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I 



A TREATISE 






ON THE 



PRINCIPLES AND PRACTICE 

OF MEDICINE 



BY 

AKTHUR El EDWARDS, A.M., M.D. 

PROFESSOR OF THE PRINCIPLES AND PRACTICE OF MEDICINE AND OF CLINICAL MEDICINE AND DEAN 

OF THE FACULTY IN THE NORTHWESTERN UNIVERSITY MEDICAL SCHOOL, CHICAGO; 

ATTENDING PHYSICIAN TO MICHAEL REESE HOSPITAL, ETC. 



THIRD EDITION, THOROUGHLY REVISED, AND REWRITTEN 



ILLUSTRATED WITH 80 ENGRAVINGS AND 23 PLATES 




LEA & FEBIGER 

PHILADELPHIA AJNT D NEW YORK 
1916 



(P 







Entered i e Act of Congress, in the year 1916, by 

I & FEBIGER, 
in the Off ji tin rian of Congress. All rights reserved. 



fk.f 



m -6 1916 



LC Control Number 




©CIA420270 

\ > 



tmp96 028691 



PREFACE TO THE THIRD EDITION 



The demand for a new edition of a work in so highly developed a 
field of medical literature is both a commendation and a summons 
to improvement. The author has spared no effort in complying. The 
real advances throughout this enormous and active domain have been 
incorporated, and the whole work has moreover been virtually re- 
written to secure increased brevity and clearness. The result is 
indicated by the fact that a vastly greater amount of information is 
furnished in a space decreased by some two hundred pages. 

A few of the additions and changes may be mentioned. Particu- 
lar attention has been given to therapeutic details in accordance 
with the recent awakening of the profession to the importance of logical 
treatment; numerous new preparations, and modified names and 
dosages, particularly for children, are explicitly specified. There are 
practically new chapters on ictero-anemia, the ductless glands, x-ray 
findings, erythremia, sepsis (infection, toxemia, bacteriemias), high 
calory-feeding in typhoid with a table of food values, sporotrichosis, 
blastomycosis, trichinosis, hook-worpi disease, pellagra, gas poisoning, 
the arrhythmias and other cardiac necroses, tropical splenomegaly and 
various other tropical affections. Due consideration has been given to 
the meningitis serum of Flexner and Jobling, Strong's work on amebic 
dysentery, Brill's disease, anaphylaxis, paratyphoid, blood cultures in 
typhoid and other bacteriemias, the "carriers of infection," the recent 
epidemics of meningitis and poliomyelitis, vaccines, serotherapy, the 
spirochete as the cause of syphilis and the recent status of tuberculin in 
its diagnostic and therapeutic application. The diagnostics and thera- 
peusis of cardiac failure, hypertension, diabetes, gastric and duodenal 
ulcer, constipation, drug addictions, neuralgias, etc., have been elabo- 
rated fully. New plates are introduced, illustrating the diphtheria 
bacillus and its cultural appearance, the Spirochete pallida and refringens, 
and x-ray plates in gastric subjects. 

The chapters on tuberculosis and syphilis are designedly amplified, 
as these diseases touch every organ, enter every specialty, and attain 
as great sociological as medical importance; indeed, an understanding 



iv PREFACE TO THE THIRD EDITION 

of these maladies is almost an understanding of medicine. The Was- 
sermann and luetin tests, congenital lues, and new matter on mercury 
and salvarsan are treated with much detail, because of their colossal 
importance. Attention has been given to numerous criticisms and many 
minor alterations have been made in the interest of logic, clarity and 
conciseness. 

So wide is the range of Modern Practice that an author who would 
cover it in a single volume, and a reader who would grasp it intelli- 
gently, must approach their respective tasks with the aid of thorough 
system. An effort has been made to deal with the subject in this 
manner, from its main divisions, which follow the most rational classi- 
fication, down to the subordinate paragraphs. Careful use has been 
made of types of various prominence to facilitate the finding of a topic 
and the appreciation of its importance. With the vast mass of material, 
an attempt has been made to so arrange the facts that the reader may 
grasp the process of reasoning. Causative pathology has been blended 
with the consecutive clinical features of disease, reasons have been 
given for facts, exceptions have been subordinated to what is usually 
found at the bedside, and the allurements of typical clinical pictures and 
dogmatic generalizations have been avoided because they hold neither 
in practice nor at the postmortem table. 

The author also conceives that a book on Practice should be well 
directed, which implies that it should deal adequately with scientific 
theories and principles, but that it should recognize that the final 
object of its existence is the application of knowledge to the cure or 
alleviation of disease. According//, an unusual amount of space has 
been devoted to treatment, to the detailed consideration of drugs and 
to numerous formula? and prescriptions ready for the student to use 
or improve upon. The physiological action of drugs has been dwelt 
upon carefully because, in the writer's experience, the symptoms of 
disease may be confounded with those of the remedies exhibited for 
its cure. The index embraces the chief references to the remedies and 
the formulae for their exhibition, and the table of contents sketches the 
general scheme of arrangement. 

The render will also find a large number of tables giving the differ- 
ential diagnosis of diseases likely to be confused, and in many instances, 
of entire subjects, such as those of the liver, brain and kidney, the 
chief eruptive diseases and those of the typhoid group. They are prac- 
tical, though necessarily schematic. Nowadays the border-lines of 
surgery and medicine overlap, and the practitioner, internist and sur- 
geon must he familiar with the province of each other. For this reason, 



PREFACE TO THE THIRD EDITION v 

as far as the scope of the treatise admits, surgical indications and results 
are introduced. 

Names and dates are employed to give credit, where it is possible, 
to the great workers in the history of Medicine. 

The writer wishes to acknowledge the extremely careful attention 
bestowed by the Publishers upon every literary and typographical 
detail, and the assistance of Dr. Milton Mandel in the proof reading. 

A. R. E. 

Chicago, 1916. 



CONTENTS. 



SECTION I. 



The Specific Infections. 

Bacterial Diseases 
Septic Infections 
Typhoid Fever . 
Erysipelas 
Pneumonia . 
Diphtheria 
Cerebrospinal Fever 
Acute Poliomyelitis 
Influenza (La Grippe) 
Pertussis (Whooping-cough) 
Cholera Asiatica 

The Plague 

Dysentery 

Shiga's Bacillary Form of Dysentery 

Amebic Dysentery 

Indeterminate Dysenteries 
Malta Fever 
Anthrax .... 

External Anthrax 

Internal Anthrax 
Glanders 

Tetanus .... 
Gonorrheal Infection 
Tuberculosis 

Tuberculosis Miliaris Acuta 

Tuberculous Meningitis . 

Tuberculosis of the Lungs (Phthisis, Consumption 

Tuberculosis of the Lymph Glands . 

Tuberculosis of the Serous Membranes 

Tuberculosis of the Brain and Meninges 

Tuberculosis of the Eye 

Tuberculosis of the Alimentary Tract . 

Tuberculosis of the Genito-urinary Tract 

Tuberculosis of the Upper Respiratory Tract 

Tuberculosis of the Heart and Vessels 

Tuberculosis of the Bones and Joints 

Tuberculosis of the Skin . 

Treatment of Tuberculosis 

Leprosy 

Non-bacterial Fungus Infections 
Actinomycosis 



17 
17 
24 
58 
62 
78 
89 
96 
102 
106 
111 
115 
118 
119 
120 
123 
125 
127 
128 
129 
130 
133 
137 
139 
146 
150 
152 
168 
171 
175 
175 
175 
177 
180 
181 
181 
183 
183 
190 
193 
193 



vni CONTENTS 

Non-bacterial Fungus Infections — 

Nocardiosis 196 

Sporotrichosis 196 

Oidiomycosis 196 

Mycetoma 197 

Aspergillosis 197 

Protozoan Infections 197 

Syphilis (Pox, Variola Magna, Lues Venerea) 197 

Acquired Syphilis 198 

Skin 201 

Lymph Glands 203 

Gastro-intestinal Tract 203 

Spleen 205 

Liver 205 

Kidneys 207 

Circulation 207 

Respiratory Tract 209 

Nervous System 210 

Eye and Ear 214 

Genitalia 216 

Bones, Joints and Muscles 217 

Mammae 218 

Diagnosis of Syphilis 219 

Congenital Syphilis 221 

Treatment of Syphilis 224 

Malaria 229 

Recurrent Fever '. 243 

Kala-azar 245 

Trypanosomiasis 246 

Other Protozoa 247 

Amebiasis 247 

Yaws, or Frambesia 247 

Trichomonas 247 

Lamblia 247 

Coccidia 247 

Infections of Doubtful Etiology 247 

Smallpox, Variola, Vaccination 247 

Chicken-pox (Varicella) 259 

Scarlet Fever (Scarlatina) ' . 260 

Measles (Morbilli, Rubeola) 270 

Rubella 275 

Typhus Fever 276 

Epidemic Parotitis (Mumps) 279 

Acute Articular Rheumatism (Rheumatic Fever) 281 

Dengue 289 

Yellow Fever 291 

Hydrophobia (Lyssa; Rabies) 294 

Febricula 298 

Glandular Fever 298 

Miliary Fever 299 

Weil's Disease (Acute Febrile Jaundice) 299 

Milk Sickness 300 

Rocky Mountain Fever 300 

Foot-and-mouth Disease 1 . . .' . 301 



CONTENTS ix 

Infections of Doubtful Etiology — 

Rat-bite Disease 301 

Psittacosis 302 

Metazoan Infections 302 

Diseases Caused by Cestodes 302 

Tenia Solium 302 

Tenia Saginata (Mediocanellata) 304 

Other Teniae Occurring in Man 304 

Tenia Echinococcus (Echinococcus Diseases) 305 

Echinococcus of the Lung 306 

Diseases Caused by Nematodes 307 

Ascaris Lumbricoides 307 

Oxyuris Vermicularis (Seat-worm, Pin- or Thread-worm) .... 308 

Trichina (Trichinella) Spiralis; Trichinosis 308 

Ankylostoma (Uncinaria) 311 

Filaria 314 

Dracunculus (Filaria) Medinensis . . 315 

Trichocephalus, Dispar or Whip-worm 315 

Strongyloides Intestinalis 316 

Diseases Caused by Trematodes (Distomiasis) .316 



SECTION II. 

Diseases of the Circulation. 

Diseases of the Heart Muscle 319 

Introductory Physiology • 319 

Dilatation of the Heart 320 

Hypertrophy of the Heart 324 

Atrophy of the Heart 327 

Fatty Heart 327 

Acute Myocarditis 328 

Acute Circum script Myocarditis 329 

Fragmentation of the Heart Muscle 329 

Chronic Myocarditis (Chronic Fibrous or Interstitial Myocarditis, Myo- 
fibrosis Cordis) 329 

Rupture of the Heart 332 

Angina Pectoris 333 

Tumors of the Heart .336 

Cardiac Thrombosis — Thrombosis Cordis 337 

Neuroses of the Heart 337 

Palpitation of the Heart 337 

Arrhythmia 339 

Tachycardia 340 

Bradycardia 341 

Diseases of the Endocardium . 343 

Endocarditis ' 343 

Acute Endocarditis ' 344 

Malignant (Ulcerative or Septic) Endocarditis 344 

Acute Verrucose or Benign Endocarditis 348 

Chronic Endocarditis, Chronic Valvular Disease 350 

Aortic Insufficiency (Corrigan's Disease) 351 

Aortic Stenosis 356 



CONTENTS 



Diseases of the Endocardium — Chronic Endocarditis 
Mitral Insufficiency . 
Mitral Stenosis 
Pulmonary Insufficiency 
Pulmonary Stenosis . 
Tricuspid Insufficiency 
Tricuspid Stenosis 
Combined Valvular Lesions 
General Symptoms of Valvular Disease 
Prognosis of Valvular Disease 
Treatment of Valvular Disease . 

Congenital Heart Disease 

Pulmonary Stenosis 

Defects of the Interauricular Septum 
Defects of the Interventricular Septum 
Patency of the Ductus Botalli 
Persistent Isthmus Aortse 
Aortic Atresia or Stenosis 
Tricuspid Stenosis or Atresia 
Transposition of the Arteries and Veins 
Valvular Anomalies . 
Anomalies in Location and Development 
Diseases of the Pericardium 

Pericarditis 

Fibrinous (Plastic) Pericarditis 
Pericarditis with Effusion 
Adhesive Pericarditis . 
Pneumopericardium 
Hydropericardium (Hydrops Pericardii) 
Hemopericardium . 
Diseases of the Arteries 

Arteriosclerosis .... 

Aneurysm 

Abdominal Aneurysm 
Acute Aortitis and Arteritis 
Rupture of the Aorta . 



and Decompensation 



357 

359 

362 

362 

363 

365 

365 

366 

370 

371 

378 

378 

379 

379 

379 

379 

380 

380 

380 

380 

380 

381 

381 

382 

382 

389 

391 

391 

392 

392 

392 

400 

408 

410 

410 



SECTION III. 



Diseases of the Respiratory Tract. 



I diseases <>f the Nose 

V.cute Rhinil is. Coryza 

I [ay Fever 

( Ihronic Rhinitis 

The Hypertrophic Form 
The \l rophic form 
' Rhinitis Fibrinosa 
Epistaxia 

Di I the Larynx 

\'iitr ( Satarrhal Laryngitis 
( 'limine ( Satarrhal Laryngitis 
Edema of t he Larynx 



411 
411 
412 
413 
413 
413 
413 
414 
414 
414 
416 
417 



CONTENTS 



XI 



Lung Cirrhosis, Fibroid Phthisis 



Diseases of the Larynx — 

Perichondritis Laryngis 

Ulcerations and Neoplasms of the Larynx 
Diseases of the Trachea and Bronchi . 

Acute Bronchitis 

Chronic Bronchitis 

Fibrinous Bronchitis .... 
Bronchial Dilatation, Bronchiectasis 
Tracheal and Bronchial Stenosis . 

Tracheal Stenosis . 

Bronchial Stenosis 
Bronchial Asthma 
E ' eases of the Lung 
Emphysema 
Bronchopneumonia 
Indurative Pneumonia, 
Pneumokoniosis 
Atelectasis . 
Abscess of the Lung 
Gangrene of the Lung 
Tumors of the Lung 

Carcinoma . 

Sarcoma and Lymphosarcoma 

Other Tumors of the Lung 
Circulatory Affections of the Lung 

Active Congestion 

Passive Congestion; Hypostasis 

Infarct; Embolism 

Edema of the Lungs 

Hemoptysis 
)iseases of the Pleura 
Pleurisy . 
Pneumothorax 
Hydrothorax 
Hemothorax 
Chylothorax 
Pleural Tumors 
Hseases of the Mediastinum 
Mediastinal Tumors 
Mediastinitis 
Mediastinal Hemorrhage 
Interstitial Emphysema 



417 
418 
418 
418 
421 
423 
423 
426 
426 
426 
427 
430 
430 
434 
438 
440 
441 
442 
444 
446 
446 
448 
448 
448 
448 
448 
449 
450 
450 
453 
453 
468 
472 
473 
473 
474 
474 
474 
475 
476 
476 



SECTION IV. 

Diseases of the Digestive Tract. 



)iseases of the Mouth . 
Catarrhal Stomatitis 
Stomatitis Ulcerosa 
Aphthous Stomatitis 
Parasitic Stomatitis 
Gangrenous Stomatitis 



477 
477 
477 
478 
479 
479 



xii CONTENTS 

Diseases of the Tongue 480 

Eczema 480 

Leukoplakia 480 

Acute Glossitis 480 

Glossitis Desiccans 480 

Diseases of the Salivary Glands 481 

Ptyalism, Salivation, Hypersecretion, Sialorrhea 481 

Xerostomia 481 

Parotitis .481 

Angina Ludovici 482 

Sialodochitis Fibrinosa 482 

Sialolithiasis 482 

Diseases of the Pharynx 483 

Acute Pharyngitis 483 

Chronic Pharyngitis 483 

Phlegmonous Pharyngitis 484 

Retropharyngeal Abscess 484 

Pharyngeal Ulceration 484 

Diseases of the Tonsils 4 

Acute Follicular or Lacunar Tonsillitis 4 ■ 

Suppurative Tonsillitis 4 

Chronic Tonsillitis N . . . 4 

Diseases of the Esophagus 4 * 

Inflammation, Necrosis, Ulceration .... T* 4 

Esophagitis 489 

Necrosis 41)0 

Ulceration ,•«.-'- 490 

Stenosis or Stricture of Esophagus 490 

Dilatation, Diverticulum v . .,.*• 4 w 

Cancer of the Esophagus "* . 494 

Perforation; Rupture; Hemorrhage of the Esophagus 495 

Motor and Sensory Disturbances of the Esophagus 495 

Diseases of the Stomach 496 

Acute Gastritis (Acute Catarrh, Acute Dyspepsia) 496 

Simple Gastritis 496 

Gastritis Toxica (Venenata) . . 497 

Phlegmonous Gastritis 497 

Diphtheritic Gastritis 4 

Parasitic Gastritis 498 

Chronic Gastritis 4 - 

Achylia Gastrica 5 

Dilatation of the Stomach; Motor Insufficiency 504 

Acute Dilatation o 

Chronic Dilatation and Motor Insufficiency 5 ' 

Changes to the Form, Size and Location of the Stomach 5 

Qlcer of the Stomach and Duodenum 50| 

Cancer of the Stomach 5i€ 

Hematemesis 5 

Neuroses of the Stomach f) 

Secretory Neuroses 5 

Hyperchlorhydria 5 

Gastrosuccorrhea (Hypersecretion; Continuous Secretion) 529 

II \|>< >secret ion 530 

Motor Neuroses of the Stomach . . . 5 



CONTENTS xiii 

Diseases of the Stomach — Motor Neuroses — ■ 

Irritative Types 531 

Depressive Motor Neuroses (Lessened Motility) 532 

Sensory Neuroses of the Stomach 532 

Hyperesthesia 532 

Gastralgia • 532 

Disturbances in the Sense of Hunger and Appetite 533 

Mixed Neuroses of the Stomach 533 

Diseases of the Intestines 534 

Acute Enteritis 534 

Chronic Enteritis 536 

Enteritis (Colitis) Mucosa or Membranacea 538 

Diphtheritic, Croupous and Phlegmonous Enteritis 539 

Intestinal Ulceration 539 

Intestinal Disorders in Infants 540 

Appendicitis 544 

Intestinal Obstruction 548 

Intussusception (Invagination) 548 

Strangulation 549 

Volvulus and Knots 550 

Strictures 551 

Tumors 551 

Foreign Bodies 551 

Dynamic Ileus 552 

Intestinal Tumors . 553 

Enteroptosis 555 

Dilatation of the Colon 556 

Intestinal Hemorrhage 557 

Piles 557 

Diarrhea 558 

Constipation 558 

Intestinal Diverticula 563 

Nervous Affections of the Bowel 563 

Neuroses of Motility 563 

Neuroses of Sensation 563 

Neuroses of Secretion 564 

Affections of the Mesentery 564 

Inflammation 564 

Hemorrhage 564 

Diseases of the Mesenteric Vessels 564 

Affections of the Chyle Vessels . . . . . .564 

Mesenteric Tumors 564 

Diseases of the Liver . 565 

Acute Yellow Atrophy 565 

Portal Cirrhosis 567 

Biliary Cirrhosis 573 

Abscess of the Liver 575 

Solitary or Tropical Abscess 576 

Tumors of the Liver 578 

Echinococcus Cysts of the Liver 580 

Multilocular or Alveolar Echinococcus 582 

Fatty Liver 582 

Amyloid Liver 583 

Anomalies of Form and Location of the Liver 584 



xiv CONTENTS 

Diseases of the Liver — Anomalies of Form and Location — 

Wandering Liver 584 

Corset Liver 584 

Affections of the Bloodvessels of the Liver 585 

Active Hyperemia of the Liver 585 

Passive Hyperemia of the Liver 585 

Pylethrombosis — Pylephlebitis 586 

Affections of the Hepatic Artery and Vein . 588 

Diseases of the Gall-bladder and Bile Vessels 588 

Icterus 588 

Cholelithiasis 591 

Cholecystitis ' 597 

Cholangitis, Catarrhal Icterus, Congenital Occlusion . . . . . 598 

Suppurative Cholangitis 598 

Acute Catarrhal Jaundice 598 

Chronic Catarrhal Cholangitis . 599 

Congenital Occlusion of the Bile Ducts 599 

Tumors of the Gall-bladder and Bile Vessels 599 

Cancer of the Gall-bladder 599 

Tumors of the Extra-hepatic Bile Ducts 600 

Diseases of the Pancreas 601 

Acute Pancreatitis; Pat Necrosis 601 

Chronic Pancreatitis 603 

Pancreatic Apoplexy 603 

Lithiasis 604 

Pancreatic Cysts 604 

Tumors of the Pancreas 605 

Diseases of the Peritoneum . 607 

Acute Diffuse Peritonitis 607 

Chronic Diffuse Peritonitis . 610 

Localized Peritonitis . 611 

Suppurative Forms 611 

Subphrenic Abscess and Pyopneumothorax Subphrenicus . . 611 

Suppuration in the Lesser Peritoneum '. 612 

Pelvic Abscess 612 

Adhesive or Indurative Forms 612 

Chronic Hemorrhagic Peritonitis ' 612 

Carcinoma of the Peritoneum 613 

Ascites 613 

Chylous and Adipose Ascites 617 



SECTION V. 

Diseases of the Kidney. 

Acute Nephritis 619 

Chronic Nephritis 624 

Chronic Parenchymatous Nephritis 624 

Chronic Interstitial Nephritis 627 

Treatment of Chronic Nephritis 633 

Passive Congestion. Embolism 638 

I '. i ssive Congestion 638 

Embolism 639 



CONTENTS xv 

Amyloid Degeneration of the Kidney 639 

Malformations of the Kidney 642 

Malformations and Structural Anomalies of the Kidney . . . • . . . 642 

Movable Kidney 643 

Anomalies of Renal Secretion 644 

Albuminuria 644 

Hematuria 647 

Hemoglobinuria 648 

Pyuria . 649 

Chyluria 649 

Lipuria 650 

Phosphaturia 650 

Lithuria 650 

Oxaluria . 651 

Indicanuria ...... 651 

Alkaptonuria 651 

Hydrochinon 651 

Hematoporphyrinuria 651 

Pyelitis. Pyelonephritis. Suppurative Nephritis 652 

Pyelitis !' .... 652 

Suppurative Nephritis 654 

Perinephric Abscess 654 

Hydronephrosis 655 

Renal Calculus (Nephrolithiasis) 657 

Tumors of the Kidney 661 

Cancer 661 

Sarcoma 663 

Hypernephroma 663 

Other Tumors 663 

Cystic Degeneration 664 

Renal Parasites 665 

Echinococcus Cysts 665 



SECTION VI. 

Diseases of the Blood. 

Chlorosis 667 

Pernicious Anemia 672 

Secondary Anemia 678 

Acute Posthemorrhagic Anemia 678 

Chronic Secondary Anemia 679 

Leukemia 680 

Acute Lymphatic Leukemia 680 

Chronic Lymphatic Leukemia 682 

Myeloid Leukemia 683 

Pseudoleukemia 687 

Erythremia 691 

The Hemorrhagic Diseases 692 

Purpura 692 

Symptomatic Purpura 692 

Purpura Simplex 692 

Purpura (or Peliosis) Rheumatica 692 



xvi CONTENTS 

The Hemorrhagic Diseases — Purpura — 

Purpura Hemorrhagica 693 

Hemorrhagic Diseases of the Newborn 694 

Syphilis Hemorrhagica Neonatorum 694 

Winckel's Disease 694 

Morbus Maculosus Neonatorum 694 

Scurvy 695 

Infantile Scurvy — Barlow's Disease . . . 697 

Hemophilia • 698 



SECTION VII. 

Diseases of the Ductless Glands. 

Diseases of the Suprarenal Glands 701 

Addison's Disease 701 

Other Affections of the Suprarenal Glands 704 

Diseases of the Spleen 705 

Acute Splenic Tumor 705 

Chronic Splenic Tumor 705 

Embolism and Abscess . . . 705 

Perisplenitis 706 

Amyloid Spleen 706 

Rupture of the Spleen . 706 

Movable or Floating Spleen . 706 

Primary Splenomegaly " . • . 707 

Diseases of the Thyroid Gland 707 

Goitre 707 

Exophthalmic Goitre (Hyperthyroidism) 709 

Myxedema 712 

Cretinism 712 

Myxedema of Adults 713 

Cachexia Thyreopriva or Operative Myxedema 714 

Treatment of Myxedema, Cretinism and Cachexia Thyreopnya . . . 714 

Diseases of the Parathyroid Glands 715 

Tetany • 715 

Diseases of the Thymus Gland 718 

Lymphatism (Status Lymphaticus) 719 

Diseases of the Hypophysis «. 719 

Acromegaly 720 

Infantilism 722 



SECTION VIII. 

Constitutional Diseases. 

Diabetes Mellitus 725 

Diabetes' Insipidus 737 

Gout " . . 738 

Rickets 742 

Obesity 746 

Adiposis Dolorosa or Dcrcum's Disease 747 



CONTENTS xvii 

SECTION IX. 

Diseases of the Nervous System. 

Diseases of the Brain . . . . . . . . 749 

Cerebral Localization 749 

The Motor Cortex 749 

The Cortex of the Parietal Lobes 753 

The Cortex of the Occipital Lobes 753 

The Cortex of the Temporal Lobes 753 

The Frontal Cortex and Aphasia 754 

Motor Aphasia 754 

Sensory Aphasia 755 

Auditory Aphasia 755 

Visual Aphasia 756 

Centrum Ovale 756 

The Internal Capsule 756 

Anterior Limb 756 

Knee ' .757 

Posterior Limb 757 

The Corpus Striatum 758 

The Optic Thalamus 758 

The Corpora Quadrigemina 758 

The Cms (Cerebral Peduncle) 759 

The Pons 760 

The Cerebellum 761 

Circulatory Diseases of the Brain 763 

Anemia of the Brain 763 

Hyperemia of the Brain 763 

Edema of the Brain . • 764 

Cerebral Hemorrhage . . 765 

Cerebral Embolism 775 

Cerebral Thrombosis 779 

Intracranial Aneurysms 782 

Sinus Thrombosis 783 

Infantile Cerebral Paralysis 786 

The Hemiplegic Form 786 

The Double Hemiplegic or Diplegic Form 787 

Brain Tumors 789 

Inflammation of the Brain 797 

Encephalitis 797 

Abscess of the Brain 799 

Dementia Paralytica 802 

Chronic Bulbar Paralysis 808 

Asthenic Bulbar Paralysis. Myasthenia Gravis 810 

Apoplectiform Bulbar Paralysis 811 

Progressive Nuclear Ophthalmoplegia . 811 

Hydrocephalus 811 

Chronic External Hydrocephalus 812 

Chronic Congenital Internal Hydrocephalus . . . ■ 812 

Acquired Chronic Hydrocephalus 813 

Diseases of the Cerebral Meninges 814 

Pachymeningitis 814 



xvm CONTENTS 

Diseases of the Cerebral Meninges — 

Meningeal Hemorrhage 816 

Acute Suppurative Leptomeningitis 816 

Serous Meningitis 818 

Chronic Leptomeningitis 818 

Diseases of the Spinal Cord 819 

General Anatomical, Physiological and Symptomatic Considerations . 819 

Diseases of the Spinal Meninges 829 

Hemorrhage 829 

Pachymeningitis 829 

Tumors of the Spinal Cord and its Membranes 830 

Tumors of the Membranes 830 

Tumors in the Cord Substance . . . .831 

Circulatory Disturbances. Hemorrhage. Trauma of the Cord .... 833 

Anemia of the Spinal Cord . . • 833 

Embolism and Thrombosis (Myelomalacia) . 833 

Hemorrhage (Hematomyelia) 833 

Caisson or Divers' Paralysis 834 

Brown-Sequard's Paralysis . . .... . 835 

Inflammation of the Cord 836 

Acute Myelitis ' 837 

Acute Multiple Disseminated Myelitis 841 

Chronic Myelitis 841 

Subacute and Chronic Poliomyelitis . 841 

Landry's Paralysis 842 

Multiple Sclerosis 843 

Syringomyelia . 846 

System Diseases 849 

System Diseases of the Sensory Tract 849 

Tabes Dorsalis, Locomotor Ataxia 849 

System Diseases of the Motor Tract . . , . . 857 

Spastic Spinal Paraplegia 857 

Amyotrophic Lateral Sclerosis 858 

Progressive Spinal Muscular Atrophy 860 

Neural Muscular Atrophy 862 . 

Muscular Dystrophy 862 

Pseudohypertrophic Muscular Paralysis 862 

Infantile Atrophic Form, with or without Facial Involvement 863 

The Juvenile Form of Erb , 864 

Combined System Diseases 864 

Hereditary Ataxia, Friedreich's Ataxia 865 

Ataxic Paraplegia 866 

Other Combined System Diseases 866 

Diseases of the Peripheral Nerves 867 

Mononeuritis 867 

Multiple Neuritis 869 

Neuroma 872 

Diseases of the Cranial Nerves 873 

Olfactory Nerve 873 

Optic Nerve . 873 

The Retina 1 873 

Optic Nerve 873 

Chiasm 873 

Optic Tract . 874 



CONTENTS xix 

Diseases of the Cranial Nerves — Optic Nerve 

Optic Centre 874 

Functional and Toxic Blindness 875 

Ocular Paralysis; Third, Fourth and Sixth Nerves . . . . . . . 875 

Paralysis of the Third Nerve 876 

Internal Oculomotor Palsy 877 

Recurrent Palsy ' . . . . 877 

Paralysis of the Fourth (Trochlear) Nerve 877 

Paralysis of the Sixth Nerve 877 

Combined Eye Paralysis 877 

Progressive Nuclear Ophthalmoplegia 879 

Sympathetic Paralysis 879 

Ocular Muscular Spasms 880 

Fifth Nerve (Trigeminus; Trifacial Nerve) 880 

Paralysis 881 

Masticatory Spasm 882 

Progressive Facial Hemiatrophy 882 

Facial Hemihypertrophy 882 

Seventh or Facial Nerve 883 

Peripheral Facial Paralysis 883 

Facial or Mimetic Spasm (Tic Convulsif) 887 

The Eighth or Auditory Nerve 887 

Meniere's Disease, Auditory Vertigo (Vertigo ab aure lsesa) . . . 888 

Ninth or Glossopharyngeal Nerve 890 

Tenth or Vagus Nerve m 890 

Pharyngeal Branches 890 

Paralysis 890 

Laryngeal Branches 892 

Anesthesia and Hyperesthesia of the Larynx 892 

Laryngeal Spasm 892 

Pulmonary Branches 894 

Cardiac Branches 894 

Gastric Branches 894 

Eleventh or Spinal Accessory Nerve (External Portion) 894 

Paralysis 895 

Accessory Spasm, Spasmodic Torticollis or Wryneck . . . . . 895 

Twelfth Nerve ' 896 

Spasm 896 

Diseases of the Spinal Nerves 897 

The Phrenic Nerve 897 

Paralysis 897 

Phrenic Spasm ...... 897 

The Posterior Thoracic Nerve 898 

The Suprascapular Nerve 898 

The Musculospiral Nerve 898 

The Median Nerve 899 

The Ulnar Nerve .899 

Combined Paralysis of the Arm Nerves 900 

Brachial Neuritis 900 

The Nerves of the Trunk 901 

The Nerves of the Lower Extremities 901 

The Lumbar Plexus 901 

Anterior Crural Nerve 901 

Obturator Nerve 901 






xx CONTENTS 

Diseases of the Spinal Nerves — The Nerves of the Lower Extremities — 

Superior Gluteal Nerve 902 

The Sacral Plexus 902 

Great Sciatic Nerve 902 

Caudal Lesions 903 

Sciatic Neuritis 903 

The Neuroses 905 

Hysteria 905 

Neurasthenia 912 

The "Traumatic Neuroses" . . . 918 

Epilepsy 919 

Infantile Convulsions 926 

Chorea and Choreiform Affections . . . 926 

Occupation or Fatigue Neuroses; Writer's Cramp 932 

Myotonia (Thomsen's Disease) 933 

Paralysis Agitans 934 

Periodic Family Paralysis ' 936 

Migraine 937 

Neuralgia '. . . 939 

Vasomotor and Trophic Neuroses . 944 

Erythromelalgia " 944 

Acroparesthesia 944 

Spontaneous Symmetrical Gangrene . 945 

Acute Angioneurotic Edema , 945 

Chronic Hereditary Trophedema 946 

Hydrops Articulorum Intermittens . • 946 

Scleroderma 946 

Ainhum 947 



SECTION X. 

Diseases of the Locomotor System. 

Diseases of the Muscles 949 

Myositis 949 

Myositis Ossificans 950 

Muscular Rheumatism (Myalgia) 950 

Amyotonia Congenita 951 

Diseases of the Joints ' . 951 

Arthritis Deformans and Chronic Rheumatism 951 

Diseases of the Bones 956 

Osteomalacia 956 

Achondroplasia 956 

Fragilitas Ossium 957 

Oxycephaly 957 

SECTION XI. 

Intoxications. Sunstroke. 

Alcoholism 959 

Acute Alcoholism 959 



CONTENTS 



xxi 



Alcoholism — 

Chronic Alcoholism 960 

Delirium Tremens 961 

Opium Poisoning ' 963 

Acute Poisoning 963 

Chronic Morphinism 963 

Lead Poisoning 965 

Acute Poisoning 966 

Chronic Poisoning 966 

Arsenical Poisoning 968 

Chronic Poisoning 968 

Food Poisoning 969 

Meat Poisoning 969 

Poisoning by Milk 970 

Poisoning by Fish 970 

Grain Poisoning 970 

Ergotism 970 

Lathyrism 971 

Potato Poisoning 971 

Pellagra .971 

Beriberi 972 

Illuminating-gas Poisoning 974 

Sunstroke > 975 

Index 979 



SECTION I. 

THE SPECIFIC INFECTIONS. 



BACTERIAL DISEASES. 



SEPTIC INFECTIONS. 



Synonyms. — Sapremia, septicemia (sepsis), pyemia, septicopyemia. 

Definition. — To understand sepsis is to understand all infections. 
Sepsis is no longer a purely surgical or obstetrical term; today it is more 
important in medicine than surgery. Intoxications are the result of the 
absorption of substances elaborated by microorganisms. Infections 
are always due to microorganisms, which enter the body and multiply 
there. Tetanus is an infection, yet it is non-contagious. Contagion refers 
to infection by direct contact, as in scarlatina, or by indirect mc^ris, 
as water infected by typhoid dejecta. Sapremia is the absorption 
of putrescent substances, but not of the germs which develop them. 
Toxemia, a broader term, includes intoxication and sapremia; toxins 
in the blood are largely the result of bacterial metabolism. Prob- 
ably all pathogenic bacteria produce toxins; the latter are divisible 
into intracellular toxins, found in the bodies of microorganisms— the 
case in most toxemias — and the extracellular toxins, thrown free into the 
circulation. Septicemia (sepsis) is the presence in the blood of micro- 
organisms (bacteriemia) — usually pyogenic — without hematogenous sup- 
puration or metastasis. Pyemia is infection, caused by microorganisms, 
which leads to hematogenous suppuration or metastasis. Septicopyemia 
is septicemia (bacteriemia) plus pyemia (metastatic suppuration). 

General Groups. — 1. Some infections — such as carbuncles, puerperal 
parametritis, diphtheria and tetanus — are local so far as the causal 
microbe is concerned, and their symptoms are due to absorbed toxins 
(toxinemia, toxemia). Local reactive inflammation seeks to protect 
the body against generalization of the microbes, by means of (i) mechani- 
cal measures, as pouring out of the leukocytes, deposition of fibrin or 
development of connective tissue ; (ii) phagocytosis ; and (iii) bacteri- 
cidal and antitoxic action of the lymph and blood serum. 

2. Other infections — such as carbuncles, puerperal sepsis, anthrax, 
and gonorrhea — at first local, may become general when their germs enter 
the blood (bacteriemia or septicemia) . Some infections, especially typhoid 
and pneumonia, once considered local, are always general. 

3. Still other infections, often resulting from the same microorganisms, 
cause metastatic suppuration (pyemia). Among, these are^im^ 



^*. 



18 BACTERIAL DISEASES 

abscesses from carbuncles, puerperal fever, typhoid osteomyelitis, pneu- 
mococcic endocarditis, and gonorrheal arthritis. It is frequently clinically 
difficult to preserve these types which so often blend; what is seemingly 
toxemia may prove bacteriemia if blood cultures are made; apparently 
pure bacteriemia may prove pyemia at necropsy; all three grades may 
occur successively; the primary infection — e. g., with scarlatina, tuber- 
culosis, and diphtheria — whether local or general, may be complicated 
by a later secondary or a simultaneous mixed infection, especially by 
the streptococcus; again the symptoms vary, first with the variety of 
microbe and its virulence; second, with its localization (in the throat, 
lung, pelvis, etc.); and third, with the physiological resistance or sus- 
ceptibility of the patient. Subjects of malignancy, cardiac, vascular, 
nephritic, cirrhotic and other diseases, readily succumb to an ultimate 
sepsis to which the name terminal infection is applied. For these reasons 
we will discuss septic infections as a whole, and indicate such special 
etiological and clinical variations as seem necessary. 

Etiology and History of Septicopyemia. — Of the numerous causal organ- 
isms, the most common are the pyogenic cocci, the pneumococcus and colon 
bacillus; less frequent are the gonococcus, anthrax bacillus, typhoid or 
diphtheria bacillus, Friedlander's pneumobacillus, meningococcus, Bacillus 
pyocyaneus, B. influenzae, B. phlegmones emphysematosa?, B. aerogenes 
encapsulatus, and least often, the Micrococcus tetragenus, the blasto- 
mycoses, the spirilli and bacilli of Vincent, the Bacillus fusiformis, and 
the proteus group. Wunderlich (1847) spoke of spontaneous pyemia, 
and Leube (1878) of cryptogenetic (occult) septicopyemia, yet careful 
clinical and necropsy investigations reveal the atrium of infection in 94 
per cent, of cases; (1) skin lesions, such as furuncles, felons, navel in- 
fection in infants, and invisible, as well as visible wounds (staphyl- 
ococcus); (2) throat (streptococcus), as in tonsillitis, scarlatina or diph- 
theria; (3) nose (not frequent in sepsis, though in meningitis the atrium 
for the meningococcus and pneumococcus); (4) ear (pneumococcus and 
streptococcus); (5) lungs (pneumococcus); (6) intestines and bile tracts, 
gall-stone infection, appendicitis, dysenteric ulcers (colon bacillus, 
typhoid bacillus); (7) urinary tract (pyelitis from colon bacillus; vesical 
and urethral infections, chiefly by the staphylococcus, far less by the 
streptococcus and gonococcus); and (8) vagina and uterus (chiefly 
streptococcus), causing puerperal infection. 

Puerperal fever, primary wound fever and severe late pyemic infection 
were known to Hippocrates. 

Boerhaave (1720) declared that secondary abscesses were due to 
pus in wounds. John Hunter (1774) associated purulent phlebitis and 
pyemia. D'Arcet (1842) drew a sharp distinction between toxemia 
and pyemia. In 1840 Virchow discovered that the "pus in the veins" 
was softened thrombi and that the "pus in the blood" was merely leuko- 
cytosis; he used the terms septicemia and pyemia in their modern 
construction. Following his work, the subject was clarified by 
bacteriology. 

General Pathology and Symptomatology. — (A) General Toxemic 
••'""•i^ t- Fever. The virulence of the germ and its toxin (rather 



SEPTIC INFECTIONS 19 

than its variety) governs the intensity of the toxemic symptoms. Fever is 
associated with cellular reactions which form specific antibodies (anti- 
toxins, lysins, opsonins, and agglutinins). It is difficult to state how far 
fever is benign and how far injurious. By toxemic disturbance of the 
cerebral centres regulating temperature equilibrium, more heat is 
produced and less eliminated. Fever is usually the first clinical symptom 
and in general the fever tends to be remittent or intermittent; (a) 
streptococcus infections usually produce irregular intermittent fever with 
moderate variations; (b) the staphylococcus and pneumococcus produce 
remittent or continuous fever; (c) the colon bacillus and gonococcus 
cause intermittent fever with great variations. Fever may be absent 
in very severe forms, especially before death, when the cells of the body 
are overwhelmed by an excessive production of toxins. 

2. Chills occur in septicemic and especially in pyemic forms and are 
usually irregular. They mark the discharge of bacteria or toxins into the 
circulation. 

3. Nervous toxemia may appear as unrest, delirium, stupor, dry tongue, 
and the status typhosus, or it may resemble meningitis. The sensorium 
may be clear. 

4. Vasomotor and cardiac weakness may be present with increased, 
irregular or hopping pulse; the cardiovascular system may suffer the 
same damage as in typhoid or pneumonia toxemia. 

5. Increased respiration, from augmented gaseous exchange, and 
bronchitis may be noted. 

6. Albuminuria and acute nephritis are common from microbic or 
toxemic injury. 

7. Septic diarrhea, in which the dark, perhaps bloody, movements 
number six to ten daily, may be observed. Tympanites is frequent from 
the toxins lowering the tone of the intestinal muscle. 

8. Acute splenic tumor is present. 

9. Anatomically we find cloudy swelling and fatty degeneration of the 
heart, liver and kidneys; a vascular, soft, moderately swollen spleen, 
with indistinct markings and wrinkled capsule; acute nephritis; hemor- 
rhages into the skin, retina, and mucous and serous membranes, with or 
without bacteria; lung edema, and, where there is marked anemia, 
there is fatty heart, increased iron deposit in the liver, hemorrhages 
by injury to the vessel walls or necrosis in the parenchymatous Organs 
or lymph glands. 

(B) Blood Findings. — 1. Bacteriemia is found in 50 per cent, of 
cases clinically, and in 95 per cent, at autopsy; 10 to 40 c.c. of blood are 
removed antiseptically from the median cephalic vein by an aspirating 
needle and mixed freely with bouillon. The importance of blood cultures, 
made daily, in severe or doubtful cases, cannot be overestimated. Some 
circulating bacteria are killed by the blood. In most streptococcic and 
staphylococcic infections, these organisms are found in the blood. 

2. Polymorphonuclear leukocytosis and iodophilia are very common, 
though not invariable, particularly in sepsis due to pyogenic organisms. 
The lymphocytes are generally decreased, e. g., in contrast to the typhoid 
formula (page 32). However, Cabot and others describe, in wound 



20 BACTERIAL DISEASES 

sepsis, boils and widespread streptococcic adenitis, an extreme lympho- 
cytosis, resembling acute leukemia. 

3. Anemia is usual, and may resemble the pernicious form. 

(C) Metastases. — They are apparent clinically, or first found at 
necropsy. Thrombophlebitis develops at the seat of primary infection, 
and disintegrated thrombi, containing bacteria, escape into the venous 
circulation. They lodge in the lungs or, passing them, reach the left 
heart, and arterial system. Purulent lymphangitis may, in the same 
way, cause metastatic suppuration. If "end arteries" are plugged, 
infarcts result; if the arteries are not terminal, small suppurative foci 
develop, especially where the circulation is slow, as in the liver, kidney 
and spleen. Not all infarcts suppurate, either because the germs are 
less virulent, or the embolic material is free of microbes. (1) Lung 
localization may cause multiple or single abscesses, and often sero- 
fibrinous or purulent pleurisy. (2) Cardiac metastasis develops in 21 
(even 63) per cent, of the metastatic group; endocarditis is localized 
chiefly on the mitral (62 per cent.) and aortic (22 per cent.) valves; it is 
attended by a heart murmur in only 60 per cent., and often by pericar- 
ditis; the heart muscle is sometimes the seat of abscesses. (3) Cerebral 
metastasis may cause meningitis, brain abscess or softening (encephalo- 
malacia with aphasia and hemiplegia) . (4) Renal localization may incite 
nephritis or suppurating infarcts, with albuminuria, cylindruria, pyuria 
and bacteriuria. (5) Splenic localization usually results in enlargement, 
frequently in pain, and rarely in perisplenic friction. (6) Localization 
in the bones may cause early fugitive bone pain, or later, fixed osteomye- 
litic tenderness over one or more bones, with inflammatory signs; in 
the joints (as in the postfebrile arthritides) it may cause simple pain, 
or serous or purulent synovitis; in the muscles it may produce abscesses, 
purulent edema, or Wagner's polymyositis. (7) In the skin ecchymoses 
develop in 50 per cent, of fatal cases, usually late, often symmetrical, 
and sometimes on the nose, fingers, toes or ears. Ecchymoses may be 
peculiarly significant of sepsis in the absence of other symptoms. Pustules 
and vesicles are less frequent; herpes occasionally develops, particularly 
in genito-urinary colon infections. Scarlatiniform, morbilliform, roseo- 
lous or urticarial eruptions are only toxemic. (8) In 33 per cent, retinal 
ecchymoses occur, first described by Litten as round, irregular spots or in 
streaks, with small white centres and appearing late or just before death. 
Least frequent is panophthalmitis, of which 33 per cent, is due to ulcera- 
tive endocarditis. (9) The peritoneum is chiefly involved in puerperal 
forms. (10) The slightly enlarged liver is more often due to toxic paren- 
chymatous degeneration and cardiac weakness than to abscess, which 
occurs in only 15 per cent, of cases of septicopyemia. Intestinal 
infarction is rare. In one type icterus is associated with meningeal 
symptoms. 

Some metastases develop, maybe years later than the original infection, 
as typhoid osteomyelitis. This bacterial latency is also noted in diphtheria 
in which virulent bacilli persist possibly for months in the throat; 
in tuberculosis where apparently healthy lymph glands may contain 
tubercle bacilli and perhaps also in diseases which recur, as erysipelas 



SEPTIC INFECTIONS 21 

and articular rheumatism. Recurrence may also be due to fastness or 
mutation of the infecting organism, resulting from enduring subinfection. 

Special Symptomatology. — This may be considered etiologically or 
topographically. Only the leading characteristics are presented. 

(^4) Etiological. — 1. Streptococcic injection, the most frequent primary 
and secondary septic infection, constitutes 66 per cent, of all forms, the 
coccus entering the blood in 33 per cent, of all fatal diseases. Its atrium 
is most often the throat and the female genitalia; it enters the veins 
in puerperal pyemia more often than the lymphatics (erysipelas and 
puerperal sepsis); it more often produces septicemia (65 per cent.) 
than pyemia (35 per cent.); the lungs are usually unaffected; endo- 
carditis occurs in 7 per cent.; and its course is chiefly acute, sometimes 
subacute (ulcerative endocarditis). 1 

2. Staphylococcic infection usually enters by the skin; the furuncle is 
the typical primary lesion. On the eyelids, nose or lips, this dangerous 
infection may reach the facial vein, then the ophthalmic vein and cavern- 
ous sinus. Furuncle of the neck may reach the transverse sinus. In- 
fections of the skin are the most frequent cause of osteomyelitis. Menin- 
gitis is known to have followed n felon. The coccus passes the throat 
with difficulty, but then with increased malignancy. It travels by the 
veins or lymphatics; it produces metastasis in 95 per cent, and endo- 
carditis in 6 per cent, of cases. Abscesses of the lung and kidneys and 
pustular skin eruptions are very frequent; the coccus is found very 
often in the blood and urine. Staphylococcic infection is usually 
acute. 

3. Pneumococcic Infections. — In all cases of pneumonia (q. v.) the 
pneumococcus appears in the blood (pneumococcemia). In actual 
sepsis following pneumonia, it enters the blood through the pulmonary 
veins. Infection through the ear or bile tracts is less frequent, but in 
the latter type, is particularly lethal; metastases occur in 25 per cent, 
and endocarditis in 6 per cent. The pneumococcus alone may produce 
pus in the joints, skin, thyroid and serous membranes. Netter states 
that pneumococcic sepsis is less severe than other types, but it is often 
malignant. It may be associated with the pyogenic cocci. It is yet 
unknown why lung infections so frequently cause brain metastases. 

4. Colon sepsis, which is less frequent, may follow wounds, suppu- 
ration in cholelithiasis, cystitis, pyelitis, or intestinal obstruction. Endo- 
carditis is exceptional, and sepsis (78 per cent.) is more common than 
metastasis (22 per cent.). Infection was hematogenous in the majority 
of Rovsing's 285 cases of colon infections of the urinary organs; the 
trouble began as acute nephritis or pyelitis in 180 cases, and fever, hema- 
turia and later, pyuria were common. 

5. Gonococcic infection is rather more benign than the other types. 
There may be the more common gonorrheal arthritis or gonorrheal 

1 Schottmueller differentiates three strains of streptococci by cultures on blood-agar: 
(i) S. pathogenes seu erysipelatos; fine colonies, with round, clear, hemolytic areola, (ii) S. 
mitior seu viridans; very fine green colonies, (hi) S. mucosus, possibly identical with the 
pneumococcus; the green colonies after twenty-four hours present a glistening, mucoid 
appearance. (The S. saprophyticus (anhaemolyticus) produces no change in blood-agar 
plates.) 



22 BACTERIAL DISEASES 

endocarditis, pericarditis and pleuritis. Thayer found the gonococcuS 
in the blood (v. Gonorrheal Infection). 

Other forms are less frequent, as typhoid suppuration in the pleura, 
bones, meninges, etc., sepsis from the pneumobacillus, meningococcus, 
etc. Pyocyaneus sepsis is attended by rapid pulse, vomiting, diarrhea, 
and a hemorrhagic diathesis. 

(B) Topographical. — The clinical varieties of sepsis are legion and 
might be extended to the chronic infections as the syphilitic spirochete 
sepsis, to the zoonoses, malaria, trypanosomiasis or certain intoxications 
as meat poisoning. (1) Ulcerative endocarditis; (2) cholangitic sepsis; 
(3) septic sore throat; and (4) otogenous sepsis (v. Sinus Thrombosis, 
Meningitis, Brain Abscess) will be considered elsewhere. The two 
following localizations are of importance to the practitioner and 
internalist : 

(5) Osteomyelitis is either a solitary metastasis or part of a generalized 
sepsis. Even when a single bone is involved, the blood usually contains 
the causal microorganism. It is due to the staphylococcus chiefly; then to 
mixed infection with the streptococcus, which is found in all fatal cases, 
or with the pneumococcus; and but rarely to the typhoid organism. 
In most typhoid and pneumonia autopsies, the causal bacteria are present 
in the bone-marrow. Acute osteomyelitis is most frequent in the growing 
bones of children. Trauma is a promoting element and the onset occurs 
with chill, fever, vomiting, diarrhea, headache, and bone pain. It is 
usually first seen and often mistaken by the practitioner. The rare chronic 
cases, which last one year or even thirty, may simulate sarcoma or syphilis. 

(6) Puerperal fever is caused chiefly by the streptococcus (95 per 
cent.). Its varieties are (a) toxemia or sapremia, caused by toxins or 
putrid decomposition products respectively. Even in cases apparently 
of this group, bacteriemia may be found (colon bacillus, saprophytes 
or streptococcus). The rare puerperal tetanus is wholly toxemic. (6) 
Lymphangitic form: lymphangitis, from infected vaginal or cervical 
wounds, may cause (i) moderate, benign, localized parametritis, (ii) Gen- 
eral septicemia, from vaginal or cervical wounds, infection following the 
lymph vessels through the pelvic cellular tissue to the general circulation. 
The symptoms appear within a day or so after delivery. Death may 
result in two to fourteen days, or encapsulation and massive cellulitis 
may develop, (iii) Lymphangitic peritonitis is more frequent (20 per 
cent, of fatal cases). It begins three or four days after delivery and is 
usually generalized and suppurative. Infection may travel directly to 
the peritoneum or, more often, by retrograde lymphatic routes (Vir- 
chow's "erysipelas grave internum puerperale")- It is more common in 
labor at term than in abortion. The symptoms are chill, fever, tense 
pulse, vomiting, abdominal pain and distention, and often effusion and 
diarrhea. In many apparently purely peritonitic cases bacteriemia is 
found. ' Early death is the rule, commonly in five to six days, but en- 
capsulation is possible, (c) The thrombophlebitic (pyemic) type occurs 
in 50 per cent, of fatal cases. It commonly begins in ulcerative or ichorous 
endometritis, in contradistinction to the lymphangitic form of vagino- 
cervical origin. Infective thrombophlebitis travels (i) from the upper 



SEPTIC INFECTIONS 23 

veins by way of the spermatic veins, to the cava and left renal vein; 
the phlebitis may actually extend into the vena cava; (ii) from the 
lower plexus, by way of the uterine veins into the hypogastric veins, 
and thence to the inferior cava. Bilateral venous thrombosis is common 
(45 per cent.). Metastases are common in the lungs, kidneys, joints, 
muscles, and spleen. Ulcerative endocarditis, meningitis and peritonitis 
may be present. The course may be stormy from predominating toxemia 
or slower with metastases. The fever is irregular, the pulse rapid, the 
chills severe, the anemia marked, and streptococcemia is present in over 
90 per cent. 

Diagnosis. — The direct diagnosis rests upon the detection of an atrium, 
the symptoms of toxemia and metastatic suppuration and the blood 
cultures. The differentiation from typhoid, malaria, and miliary tuber- 
culosis is fully considered on pages 46 and 47. Solitary local or visceral 
symptoms, as osteomyelitis, arthritis, endocarditis, etc., may cause con- 
fusion if not viewed in their broad relations to a possible sepsis. 

Prognosis. — The prognosis depends upon the organism, its virulence 
and dissemination, the patient's physiological resistance (whence the 
obviously poor outlook in terminal infections), and finally on the surgical 
accessibility of the primary lesion or metastatic foci. Only 17 per cent, 
of Lenhartz's cases with bacteriemia recovered, yet recoveries are recorded 
in cases of gonococcemia and streptococcemia. A stormy onset and chills 
are ominous. A case of Lenhartz with empyema, lung abscess, pan- 
ophthalmitis, diffuse venous thrombosis and multiple osteomyelitis 
recovered. Puerperal infections, with the large wound surface and 
frequent hemorrhages, are severe, the mortality of all forms being 55 
per cent., and of severe forms 65 per cent. (Curschmann) . The strepto- 
coccus has been regarded with particular dread; however, Bertelsmann 
states that the prognosis is twice as favorable as in staphylococcic in- 
vasion. 

Treatment. — Surgical prophylaxis, even in apparently insignificant 
wounds and obstetrical asepsis is important, especially in subjects 
reduced by general diseases. Treatment of existing sepsis consists 
in giving the largest possible amount of food which can be digested; 
in free administration of salt solution by rectum or transfusion, to flush 
the toxins through the kidneys; and in the free use of alcohol The treat- 
ment of hypostasis, diarrhea, vomiting and chills is symptomatic. The 
temperature is seldom influenced by drugs safely. The internal use of 
germicides is justly abandoned. We have not observed the slightest 
benefit from Crede's silver ointment. Crede's collargol has been used 
with benefit, intravenously, in doses of one to two and a half drams. 
Nuclein and 5j-ij of fresh brewers' yeast are also advised. Surgical 
intervention is indicated whenever definite accessible foci are localized. 

Vaccine and Serum Therapy. — Nature heals and the progress to re- 
covery is usual, if infection is not too rapidly fatal. The so-called im- 
munity principles reside in the phagocytes and soluble, probably protein 
bodies, preformed in the body and increasing under the stimulus of 
infection. The various portals of entrance of the infective agent into 
the body are detailed above; whereas the surfaces of the body are 



24 BACTERIAL DISEASES 

inhabited by myriads of bacteria, they resist infection usually, the 
epithelium being protective, the hydrochloric acid of the stomach, 
the overgrowth of the infective virus by the normal flora of the intestine 
and the acid reaction of the vagina combating localization, etc. Gaining 
access to the body, the microorganisms produce toxins, which in turn 
excite the production of antitoxins. The antitoxin is, then, a reaction 
product of the organism against the toxin. Immunity is active when the 
body, in response to infectious germs (antigens), protects by producing 
its own antibodies; it is passive when protection is achieved, e. g., by the 
use of antidiphtheric serum in which the antibodies formed in the blood- 
serum of another animal are employed. The immunity or protective 
forces of the body are the bacteriolysins which destroy the bacteria, the 
agglutinins which clump the virus, the antitoxins which neutralize the 
toxin and the opsonins which so alter the bacteria that they fall an 
easy prey to the phagocytes. 

Guided by the opsonic index, bacteria, dead or alive, may be injected 
to stimulate the lagging reactive powers of the body; the bacteria are 
the antigen. Vaccine therapy is indicated, theoretically, only in subacute 
and chronic infections; in acute general infections, particularly of the 
fulminating type, vaccines are contra-indicated, since they expose the 
patient to greater danger, by imposing the negative phase (in which the 
opsonic index is lowered). In septicemia, pyemia and grave sapremia, 
vaccines should be avoided or employed only with the utmost caution. 
In surface infections, in furunculosis, in lingering infections from mild 
types of parasites, and in infections with slow invasion, vaccines sometimes 
may be useful. The average interval of inoculation is five to ten days. 
The range of dosage is 100 to 1000 millions in staphylococcic infections; 
5 to 200, in streptococcic; 10 to 200 in pneumococcic ; 5 to 500 in gono- 
coccic; and 10 to 200 in colon infections. Vaccines should be autogenous. 
In commercial stock vaccines dangers linger beyond those inherent 
in vaccine therapy in general; the uncertainty of the source of these 
cultures, of their age, potency, dosage and purity are most important. 

Antistreptococcic and other sera are most uncertain. 

TYPHOID FEVER. 

The name (typhos, stupor) refers to the clouded mentality, and dates 
from Hippocrates. Bright, Louis and others recognized that ulceration 
of the bowels occurred in certain continuous fevers, but typhoid was first 
described as a disease separate from tvphus by Gerhard and Pen nock 
(1837). 

Definition. — Typhoid fever is a general infection, characterized — 

1. Etiologically by the Bacillus typhosus. 

2. Anatomically by hyperplasia and ulceration of the lymphatic 
structures of the intestine, hyperplasia of the spleen and mesenteric 
glands, and by parenchymatous degeneration in other organs. 

3. Clinically by a characteristic fever, roseolous eruption, enlarge- 
ment of the spleen, slow pulse, a peculiar serum reaction, typhoid 
bacillemia, and often by intestinal symptoms. 



TYPHOID FEVER 25 

Etiology. — The typhoid bacillus was first detected by Eberth and Koch 
(1880), and first cultivated by Graffky (1884). 

1. Characters. — It has thick, rounded ends, is three times as long 
as wide, in length is one-third the diameter of a red blood corpuscle, and 
its numbers are usually proportionate to the degree of infection. It is 
polymorphous, sometimes thread-like, contains no spores, is flagellated 
and actively motile. It is a facultative anaerobe growing on various 
media, especially on agar, gelatin and, characteristically, on potato. 
It does not produce acid, indol, ferment lactose or coagulate milk. 
It stains with aniline dyes but not by Gram's method; it produces an 
endotoxin only by the disintegration of the bacillus itself. 

Typical lesions have been produced in chimpanzees and goats. 

Its tenacity of life is great, the germ persisting for years in bone lesions 
and from three weeks to three months after death. It resists drying 
for months but in water seldom lives longer than three weeks and its 
multiplication is prevented by saprophytes. The germ may live for 
months in ice, sour milk, feces or in the upper layers of the soil. It may 
survive a year in soiled clothes, which explains contagion in washer- 
women. It is killed in a few hours by direct sunlight. 

2. Location. — It is found in the typhoid ulcers, the lymphatics of 
the mesentery, the spleen, the feces, blood, gall-bladder, urine, roseolse, 
less frequently in the lungs, esophagus and mouth, and in various second- 
ary foci, as in pleurisy, pneumonia (sputum), endocarditis, meningitis, 
parotitis, osteomyelitis and abscesses. It has been isolated from the 
blood of the fetus in maternal typhoid infections. 

3. Entrance. — Its chief and probably sole atrium is the digestive 
tract, the infection being carried in water, milk, butter, ice, vegetables 
or oysters. Water or milk infection is the usual explanation for 
"explosive" epidemics. As shown in the Spanish-American and Boer 
wars, dried feces containing the bacilli may be carried by sand, flies, 
cockroaches and Other insects. 

4. Exit. — The germ leaves the body chiefly in the feces and urine, 
which are dangerous far into convalescence; they are the chief means 
of dissemination, the disease being less often conveyed directly from one 
individual to another, although direct infection occurs in hospitals and 
camps. Lentz found that after a typhoid attack 4 per cent, of persons 
become "chronic carriers of typhoid bacilli/' the microbes remaining 
in their dejecta for one, fifteen or even fifty-four years. Soper describes 
a cook who, though perfectly well herself, was a " bacillen-trager" and 
caused 26 cases of typhoid fever in five years, and 54 typhoid infections 
are attributed to a dairy hand. The bacilli-carriers are twofold: the 
primary, who carry bacilli in the blood or stools, but resist infection 
or reaction and the secondary carriers, who have suffered infection — 
the more common class. 

Alimentary infection is the most common, occurring by water in 71 
per cent, of typhoid infections, by milk in 17 per cent., by flies in 4 per 
cent, and by clothes, dust, etc., in 8 per cent, (direct contact, 3 per cent.), 
in 35,674 cases (Schiider). Kayser holds that milk causes 27 per cent., 
water 15 per cent., and typhoid-carriers 10 per cent. 



26 BACTERIAL DISEASES 

Predisposing Etiology.— 1. Reduced Physiological Resistance. — 
Reduced resistance, as from overwork, mental depression; decreased 
hydrochloric acid formation or dilated stomach, is a frequent predisposing 
cause; yet typhoid very often occurs in the robust. It is claimed that the 
weak or emaciated are immune — e. g., those with syphilis, tuberculosis, 
cancer, endocarditis or anemia. Most cases occur in time of war among the 
poorer classes, or among recent residents in typhoid localities (Trousseau) . 

2. Season. — For unknown reasons most infections develop in the late 
summer and fall (" autumnal fever"). 

3. Age. — The years from fifteen to twenty-five include 56 per cent, 
of cases; a few cases occur in the first year of life. Their number 
increases from the first to the fifth year. Between the fifth and fifteenth 
years as many are affected as after thirty-five. The disease is relatively 
rare after fifty. 

4. Geographical Distribution. — Although it is the most common 
continued fever in temperate climates, it is a world-wide disease and 
sustains a most intimate relation to the water supply, the disposal of 
sewage, the density of population and personal hygiene. 

Immunity. — Immunity bears no relation to the severity of the disease; 
usually conferred after one attack, it is not life-long nor as frequent 
as, e. g., in scarlatina. In the Hamburg epidemic (1887) 2.4 per cent, 
of the cases were second attacks. Second attacks may equal or exceed 
the original in severity. 

Symptoms.— The general clinical picture offers more variability than 
any other infection. Typhoid is not an intestinal disease, but a general 
infection, with bacillemia. Its forms are: 

1. The typical enteric, frequently with diarrhea, tympany, hemor- 
rhage and perforation. 

2. The septicemic, without any or with very slight intestinal lesions; 
the Widal reaction and bacillemia are present. 

3. Other localizations than enteric, e. g., in the lung, bone, etc. 

4. Mixed infections — malaria, streptococcus, colon bacillus, etc. 

5. Paratyphoid, with close clinical resemblance to typhoid but with 
organisms differing culturally and otherwise (p. 47). 

The incubation lasts two or three weeks, with symptoms more vague 
than in other infections, e. g., depression, pains in the head, back or 
limbs, disturbed sleep, chilliness, anorexia, epigastric oppression, con- 
stipation or diarrhea. The incubation was three days in a girl who 
drank a typhoid culture with suicidal intent. 

The first tveek corresponds anatomically to the intestinal catarrh 
and the beginning of medullary infiltration of Peyer's plaques. The 
disease dates from the fever, which each evening is from 1° to 1.5° 
higher than on the previous day, until a temperature of 103° to 104° 
is reached. The pulse is full, dicrotic and rapid, but slow in proportion 
to the fever. The tongue is coated white. Thirst, anorexia, dry cough, 
enlarged spleen, eruption of rose spots and typhoid bacillemia are found. 
The abdomen shows slight distention and pain or tenderness over the 
ileocecal region or epigastrium. Headache, constipation, and apathy 
are usually present. 



TYPHOID FEVER 27 

The second week corresponds to the end of medullary infiltration and 
the beginning of eschar formation. The fever is higher and usually 
continuous; the morning remission is less. The pulse is full, faster and 
less dicrotic. The Widal test appears. The tongue is dry and glazed, 
as are also the lips, pharynx and mouth, to which the mucus adheres. 
The face is apathetic, its lines obliterated, the mouth half-open and the 
upper lip retracted, showing sordes. The voice is weak. The bron- 
chitis increases, and the urine is febrile. Meteorism appears and 
yellow pea-soup dejecta, involuntary in severe cases. Roseola? de- 
velop during this week. Nervous symptoms increase with higher fever; 
delirium follows; the patient becomes less querulous; and euphoria 
from narcosis by the toxins is the rule, while pain suggests complications. 
The toxemia is due to endotoxins liberated from typhoid bacilli, killed 
by the tissues. The patient may begin to recover through the opsonins, 
bacteriolysins and agglutinins, overcoming the toxins, or may die at 
this stage from hemorrhage, nervous toxemia, etc. 

The third week is the stage of ulceration. The fever gradually declines 
with marked morning remissions and unaccountable variations. The 
pulse is smaller and faster (100 to 120), and loses its dicrotism. The 
tongue clears and the roseola? are replaced by miliaria from sweating. 
Diarrhea may be seen for the first time in this week. When the fever 
falls the emaciated patient complains of hunger, weakness and pain. 
Death may occur in the typhoid state from heart weakness, pulmonary 
inflammation, paralysis of the nerve centres, hemorrhage or per- 
foration. 

The fourth week (cicatrization) usually marks convalescence, as the 
average typhoid runs three to six weeks; in severe cases the symptoms 
of the third week may continue. Convalescence may be uneventful, 
or marred by slight fever, rapid pulse, weakness, etc. 

Symptoms in Detail. — To avoid repetition, and to explain anatomi- 
cally the clinical symptoms, the typhoid pathology will be incorporated 
under the appropriate organs, and complications and sequels classified 
with the usual typhoid manifestations. 

1. Fever. — Fever is a cardinal symptom of typhoid; it is toxemic, 
the toxins so affecting the heat centre (in the corpus striatum), that heat 
production is increased and its elimination decreased. It is subacute, 
averages three or four weeks in duration, usually comes on without a 
chill, and resolves by lysis. Wunderlich diagnosticated typhoid from the 
fever chart alone. In the first week, corresponding to the catarrh and 
medullary infiltration, the evening temperature is 0.6° to 1° more than in 
the morning, and the ascension is ladder-like. In the second week, cor- 
responding to the end of infiltration and to the formation of the slough, 
the fever is continuous from one-half to three weeks. In the third week 
(ulceration) the fever is remittent (the amphibolic stage or stadium 
hecticum). The fourth week (cicatrization) is the stage of "steep curves/' 
lasting from three to eight days. When a sudden drop occurs, recurrences 
and relapses are not infrequent. 

Convalescence. — At first the typical curve is subnormal, with a later 
gradual rise to normal. 



28 



BACTERIAL DISEASES 



Atypical Fever Course. — As to onset, two variations may be observed. 
(1) There is a sudden explosive onset in 10 per cent, of typhoids. The 
writer saw a sudden rise to 106° on the second day. (2) When there is an 
initial chill every other disease should first be excluded, yet Osier observed 
chills in 22 per cent, of his cases (a) at the onset, especially in children, 
and in light forms; (b) throughout the course, and accompanied by 
sweats, the sudoral type; (c) in complications — pneumonia, otitis media ; 
(d) after antipyretics, tubbing, or (e) in defervescence from secondary 
sepsis. 

In the second week especially high temperature suggests complications ; 
if the fever becomes very high, the course is apt to be severe. In a fatal 
case, the writer observed fever ranging from 106° to 108° for one week. 
Sometimes a pseudocollapse may occur, particularly in subjects between 
twenty-five and thirty years of age. In the third or fourth week the 



PULSE 


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FEVER FEVER 



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Fig. 1. — Typical typhoid-fever curve. The heavy line marks the temperature curve, and 

the broken line the pulse curve. 

fever exceptionally may decline by crisis; a brusque defervescence 
occurs in 29 per cent, of cases (Jaccoud). 

The fever may be intermittent or remittent throughout the disease, 
especially in children, the aged and in severe cases; protracted irregu- 
larity may suggest miliary tuberculosis or sepsis. 

In the typus inversus, seen chiefly in children and the aged, the morning 
temperature is higher than the evening record. Afebrile typhoid is 
exceptional. Modification of temperature may be caused by excitement, 
entrance to the hospital, relapse, hemorrhage, abortion, peritonitis 
and other complications. 

2. The Splenic Tumor is. a cardinal symptom, occurring early and 
persisting in exacerbations and relapses. In importance and size, it 
ranks third to the splenic enlargement of malaria and sepsis. Its cause 
is the bacillus or its toxin which produces splenic hyperemia and hyper- 
plasia — changes analogous to those in the intestinal lymph structures — 
and endothelial proliferation in the splenic vessels (Mallory). In the 



TYPHOID FEVER 



29 



first week the spleen is hyperemic and swollen to twice its normal size. 
Its markings are indistinct. In the second week it is darker and more 
pulpy. By the fourth week it usually has disappeared, but as long as 
splenic tumor persists the disease persists. 

Frequency. — (a) Anatomically the splenic tumor is present in 98.4 
per cent, of the cases. Its rare absence is explained by capsular thicken- 
ing or induration or infarction of the organ. (b) Clinically, it is present 
in 75 to 90 per cent. The percentage varies with the skill and the method 
of examination (the sign being often absent in children, in adults older 
than forty-five years, or after hemorrhage). It should be palpated 
with the patient in the right diagonal position; the examiner should 
sit on the right side of the patient palpating with the right hand pressing 
evenly on the abdomen, and the left hand hooked beneath and lifting 
up the lower left ribs. If the palpating fingers are not pressed too deeply 
into the splenic region, the spleen is almost invariably detected. Tympany 



DAY 


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Fig. 2. — Typhoid fever, irregular fever curve throughout the course. 



may obscure the splenic tumor. Percussion of the spleen gives utterly 
unreliable results. The author has twice seen the spleen ruptured by 
rough palpation. Rare complications are abscess, infarct and spontaneous 
rupture (38 instances, Bryan, 1909). 

3. Skin. — (a) Rose spots (roseola typhosa, tdche rosee lenticulaire 
of Louis) constitute the third cardinal symptom. They are round spots, 
varying in size from a pin-head to a lentil (lenticular), rose-colored, 
slightly elevated, purely hyperemic and therefore disappearing on pressure 
and reappearing on its release. Pustulation is rare (5 cases, Eggleston), 
as also are fusion, vesiculation and hemorrhage — the term petechia being 
inappropriate. They usually appear from the seventh to the tenth day. 
They occur in crops, during two weeks, each crop lasting from three to 
five days. Occasionally they outlive the fever. They appear on the 
lower chest and abdomen, though sometimes twenty-four hours earlier 
on the back, because of its warmth, They rarely occur on the neck or 



30 BACTERIAL DISEASES 

face, and are more frequent on the proximal parts of the extremities 
than on the distal. (If many spots appear here, they are probably 
not roseola?.) They number five to ten, or even thirty. They are more 
abundant in women, less so in children and the aged, and seldom so 
numerous as to resemble measles closely. Eichhorst found them con- 
stantly in 2044 cases, Osier in 93 and Murchison in 33 per cent. Typhoid 
bacilli in the roseola? (in 100 per cent.) may establish a doubtful diagnosis, 
but rarely an early one; in miliary tuberculosis, meningitis and pneu- 
monia, roseola? are very rarely encountered. 

(6) Other Cutaneous Manifestations. — The typhoid odor is musty 
or semicadaveric. Furunculosis is the most common cutaneous compli- 
cation. Miliaria are frequent, though less than in sepsis; usually appear- 
ing in the third or fourth week, they indicate convalescence. The author 
has observed herpes only ten times in upward of 2000 cases; it is far 
less frequent than in pneumonia, malaria, typhus, meningitis and in- 
fluenza. Decubitus occurs in 1 per cent., mostly in severe and hospital 
cases. (See Therapy.) Noma is a rare complication. In 204 cases of 
gangrene collected by Keen, 50 per cent, occurred in the leg and 25 per cent, 
in the face, neck and trunk. Sweats and chills occur in the " typhus sudo- 
ralis," especially in the latter half of the fever course, described in Naples 
by Borelli and in Paris by Jaccoud. Edema is due most frequently to 
phlebitis, sometimes to anemia, and rarely to nephritis. The skin some- 
times shows atrophic stria? cutis distensse like those of pregnancy. Other 
cutaneous manifestations are: Urticaria; desquamation (in 7 per cent.); 
erythema, even of the nodose or exudative forms; morbilliform rashes; 
purpura; pelioma typhosum or the tdche bleudtre — pale blue spots, 
measuring 4 to 10 millimeters — due to pediculosis and therefore seen 
in parts nearest the pubic or axillary hair (Piednagel, 1837) ; erysipelas 
or phlegmon; and alopecia after the typhoid attack, rarely followed by 
permanent baldness. 

4. Circulation. — (a) The slow pulse is the fourth cardinal symptom. 
It is lower than the fever would justify, especially in men under forty 
years, e. g., pulse 90 with the fever 103°. Its slowness is due to an 
inhibitory action of the toxins on the medulla or the heart. The pulse 
may range from 50 to 60, with the fever above 103° and the respirations 
above 40. Slowness is of good import. Dicrotism, evidenced by a 
double shock, occurs in 80 per cent, of cases, which, with slowness, 
suggests typhoid. It is usual in adults, but is absent in children and 
often in adults at the fastigium in very severe cases. Since it indicates 
lack of arterial tone, it is also absent in arteriosclerosis, or in vasomotor 
paralysis. The systolic blood-pressure is 115 to 125 mm. A fast pulse 
early in the typhoid course is a poor prognostic, especially in men 
(heart or lung inflammation, perforative peritonitis, hemorrhage and 
severe intoxication). It may also run up on visiting days, in women, 
children, emaciated and nervous individuals, or in the stage of great 
temperature variations. Irregularity or crossing of the pulse and tem- 
perature curves is ominous. Early in convalescence, when there is 
subnormal temperature, the pulse is usually normal in rate or slow, 
from depressed conductivity or myocarditis. Later it is usually above 



TYPHOID FEVER 



31 



normal, especially after getting out of bed, or after a bowel movement. 
On the whole, bradycardia in convalescence is more common than 
tachycardia. 

(6) Heart Muscle. — Parenchymatous degeneration, evidenced by albu- 
minous granules, nuclear swelling and pigmentation, makes the heart 
flabby, soft, pale and even waxy. Fatty and hyaline degeneration, 
vacuole formation, periarteritis, endarteritis and segmentary myocarditis 
are the usual findings in fatal cases. Interstitial myocarditis, like that of 
diphtheria or scarlatina, occurs in over 50 per cent, of typhoid cases. 
Its clinical signs appear at the end of the second week, lasting into the 
fourth week, or develop first in convalescence. The symptoms are 
gradual dilatation of the left ventricle, weak tones (especially the first 
tone at the apex), accentuation of the second pulmonic, a systolic bruit, 
and a fast, irregular pulse. Tachycardia, without myocarditis, may 
result from the toxins acting on the medulla oblongata. It usually 
regresses completely, and chronic myocarditis rarely develops. 

Dilatation of the right heart may be observed in severe cases. Less 
frequent are the following complications: Cardiac thrombosis and 
embolism; pericarditis, once in 1000 typhoid autopsies, mostly fibrinous 




Fig. 3. — Pulse tracing in typhoid, showing dicrotism. 



and in complicating sepsis; and endocarditis, once in 1000, mostly 
mural over myocarditic patches, sometimes due to Eberth's bacillus. 
Collapse, with its usual signs, may cause death from heart degeneration, 
or from toxic vasomotor paralysis (as in diphtheria or pneumonia) ; myo- 
carditis is the most frequent cause, while pulmonary embolism, uremia, 
cerebral hemorrhage, etc., are far less common. Sometimes no clear 
cause is discovered at autopsy. Sudden death is recorded in 80 instances 
(Dieulafoy). Collapse develops most often during convalescence and 
mostly in strong men (80 per cent, of Dewevre's 140 cases) (see 
Prognosis) . 

(c) Vessels. — Phlebitis typhosa occurs in 1 per cent, of cases, being 
marantic, or infective due to Eberth's bacillus or pus cocci, when pain 
and fever are present; it occurs chiefly in males and is usually left-sided, 
since the left iliac vein has a slower current, being crossed by the right 
iliac artery. The symptoms are pain, coldness, edema and sometimes 
a tender, palpable cord, manipulation of which may precipitate embolism. 
Thrombosis usually occurs in the saphenous vein where "it empties into 
the femoral, sometimes in the popliteal vein, and rarely in the arms. 
It may extend from the leg to the cava, when the other leg may be 



32 BACTERIAL DISEASES 

involved. There is some danger of detachment, pulmonary embolism, 
and sudden death; but relative recovery is usual after two or three 
months. L. A. Connor believes that thrombophlebitis develops in 10 
to 15 per cent, of typhoids and causes embolism (33 per cent.), post- 
typhoid chills, and "tender toes" (usually considered as a plantar neuritis). 
Arteritis typhosa, most often femoral, is rare, W. W. Keen collecting 
only 44 cases, and it is specific, caused by the typhoid bacillus. Sponta- 
neous gangrene was noted in 44 typhoid patients, among 180 cases of 
gangrene in youth after various infections (Barraud, 1904). Arterio- 
sclerosis may be initiated by typhoid. 

(d) The Blood. — The red blood cells average 4,000,000. Anemia is most 
frequent during the third week or in relapses. An apparent increase 
of the red disks may result from loss of fluids, as from diarrhea. The 
hemoglobin decreases slightly in excess of the oligocythemia. The leuko- 
cytes decrease from 8000 to 1700, averaging 5000 per cubic millimeter. 
Leukopenia is more common in typhoid than in any other febrile condition 
and helps to differentiate it from pneumonia, sepsis, meningitis, etc. 
Severe infections always exhibit a low count; the converse is not true. 
The polymorphonuclear neutrophiles are absolutely and relatively 
decreased to below 60 or 50 per cent., while they are increased in most 
other infections. The large mononuclear and transitional forms are 
relatively increased. The eosinophiles are greatly decreased; their 
return is a good prognostic. Leukocytosis occurs only in complicating 
inflammations. 

Typhoid is a primary bacillemia or septicemia (Frankel and Simmonds, 
1885). The bacilli reach the blood from the lymphopoietic organs, and 
from the blood reach the feces secondarily by way of the bile or by 
ulceration of Peyer's patches. A positive blood culture is the safest and 
surest means of diagnosis in the first week of typhoid. Cultures, repeated 
day after day, are positive in 100 per cent, in the first week, in 71 per cent, 
in the second, and in 36 per cent, in the third week. Convalescence 
is rapidly established as soon as the bacillemia ceases. 

The Gruber-Widal Test. — The agglutination and immobilization of 
typhoid bacilli occur when they are brought in contact with a typhoid 
serum. The agglutinins are produced by the tissues reacting to the 
bacilli. Gruber pointed out the value of the test in proving the existence 
of a previous typhoid, while Widal applied the laboratory facts at the 
bedside. 

Technique. — A bouillon culture, not more than eighteen hours old, 
is used, taking forty parts of the bouillon and one of the blood (dilution 
of 1 to 40), since the test is quantitative rather than qualitative. The 
test may be made macroscopically in the test-tube, or on the microscopic 
slide, where immobilization, clumping and agglutination of the bacilli 
may be observed, sometimes in a very short time — an hour is the usual 
time-limit for the test. Ficker employs dead cultures with equally 
accurate results, and this method is more convenient and safe than the 
use of living bacilli (Plate, I). 

Significance. — The reaction may be found thirty years after a typhoid 
attack. It is sometimes absent in typhoid, particularly in severe cases, 



PLATE I 



FIG. 1 




Bouillon Culture of Typhoid Bacilli before the Addition of Diluted 
Typhoid Serum. X 500. (After Cabot.) Serum diagnosis. 



FIG. 2 




The Same, Five Minutes after the Addition of Typhoid Serum 
(dilution 1 to 10), showing Typical Clump Reaction. 

X 400. (Cabot.) 



TYPHOID FEVER 33 

and it often develops late, e. g., not until the seventeenth or sixty-seventh 
day. Cabot found the reaction in 97 per cent, of 5978 typhoid cases. 
In Osier's series it appeared in 93 per cent, before the eighth day. When 
it appears in the first week, it is due to a "silently developing" infection 
(Widal), i. e., the typhoid is more advanced than we appreciate. The 
test is most significant when it is absent early and develops later. Typhoid 
bacillemia decreases as the Widal develops. The Widal reaction is 
specific; its occasional occurrence in icterus is probably due to a previous 
attack of typhoid. Some maintain that the reaction is not one of infec- 
tion, but one of immunity, agglutination becoming most marked toward 
the end of the disease. 1 

5. Nervous Symptoms. — Typhoid was once called "nervous fever" 
(jebris nervosa, nervenfieber) . The nervous system may be conspicuously 
involved even in the incubation stage. 

(a) Headache. — Toxemic headache is almost invariable, being most 
often frontal or occipital, constricting or throbbing. It disappears 
in the second week, but if it lasts or develops late, it may indicate 
meningitis. Insomnia may be both early and lasting. The early ex- 
citation passes into the later depressive euphoria of the typhoid state. 

(6) The typhoid state begins in the second week (v. s.) with apathy 
and delirium, which is usually mild. The patient may attempt to get 
out of bed, and, in alcoholics, delirium tremens may be simulated or 
actually develop. In mild cases delirium lasts into the third week. In 
irritable subjects or in overwhelming intoxication, we may have photo- 
phobia, stupor, coma, loud breathing with an open mouth, involuntaries, 
waving of the hands (floccitation) , leaping of the tendons (subsultus 
tendinum), picking of the bedclothes (carphologia) , trismus, contractures, 
grinding of the teeth and rigid neck, which symptoms are due to toxemia. 
In coma-vigil the patient is semicomatose subjectively, but the open, 
unseeing eyes give a "watchful" appearance. Anatomically a "wet- 
brain" is found. Convulsions (0.2 per cent.) may develop in children, 
in severe intoxication, or from cerebral complications as meningitis, 
encephalitis, embolism, etc. 

(c) Nervous Complications. — The author has seen five typhoids taken 
to the detention hospital in the third week under a diagnosis of mania. 
Psychoses are due to the exhausting inanition of protracted toxemia, 
or sometimes an hereditary predisposition. They are generally post- 
febrile and of the depressive variety such as melancholia ; alienists assert 
that one-third to one-fifth do not recover. Two-thirds of juvenile cases 
recover (Edsall) . Typhoid may cure a previous insanity. 

Meningitis occurs in 0.5 per cent, of cases, generally as a late complica- 
tion. Meningitis may be due to the pneumococcus, pyogenic cocci, 
tubercle bacillus (4 cases recorded) or Eberth's bacillus, which has been 
found on lumbar puncture in over twenty-six cases (Cole), of which 
half were serous and half suppurative. Typhoid meningitis may develop 
without typhoid lesions in the bowel (Henry). In a patient recovering 

1 Chantemesse reports an ophthalmoreaction, similar to the tuberculin reaction of 
Calmette. Gay has devised a skin test; and a hemolytic test is suggested, similar in 
principle to the Wassermann test. 

3 



34 BACTERIAL DISEASES 

from typhoid and exhibiting no meningeal symptoms, bacilli were found 
in the cerebrospinal fluid (Stuhmer). Meningitis must not be con- 
founded with pseudomeningitis or "meningismus,'' in which toxemia 
produces irritative meningeal symptoms as described under typhoid 
state (v. s.). The writer observed hemorrhagic pachymeningitis. 

In the brain, edema, degenerated and pigmented ganglionic cells, and 
nuclear multiplication are the most common findings at the autopsy. 
Hemorrhage, embolism, arterial and sinus thrombosis, and abscess 
(sepsis) are rare pathological complications. Aphasia, monoplegia, 
hemiplegia and paralysis of the cerebral nerves are rare clinical compli- 
cations. The author twice noted hemiplegia developing suddenly in 
convalescence, probably embolic from detached heart-clots, the patients 
being allowed to leave the bed too soon. Forty cases of hemiplegia 
in typhoid are on record. 

In the cord, myelitis, multiple sclerosis, infantile paralysis and 
Landry's paralysis are rare complications. The knee-jerks are some- 
times increased, especially in emaciated subjects, and ankle-clonus may 
appear. 

Neuroses may complicate convalescence, such as chorea, hysteria, 
neurasthenia, Basedow's disease, tetany, paralysis agitans, etc. 

Neuritis in the single or multiple form (q. v.) may follow typhoid. 
It constitutes the "tender toes" of Hanford and always results in recovery 
(see Phlebitis, p. 32). 

6. Digestive Tkact. — The upper lip is retracted and bleeds easily. 
Sordes of dried saliva, food and epithelium are observed on the teeth and 
gums. Though the tongue shows nothing characteristic, early it is white 
on the dorsum, moist, flabby, and therefore indented by the teeth and its 
edges are red. It may be moist throughout the disease. The coating 
is explained partly by the milk diet and lack of mastication. In the second 
week it becomes dry (from the fever, lack of saliva and mouth-breathing), 
small and fissured; it bleeds, and a brown coating replaces the white. 
In the third week or later, a triangular patch clears at its tip. Typhoid 
bacilli are said to occur in the mouth in 50 per cent, of cases. Acute 
glossitis is a severe, yet rare complication. 

The throat is swollen, granular and eroded. Angina may usher in the 
disease and lead to a wrong diagnosis; usually of the ordinary type, it 
may be due to the typhoid bacillus. The phlegmonous type is very 
dangerous. Letulle observed yellowish or pinkish-gray ulcers on the 
uvula or anterior pillars in one out of every three cases. 

Parotitis, occurring in 1 per cent, of cases, became less frequent since 
special care of the mouth has lessened infection ascending Steno's duct. 
It is usually one-sided, is due to the typhoid bacillus or pyogenic cocci, 
and is usually seen on the fifteenth day. The prognosis is poor, especially 
when due to metastasis. Two personal cases, caused by the typhoid 
bacillus, recovered. Ulceration of the esophagus is very rare; the 
cicatrized ulcer may produce later stenosis (12 cases, J. E. Thompson, 
1904). 

In the stomach specific typhoid lesions are rarely observed; hema- 
temesis may occur. Early and severe epigastric pain rather contra- 



TYPHOID FEVER 35 

indicates typhoid. Incipient nausea and vomiting occur mostly in nervous 
women or children; at the height of the disease they suggest meningitis, 
overfeeding or perforation, and in convalescence dietetic errors. Anorexia 
is observed during the onset and fastigium; great hunger denotes con- 
valescence. 

Specific changes in the intestines: (a) Hyperemia, catarrh and beginning 
medullary infiltration in the lymphoid structures during the first week, 
most changes being observed in the lower ileum, whence the name 
ileotyphoid. (b) Medullary infiltration or hyperplasia, during the second 
week, occurring first in Peyer's patches and then in the follicles. The 
patches are oval and parallel with the long axis of the gut; they lie oppo- 
site to the mesenteric attachment, are 3 to 5 millimeters high, and are 
at first red, then paler from compression of the bloodvessels. The solitary 
follicles, even to the sigmoid flexure (colotyphoid), may be principally 
enlarged. These changes are not distinctive of typhoid, but are more 
significant in adults than in children, in whom they are frequent in 
digestive diseases, the exanthemata and diphtheria. The lymphoid 
swelling is explained by proliferation of the endothelial cells of the 
vessels to act as phagocytes; when they degenerate, fibrinous thrombi 
develop (Mallory). Medullary infiltration need not advance to ulcera- 
tion; regression may occur, and the lymphatic structures then assume a 
"shaven beard" appearance, (c) Ulceration occurs in the third week 
from anemic necrosis, slough formation and exfoliation of small particles. 
The typhoid ulcers are usually seen without opening the gut. They 
have an irregular oval outline, sharp, steep, often undermined edges, 
with a red floor generally composed of the muscular coat. The lower 
ileum is most affected and in extreme cases may present almost no 
normal surface. The solitary follicles, both in the large and small gut, 
ulcerate at their apices. As to localization of the typhoid ulcer, Baer 
states that it may occur in any part of the digestive tract (v. s. mouth). 
The pharynx is affected in 2 per cent, of the cases, the esophagus in 4 per 
cent., the stomach in 2 per cent.; 97 per cent, of the ulcers develop in the 
small intestine, 89 per cent, in the ileum, 2 per cent, in the appendix, and 
33 per cent, in the large intestine, (d) Cicatrization occurs by granulation 
tissue and growth inward of the epithelium. The cicatrix is depressed, 
slightly pigmented and does not narrow the intestinal lumen. Slight 
bowel lesions are usually present in most cases reported "without in- 
testinal lesions. " 

The mesenteric glands are swollen in the second week, contain typhoid 
bacilli and are altered like the intestinal lymphatics. The swollen glands 
usually regress, but may soften, sometimes causing peritonitis or simula- 
ting perforation. Six cases of suppuration are recorded; Le Conte 
reports a recovery after operation. 

No parallelism exists between the frequency, constancy or severity 
of the clinical symptoms, and the degree of anatomical involvement, 
e. g., in ambulant cases there may be perforation or hemorrhage, or lethal 
cases may occur with little intestinal change. 

Meteorism is less common than usually described. It occurs mostly 
in the duodenum or jejunum above the ulceration, but sometimes involves 



36 BACTERIAL DISEASES 

the colon. If much tympany develops the prognosis is poor, since meteor- 
ism is due to toxemic paresis of the intestinal musculature rather than 
to local ulceration; tympanites develops in four-fifths of the fatal cases. 
The heart and lungs may be crowded upward. It may occur with hemor- 
rhage or perforation. 

Abdominal tenderness and pain occur in half the cases; they are due 
to : (a) Local bowel conditions, as gas, constipation, inflammation in the 
ileocecal region, or perforative and peritonitic complications; (b) to 
splenic or hepatic tumefaction; (c) distended bladder; (d) muscle 
changes or cutaneous hyperesthesia, so frequently observed in fever of 
any variety; (e) pleurisy or phlebitis, etc.; (/) typhoid appendicitis 
may simulate ordinary appendicitis which is differentiated only by 
the blood count, seroreaction or clinical evolution (the fever, rose 
spots, etc., preceding local pain and tenderness). Gurgling has no 
diagnostic value in typhoid. A thickened ileum may be palpated. 

The stools are not pathognomonic save that the Bacillus typhosus, 
present in 30 per cent, of cases, reaches the bowel by the bile or through 
the ulcers. The dejecta are thin, offensive, pea-soup-like and alkaline. 
Because the feces are poor in mucus, two layers form on standing, an 
upper, cloudy, and a lower, yellowish-gray, granular and flocculent layer. 
The stools contain red corpuscles and triple phosphates, the latter more 
abundantly than in any other disease. Shreds or sloughs may also be 
found. 

Diarrhea in the febrile stage occurs in 25 per cent, of cases. Three 
to six stools daily are the average; if this is exceeded, the type of the 
disease is severe; prodromal diarrhea rarely occurs. Diarrhea is a measure 
of the degree of toxemia or of colonic involvement, and is not a result of 
ulceration of the small intestine. 

Hemorrhage is seen in 5 per cent, of cases. It usually occurs after the 
first two weeks, and is less frequent in relapses and in children (1 per 
cent.). Ulceration into the muscularis is its chief cause. Oozing, from 
simple hyperemia and bleeding in the hemorrhagic forms are exceptional. 
Bleeding is more common in ambulatory and delirious patients. There 
are no symptoms if the hemorrhage is small (occult hemorrhage); if it 
be large, acute anemia develops, with collapse, evidenced by a fast pulse, 
lowered temperature and pallid skin. The intellect often clears, the 
spleen becomes smaller and fresh blood, or, later, black, tar-like movements 
are voided (manifest hemorrhage). The abdomen is often distended. 
There may be dulness on percussion from blood retained in the bowel, 
if the peristalsis is weak and the hemorrhage is very profuse. In two 
rapidly fatal cases one and two pints of blood were vomited. Confusion 
with bleeding piles and bismuth stools is possible. The average number 
of hemorrhages is four. 

Some patients improve at once after hemorrhage, as was remarked 
by Graves and Trousseau; yet 30 to 50 per cent. die. Large blood clots 
are ominous, indicating erosion of a large artery. Hemorrhage may cause 
death within an hour (Trousseau, Leymaire). 

Perforation occurs mostly at the time of eschar formation, at the 
end of the second or in the third week; but it may also occur later — 



TYPHOID FEVER 



37 



in the third to fifth week (Leube). Scott found that 92 per cent, occurred 
between the second and fifth weeks. It develops in 10 per cent, of fatal 
cases and in 3 per cent, of all cases, but it very rarely occurs in children 
under five years ; after this year perforation is half as frequent as in adults. 
Scott's figures, in 9713 cases, show perforation in one-third of all fatal 
cases. Perforation is usually low in the ileum, 81 per cent. ; or in the 
colon or sigmoid, 12 per cent. ; in the appendix, 3 per cent. ; in Meckel's 
diverticulum, 2.4 per cent.; in the jejunum, 1.2 per cent.; according 
to Fitz's figures. In 83 per cent, but one perforation is found; several 
may occur, twenty-five being observed in one patient. It is promoted 
primarily by deep ulceration, and secondarily by movement, straining, 
coughing, constipation or tympanites; in 75 per cent, of cases perforation 
occurs in severe infections. Three types are encountered: (1) Least 
frequently, undiscovered latent perforation; the typhoid state masks 
the perforation, which affords an unpleasant postmortem surprise. (2) 



PULSE 


TEMP. 

104 














180 


103 










/\ 




110 


102 








/ 
s 
s 




i j 




100 


101 






y N 






*. 


90 


100 


--s 




"A 








80 


99 














70 
































2ND WEEK 


FOL 


R COPIOUS 

HEMORRHAGE 


STC 
S TR/ 


)OLS WITHOUT 
,CES OF BLOOD 



Fig. 4. — Typhoid-fever curve, with fall of temperature (solid line) after hemorrhage and 
rise of pulse (broken line). Note crossing of curves at A. 



More frequently, cases with gradual onset, and ambiguous symptoms. 
(3) Most frequently, cases with sudden symptoms and more or less clear 
diagnosis. The symptoms of perforation are: (a) Pain due to the per- 
foration itself (in 75 per cent.), usually localized in the hypogastrium 
or right lower quadrant of the abdomen and followed later by the pains 
of peritonitis. In 70 per cent, the pain is sudden and severe; in 20 
per cent., gradual in onset; and in 10 per cent., absent, (b) Tenderness 
on palpation (75 per cent.), evidenced by the board-like rigidity of the 
abdominal muscles, (c) Limitation of the respiratory movements of the 
abdomen, due to pain and tenderness, id) Vomiting of gastric contents 
or fecal matter, {e) Intestinal obstruction. (/) Abdominal distention, 
appearing possibly for the first time — in which event its significance is 
enhanced — or increasing, if already present; nevertheless the abdomen 
may be flat; in one typhoid patient, seen first in a dying condition, 
the scaphoid abdomen contained three pints of pus. Abdominal dis- 



38 BACTERIAL DISEASES 

tention crowds upward the diaphragm, heart and lungs, and causes 
hurried breathing, (g) Disappearance of the hepatic flatness by reason 
of free gas in the peritoneum. This is more significant if the abdomen 
was not previously distended. Perihepatic adhesions prevent oblitera- 
tion of the liver dulness; a gas-distended colon may overlie the liver, 
and in some cases the colon normally overlaps the liver. W. W. Herrick 
suggests the detection of pneumoperitoneum by introducing a blunt 
needle attached to a wash bottle, (h) Other occasional abdominal 
findings are flatness in the flanks, caused by fluid; the Beatty-B right 
friction-rub ; absence of peristalsis, rectal or vesical pain or tenderness. 
(i) Marked leukocytosis is found in but half the cases and special emphasis 
on its absence is most misleading, (j) Sudden fall of temperature, rapid 
rise in pulse-rate and other signs of shock may occur at the time of per- 
foration, though less frequently than the usual descriptions indicate. 
The writer has seen the pulse-rate remain normal. Dieulafoy's case, 
successfully operated upon for perforation, resulted fatally from two 
later perforations. The sudden clearing of the patient's intellect may 
deceive the inexperienced physician. In the advancing generalized 
peritonitis, the fever, if it has fallen, rises; the pulse becomes rapid, 
small and thready; the skin clammy and dusky, and the features pinched 
(facies Hippocratica) . Hiccough is common. The peritonitis rarely 
remains local; in six of the author's cases, the local abscess ruptured 
later. Ninety-eight per cent, of unoperated perforations die. Hemor- 
rhage and perforation may occur in association or in succession. 

Peritonitis occurs, frequently in ambulatory cases, from rupture of 
the bowel, gall-bladder, spleen or lymph glands; occasionally from 
post-typhoid appendicitis; or without rupture of any organ or tissue 
(in 2 per cent, of fatal cases). 

The liver in the early stages is anatomically hyperemic, large and 
firm; later its lobular markings become indistinct from cloudy swelling 
and fatty change. The organ is softer, and Wagner's lymphomata 
and some focal necrosis occur. Clinically, some tenderness is not 
unusual and at times may lead to an incorrect diagnosis of liver abscess 
or cholecystitis. 

Icterus is very rare (0.5 per cent.), and its absence is of diagnostic 
value. Icterus may occur from duodenal catarrh, gall-stones, cholecys- 
titis or abscess. The author has seen icterus but once in typhoid fever. 
Single liver abscess is rare, as are suppurative pylephlebitis and sup- 
purative cholangitis. Thirty cases of liver abscess are on record (von 
Eberts, 1911) and six instances of abscess with pure typhoid cultures 
(Venema). Suppuration generally follows mild infections; icterus is 
present in 15 per cent., and in 50 per cent, the abscess is seated in the 
right lobe. 

Typhoid favors the formation of gall-stones, which may develop months, 
years or decades later. 

Cholecystitis has been reported by Chiari and others; thirty-nine per- 
forations are on record, among 154 cases (Thomas, 1907). Tenderness, 
pain, muscular rigidity and enlarged gall-bladder are found in most 
cases. Typhoid bacilli from hematogenous infection are found in the 



TYPHOID FEVER 39 

gall-bladder, free or in its walls, in nearly all autopsies, although seldom 
having produced symptoms. 

7. The Respiratory Tract. — This is the seat of frequent and mani- 
fold symptoms and complications. 

(a) The Nose. — Epistaxis occurs in 20 per cent, of cases, usually 
early and in young subjects; it is often profuse, sometimes dangerous, 
but rarely lethal. Croup and diphtheria are rare. The author has seen 
but two cases, begin with profuse coryza. 

(6) The Larynx. — Ulceration of the swollen hyperplastic lymph 
follicles (like the intestinal changes), occurs in the posterior wall, followed 
often by edema glottidis. These "bed-sores" are found in 12 per cent, 
of lethal cases. Perichondritis and necrosis are attended by pain, aphonia, 
stenosis, mediastinitis, cervical cellulitis and diffuse emphysema, indi- 
cating tracheotomy; the author has seen but three cases. Dupuy 
collected 255 cases of perichondritis and submucous laryngitis, and 
believes they explain 3 to 10 per cent, of typhoid fatalities. Without 
operation the mortality is 98 per cent. 

(c) Air Tubes. — A dry catarrh of the trachea and bronchi is very 
frequent. Rales, retrosternal rawness and pain are present in the bron- 
chitis of typhoid. Bronchiolitis is regular and specific. It is found 
especially in the lower lobes. Coughing in early typhoid is of value in 
differentiation from simple intestinal catarrh. The outlook is less favor- 
able when severe and early coughing occurs. 

(d) Lungs. — Hypostasis, from a dorsal decubitus and weak heart, 
is often relieved by change of posture. It is very common in weak 
adults and in severe infections. The percussion note is tympanitic or 
dull; the fremitus is increased if the patient is not too stupid to talk, or 
decreased from stagnation of secretion; the breathing, especially the 
expiration, is distant or sometimes bronchial. Rales, moist, crepitant 
and subcrepitant, are heard. 

Lobar pneumonia may, in rare instances, dominate the early clinical 
picture (pneumotyphoid) and is of two types: The more frequent 
type, (a) in which at the height of the disease, the pneumonia is a true 
complication, due to the pneumococcus or sometimes to the colon bacillus 
and streptococcus. The pneumonic symptoms are atypical, as in most 
secondary pneumonias, often without chill, with a slower course, and 
often ending by lysis or, less often, with such complications as abscess 
or gangrene. More than one-half of these cases die. The less frequent 
second type (b) is due to Eberth's bacillus. The course is that of an 
initial pneumonia, which does not end typically, but shows later a 
typhoid temperature, rose spots, Widal reaction, etc. These cases are 
confusing in their incipiency, and the typhoid is apt to be overlooked. 
Lobular pneumonia, from inhalation, pus cocci or Eberth's bacillus, is a 
complication. Abscess follows pneumonia or sepsis; it occurs in 0.7 
per cent, of fatal cases. Infarct occurs in 6 per cent, of typhoid fatalities, 
thrombi from the leg reaching the lungs by way of the right heart and 
accompanied by hemoptysis, chill, temperature, pain, etc. Gangrene 
(1 per cent, of typhoid autopsies) is usually metapneumonic, but may 
be caused by perichondritis or aspiration of food. 



40 BACTERIAL DISEASES 

(e) Pleura. — Serofibrinous pleurisy (1.6 per cent.) is rare unless the 
lungs are diseased. Postmortem statistics show it in 6 per cent. Empyema 
(0.2 per cent.) is due oftenest to Eberth's bacillus. In 1903, 55 cases 
of pleurisy were collected in which the typhoid bacillus was found. 

(/) Tuberculosis. — Acute caseous pneumonia, subacute tuberculous peri- 
bronchitis with a few bacilli, fever and aggravation of the bronchial 
symptoms, or occasionally miliary tuberculosis, may occur. The sooner 
tuberculosis begins after typhoid the more unfavorable is its course. 

8. Genito-urinary Tract. — (a) The urine is febrile, i. e., decreased, 
acid, concentrated, with a high specific gravity, but the amount of urine 
depends upon the amount of water ingested. Water is retained in the 
tissues in protracted fevers. Typhoid bacilli are present in 30 per cent, 
of cases and may give the urine a glistening appearance. Bacilluria is 
hematogenous and occurs in severe infections; it is favored by retention 
and albuminuria ; the bacilli multiply in urine of low acidity and usually 
disappear spontaneously, but may persist months or years; cystitis is due 
to other organisms (Connell). In convalescence, the urine is increased, 
is neutral in reaction, and has a lower specific gravity. (6) Serum 
albumin, globulin and rarely peptone are found in febrile albuminuria. 
Serum albumin is found in 50 per cent, of the cases; cylindruria is ap- 
proximately half as frequent. The prognosis is three times as unfavorable 
when albumin is found. Albuminuria appears from the seventh to the 
tenth day, and its average duration is twelve days. It corresponds 
anatomically to parenchymatous and fatty degeneration of the kidneys. 
(c) Nephritis in typhoid is of the acute parenchymatous type. It is 
often hemorrhagic, and occurs usually in the first three weeks but oc- 
casionally in convalescence. It is found in 1 per cent, of cases, mostly 
in men, rarely in children. Nephritis indicates a severe infection, from 
which 50 per cent, of the cases die. Uremia and suppression of urine 
are rare. If not fatal, nephritis usually regresses entirely and rarely 
becomes chronic. Early marked renal symptoms constitute the nephro- 
typhoid of French writers. Miliary typhoid abscesses in the kidney 
may keep up the bacilluria. (d) The urine of typhoid exhibits the diazo 
reaction of Ehrlich, due to incomplete oxidation of the proteid metabolism 
of the aromatic sulphates. The author found it in 98 per cent, of his cases. 
It occurs in the early stages of the disease, at the acme and during re- 
lapses. It closely parallels the bacillemia. It is a valuable sign, though 
not of differential value. Its absence somewhat contra-indicates a 
florid typhoid, (e) Cystitis and pyelitis occur, due chiefly to pus organisms 
or colon bacilli. Simple retention of urine is common in the typhoid 
state. Hemoglobinuria is rare. Typhoid bacilli may form the nuclei 
of renal stones. (/) The genitalia are more often implicated in women 
than in men. Menstruation often appears early at the onset of typhoid 
and is suppressed in 60 per cent, of the cases. Hematocele, endometritis, 
vaginal erosions, ulcers, inflammation, gangrene and mastitis are rare 
complications. Pregnancy is of grave import, especially in its later 
stages. At the acme of the fever, abortion and premature delivery 
intervene in 65 per cent. The maternal mortality is increased twofold 
at least. Blumer and Dobbin report puerperal infection from the typhoid 



TYPHOID FEVER 41 

bacillus. Orchitis usually develops late or in convalescence, with chills 
and fever. Velpeau described the first instance. J. G. Beardsley collected 
102 cases, chiefly due to the typhoid bacillus. The patient generally 
recovers in two weeks. It is frequently associated with urethritis. 
Emissions are common in convalescence. 

Adrenal Function. — According to Sergent, adrenal insufficiency may 
ensue in typhoid or other infections; peritonitis and hemorrhage may 
be simulated at the height of the disease, and anemia, prostration and 
psychasthenia may be evident in convalescence, exhibiting prostration, 
lowered temperature, the white dermographic line, low arterial tension 
and collapse, and relieved by adrenal therapy. 

9. Special Senses. — Ocular muscle paralysis (neuritis) and inflam- 
mation are very uncommon. In convalescence, mydriasis and paralysis 
of accommodation often result from exhaustion. Uhtoft, in 253 cases 
of optic neuritis, found 17 cases following typhoid. Involvement of the 
ear includes functional toxemic disturbance of hearing, abscess and 
otitis media (2 per cent.). Mastoid disease and meningitis are very 
exceptional. 

10. Muscles, Thyroid Gland and Bones. — The muscles ana- 
tomically are dry, of a smoked-meat appearance, and may be the seat 
of hemorrhage, rupture, granulofatty or waxy degeneration, and abscess, 
due to Eberth's bacilli and pus cocci. Myositis may explain some 
instances of muscular tenderness with cramps. 

In the thyroid gland a strumitis typhosa, with suppuration or re- 
gression, is due to the typhoid bacillus. Recovery is the rule. 

Bone disease is more frequent than the 237 cases of Keen indicate. 
Periostitis is the more common. These post-typhoid complications are 
due to the typhoid bacillus (75 per cent.), or pus cocci (25 per cent.). 
They attack the tibia (38 per cent.), the ribs (13 per cent.), femur, 
ulna, temporal bones, etc., occur chiefly in young individuals and are 
characterized by indolence and recurrence. Osteomyelitis may resemble 
syphilitic or tuberculous osteopathies. Typhoid bacilli have been found 
fourteen years after typhoid in osteomyelitic fistulas; this typhoid 
septicopyemia is a striking instance of bacterial latency. Arthritis 
may be typhoid, gonorrheal or septic. Keen noted eighty-four cases. 
It may be poly- or mono-articular, serous or purulent. The hip is most 
frequently affected. The " typhoid spine" of Gibney, of which Elkin 
and Halfpenny collected 94 cases (1914), is characterized by pain, often 
referred to the belly, tenderness and stiffness in the back; these seem 
to be root symptoms. It is clearly an embolic spondylitis. 

Anomalous Courses. — 1. Malignant. — The malignant or hyperpyretic 
form is rare. It is severe even in the earliest stages. The temperature 
rises rapidly and there may be hyperpyrexia. The pulse is weak and 
rapid. Meteorism, diarrhea and albuminuria are present, and death 
usually follows the deep intoxication. 

2. The slow severe form lasts four weeks to four months. The 
fever is often remittent with frequent exacerbations. Defervescence 
may occur or death intervene, marasmus alone being found at autopsy. 
The severe types of typhoid have decreased during the last two decades. 



42 BACTERIAL DISEASES 

3. Typhus Abortivus. — Typhus levissimus, typhoidette, exhibits a 
short, mild-course temperature with a short initial stage, or often a crisis, 
lasting one to three weeks. Bronchitis is frequent, splenic enlargement 
is constant and meteorism, diarrhea, roseolse, hemorrhage and per- 
foration are rare. Relapses are more frequent. 

4. Typhus Ambulatorius. — Typhus ambulatorius (latent or walking 
typhoid) occurs especially in men, who often endure it by the help of 
alcohol. There are two types: (a) the lighter and atypical, and (b) the 
usual course, very often ending in hemorrhage, perforation, etc. The 
temperature often is not high, but is usually less at night than during the 
diurnal activity. The pulse is faster because of exertion. The spleen 
is often enlarged and the roseolse are frequent. 

5. Typhus Afebrilis. — The afebrile form is most often encountered 
in family practice. It may be ambulatory and is diagnosticated by the 
pulse, spleen, roseolse, Widal test, etc. Atypical cases have increased 
in recent years. 

6. Hemorrhagic. — The hemorrhagic form is characterized by nasal, 
subcutaneous and intestinal hemorrhages — the blood dissolution of the 
older writers. It occurs especially in children and alcoholics (0.1 per 
cent, of typhoid cases). The prognosis is usually bad. The four cases 
which the author has seen occurred in 1900, in St. Luke's Hospital, 
where a severe house epidemic prevailed. 

7. Visceral Forms. — The so-called visceral forms may cause confusion. 
They include the gastric or bilious types, nervous fever, meningotyphoid, 
cerebrotyphoid (mania, psychoses), laryngo-, tonsillo-, nephro-, and 
pneumoty phoid . 

8. In children the course is shorter and milder. The younger the 
patient, the less is the fever. Epistaxis is less common. The pulse is 
faster than in adults, though after the twelfth year it is equally slow. 
Roseola? occur as often in children as in adults, and in some cases are 
abundant and confluent (between the fifth and tenth years). Bed-sores 
are very rare, but noma is more frequent than in adults. The nervous 
system is generally less involved in children, though if the infection is 
severe, convulsions, irregular pupils, rigidity of the neck, etc., may 
occur (see Typhoid State). Neuralgias and psychoses are rare. The 
frequency of aphasia has not yet been explained. Atelectasis, hypostasis 
and lobular pneumonia are more frequent. Children exhibit less meteor- 
ism, hemorrhage (1 per cent.) and perforation. There are fewer ana- 
tomical changes. Splenic enlargement is palpable in 50 per cent. Initial 
vomiting, pain and perhaps diarrhea, are more frequent. Albuminuria 
and nephritis are relatively rare. In infants: Griffith and Ostheimer 
assembled 325 cases in infants, of which 139 occurred under one year, 
187 in the second, and 68 between two and two and one-half years. 
The mortality under one year (v. i.) was 73 per cent., and of the entire 
group, 50 per cent. Typhoid is rare in the first two years of life, and 
is sometimes overlooked, being very atypical. The course is short. 
Bronchitis, splenic tumor and roseolae are infrequent. If the disease is 
severe, a very high temperature, meningeal symptoms, and initial 
vomiting occur, and also a 50 per cent, mortality caused by toxemia, 
pneumonia, perforation or ulceration of the larynx. 



TYPHOID FEVER 



43 



9. In the Aged. — Typhoid is infrequent after the fortieth year. 
The fever is lower, atypical and often absent. The pulse is faster, 
irregular and without dicrotism. There is greater lung congestion, 
owing to weakness of the right heart, and lung complications are more 
frequent. The nervous symptoms are dominant, often occurring with 
great depression. Roseola? are fewer and bed-sores are more frequent. 
The spleen is less often enlarged because of old infarcts, induration and a 
thicker capsule. Tympany and hemorrhage occur more often. Con- 
valescence is naturally slower. In 1903, the author had under his care, 
in Wesley Hospital, a woman, aged fifty-seven and her mother, aged 
seventy-two, both with typhoid, ending in recovery. 

Relapses and Exacerbations. — Relapses and exacerbations differ in 
degree only. Their explanation is probably involved in the immunity 
problem, an exhaustion of the antibacterial forces of the body. In the 
relapse, the temperature falls to normal or nearly normal, for five days 
on the average, and then fever and other signs of typhoid reappear. 
It occurs in 9 per cent, and varies with the epidemic, sometimes occur- 



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HIGH FEVER REMISSION EXACERBATION LYSIS APYREXIA RELAPSE 

Fig. 5. — Showing remission, exacerbation, lysis, and relapse. 

ring in as much as 35 per cent. Relapse is more likely to occur (a) in 
light or moderately severe cases (75 per cent.) than in severe ones (25 
per cent.) ; (b) when the splenic tumor does not disappear (but the spleen 
may have been enlarged from some previous disease, as malaria); (c) 
when the temperature in convalescence does not become subnormal; 
(d) when the pulse is variable and rapid; and (e) more commonly in 
young than in old subjects. 

The fever runs the same course as in the first attack, and averages 
ten days. The pulse is faster and less dicrotic. There are less roseola?, 
nervous and respiratory symptoms, hemorrhage (4 per cent.) and per- 
foration (0.7 per cent.), whence, as a rule, the prognosis is relatively 
good. There are seldom more than two relapses — three or four being 
very rare. The author has seen five relapses, covering, with the original 
attack, as many months. They may be afebrile, with a return of the 
roseola?, spleen, etc. Relapses should not be confused with Biermer's 
" after fever," due to inanition or possibly, sepsis. Recrudescence is 
renewal of the fever after it has lessened, but not entirely subsided, and 
in 50 per cent, is followed by more severe symptoms. 



44 BACTERIAL DISEASES 

Convalescence. — Convalescence requires two or three weeks and is 
not certainly established until subnormal temperature is observed. The 
pulse tends to run high on exertion or excitement. Anemia, emaciation, 
phlebitis, tuberculosis, psychoses, bone, muscle and other complications 
may intervene. If the appetite is poor in convalescence, complications 
are to be expected. 

Diagnosis. — General Rules. — 1. Observe long and carefully. Say 
that a diagnosis is impossible in the first few days. 

2. No single sign is absolutely diagnostic, except bacilli in the blood 
and the Widal reaction. 

3. Diagnosticate from positive findings and careful exclusion. 

4. The typhoid state only indicates toxemia, not typhoid. 

5. In doubtful cases remember the great statistical frequency of 
typhoid. 

6. Remember its manifold forms, e. g., pneumotyphoid, etc. 

7. Be on the safe side in light, ambulatory or abortive cases as to the 
diagnosis and treatment. 

The Cardinal Signs are: (a) Bacillemia is found in practically all 
early cases. 

(b) The serotest is successful in 97 per cent, of cases; its absence 
does not exclude typhoid. 

(c) The eruption has a diagnostic value in its location, occurrence 
in crops, time of appearance and short duration. 

(d) The slow and dicrotic pulse is suggestive. 

(e) The fever curve shows a gradual, step-like onset, continuous 
fastigium, steep curves in the breaking stage and subnormal register 
in convalescence. 

(J) Splenic tumor is per se suggestive after the first week. Splenic 
puncture, to detect bacilli, is never permissible. 

Secondary Signs. — These are, in order of importance, the typhoid 
tongue, the stools, bronchitis, typhoid state, leukopenia, intestinal 
symptoms and the diazo reaction. 

Symptoms contra-indicating typhoid are coryza, early vomiting 
and sweating, herpes, endocarditis, retraction of the abdomen, negative 
diazo test, leukocytosis (unless some complication has occurred), icterus 
and rigors. Any of the above symptoms may, exceptionally, complicate 
typhoid. 

Differential Diagnosis. — Differentiation may be most difficult from acute 
miliary tuberculosis which may develop in typhoid. Typhoid may be 
complicated with septicemia, very rarely with malaria in this climate, 
or with meningitis (v. table on pages 46 and 47). 

Exanthematous typhus (q. v.) and recurrent fever (q. v.) are easily dis- 
tinguished. Exanthematous diseases are rarely confused, except, perhaps, 
in the initial stage. In 75 instances typhoid and scarlatina coexisted 
(Fournier). An extensive eruption of roseolas resembling measles is easily 
distinguished by the catarrhal symptoms, temperature curve and course. 

Fibrinous pneumonia rarely resembles typhoid, and still more rarely 
occurs with typhoid in its earliest stages by the localization of typhoid 
bacilli in the lungs. Though typhoid may begin with severe bronchitis 
or pneumonic symptoms, the intestinal and cardinal findings of typhoid 



TYPHOID FEVER 45 

usually appear after a few days. Sudden onset with chill, pain in the 
side, abrupt rise of pulse and temperature, rapid respiration, bloody, 
viscid sputum, herpes, leukocytosis, and a tympanitic note and a few 
crepitant rales over one lobe, followed later by typical pneumonic in- 
filtration as consolidation advances from within toward the periphery of 
the lung, establish the diagnosis of pneumonia on the second or third day. 

In intestinal anthrax fever, splenic tumor and nervous symptoms 
are accompanied by hemorrhagic vesicles in the mouth, vomiting, colic, 
hemorrhage from the intestine and kidney, cyanosis and dyspnea, an- 
thrax bacilli in the blood, urine, stools or sputum, and inoculations 
establish the diagnosis. 

Febrile gastritis rarely simulates typhoid; the rare fever is low or 
irregular, and early gastric symptoms are not common in typhoid. With- 
out blood cultures, paratyphoid may not be distinguished from acute 
gastro-enteritis. Febrile enteritis is characterized by much mucus in the 
stools, whereas the typhoid stool seldom contains much mucus. Splenic 
tumor is most uncommon in enteritis. The fever in enteritis is lower 
or more irregular and the bronchitis, slow pulse and other cardinal 
signs of typhoid, are absent. Cases of typhoid developing suddenly may 
be confused at first, with grippe, diphtheria or other diseases. Febrile 
syphilis seldom causes diagnostic trouble but must be considered in 
dubious cases. 

Paratyphoid.— The paratyphoid bacillus resembles the typhoid bacillus 
morphologically but differs biologically; in cultures it forms no indol, 
therein resembling the Bacillus typhosus, but like the colon bacillus 
it ferments grape-sugar. In Bacillus A, the growth on potato is very 
thin; in Bacillus B, very thick; it may very closely resemble Gart- 
ner's bacillus enteritidis. Infection may occur from milk, water and 
tainted meat. The bacilli are found in the stools, blood, roseolse and 
urine, and agglutinate in higher dilutions (1 to 1000 or 2000) than the 
typhoid bacilli. The first clear cases were reported by Schottmuller, 
in 1900 and Gwynn, though the term paratyphoid was first employed 
by Achard and Bensaude in 1896. Paratyphoid constitutes 4.5 per cent, 
of cases with the general clinical picture of typhoid fever. In para- 
typhoid the temperature is more brusque in onset, shows greater re- 
missions, and may end by crisis. The pulse is slow and dicrotic. Roseola? 
are present in 80 per cent., the spleen is less often enlarged and no leuko- 
cytosis is observed. Prodromal catarrhs, reddening of the throat, 
diarrhea, cervical adenitis, edema of the lids, vomiting, rigors, epigastric 
pain, herpes, myositis, arthritis, pleurisy, endocarditis and meningitis, 
are more common than in typhoid and may enable the practitioner to 
differentiate paratyphoid, clinically. The diazo reaction is positive 
in 45 per cent. The clinical course covers two to four weeks. Relapses 
are common. The infection is usually mild and rarely fatal (3.6 per cent.). 
Ulceration of the intestinal lymph structures is rare in the fatal cases, 
though other necroses occur, thus explaining the hemorrhage (5 per cent.). 
Pneumonia and perforation are unknown. Nervous symptoms are not 
prominent. The blood seldom responds to the Widal test. Grunberg 
and Roily hold that the Widal reaction is less a specific than a group 
reaction, as they found agglutination in the paratyphoid group by typhoid 



46 



BACTERIAL DISEASES 



Pathognomonic 
signs. 



Pulse and circulation. 



Fever. 



Splenic 
enlargement. 



Blood. 



Typhoid: 

Typhoid bacilli 
in the blood, 
urine, roseolae 
or stools. Wi- 
dal test. 



Relatively slow dicrotic 
pulse early in the dis- 
ease, especially in men, 
and in not too severe 
infections. Endocar- 
ditis and pericarditis 
very rare. 



Typical rise, acme, de- 
fervescence, and sub- 
normal in convales- 
cence. Remissions 
and intermissions f ol- 
lowing continuous 
fever speak for ty- 
phoid. Responds to 
hydrotherapy as a 
rule. Sometimes 
chills at onset or in 



Very frequent; 
larger than in 
miliary tu- 
berculosis; 
appears in 
first week. 



Bacilli in blood, 
early; Widal test 
later. No leuko- 
cytosis unless com- 
plications, but 
leukopenia. Poly- 
morphonuclears 
decreased. Eosin- 
ophilia rare. Late 
anemia. 



Miliary 

Tuberculosis: 
Rarely tubercle 
bacilli in the 
blood or splen- 
ic pulp; tuber- 
cles in the 
choroid. 



Rapid, 120 or more, 
high even during re- 
missions ; slowed in 
tuberculous meningi- 
tis and in the aged. 
Dicrotism uncommon. 
Sometimes pericar- 
dial rub. 



No cycle; irregular or 
remittent. Seldom 
long continued, and 
if so, longer than in 
typhoid. Exacerba- 
tions with renewed 
dissemination of tu- 
bercle bacilli. Brain 
involvement may 
lower fever or make 
it variable, as in- 
versed type. 



Less frequent; 
smaller and 
usually ap- 
pears later. 



Sometimes tubercle 
bacilli in blood. 
No Widal. Leuko- 
cytosis not often 
but more than in 
typhoid. Eosino- 
philia more fre- 
quent. 



Malaria : 

Plasmodium in 
the blood. 



Pulse moderate in rate; 
sometimes dicrotic; 
very rarely endocar- 
ditis. 



Intermittent, begin- 
ning very often with 
chills ; type varies 
(quotidian, tertian, 
etc.) ; often rises high 
at once ; if continuous 
(subcontinuous), at 
least made irregular 
by quinine or usually 
wholly abolished (for 
a time at least). 



Much en- 
larged; more 
than in ty- 
phoid; and 
persists fre- 
quently as 
ague-cake. 



Plasmodium, mel- 
anemia, no leuko- 
cytosis save in 
pernicious forms. 
Great and early 
anemia. No 
Widal. 



Sepsis (Including 
Endocarditis) : 
Cultivation of 
pyogenic or- 
g a n i s m s , 
pneumococcus, 
etc., from the 
blood or va- 
rious foci. 



Usually fast and irregu- 
lar ; cardiac localiza- 
tions very frequent in 
sepsis, puerperal es- 
pecially, and in endo- 
carditis (a cardiac 
form of sepsis). Car- 
diac enlargement, 
thrill, bruit, accentu- 
ated pulmonic tone, 
etc. 



Chills, sweats, steep Especially en- 
elevations, and sud- larged from 
den depressions al- \ sepsis and in- 
most always at some j farcts. Also 
time, and usually j often the 
repeated with each lymph nodes, 
discharge into the I 
blood of infective 
material. 



Various organisms. 
Marked polymor- 
phonuclear leuko- 
cytosis very fre- 
quent; sometimes 
absent in endo- 
carditis. Seldom 
eosinophilia. No 
Widal. 



Meningitis: 

Lumbar punc- 
ture (a) men- 
ingococci, tu- 
bercle bacilli, 
pyogenic or- 
ganisms, etc. ; 
(b) increased 
turbid fluid, 
etc. 



Rate differs with type; 
variable. 



Differs with variety, 
but seldom as high 
as typhoid; no cycle. 



Rare. 



Leukocytosis in ep- 
idemic and puru- 
lent types; rarer 
in tuberculous. 
No Widal. 



serum. A mixed infection with typhoid may occur. In about half the 
cases due to the paratyphoid B, the symptoms are choleriform. Bacilli- 
carriers are as important as in typhoid; a wide-spread house epidemic 
occurred from kitchen infection among the patients and physicians in 
the Allgemeines Krankenhaus in Vienna. 

Trichinosis is differentiated from typhoid by the history, muscular 



TYPHOID FEVER 



47 



Skin. 



Lungs. 



Nervous system. 



Sputum, urine. 



Alimentary tract. 



Roseolse, typical in 
location, crops, 
appearance, con- 
taining typhoid 
bacilli. Sweating 
and miliaria less 
often and later. 
Icterus rare. 
Herpes rare. 



Roseolae absent or 
extremely rare, 
and then not in 
crops. Drench- 
ing sweats com- 
mon. Herpes 
more than in ty- 
phoid. Skin ane- 
mic and very 
often cyanotic. 



In severe, eyes sub- 
icteric or marked, 
very frequent and 
urticaria the next 
most frequent ex- 
anthem. 



Frequent sweating, 
miliaria. Septic 
polym orphous 
rashes. Subic- 
terus, frequently 
purpuric skin 
eruptions, herpes 
not uncommon. 



Herpes in epidemic 
c er ebr ospinal 
form. Tache 
cerebral e. 



Breathing somewhat 
increased from toxe- 
mia (cerebral breath- 
ing) , hypostasis or 
other complications 
Rales below and be- 
hind. Tympanitic 
note never heard in 
typhoid. 



Early headache, re- 
placed later by de- 
lirium, typhoid 
state; actual men- 
ingitis very rare ; 
intoxication may 
closely simulate 
meningitis. Very 
rarely disk changes. 



Typhoid bacilli in 
urine. Diazo test 
in nearly all cases. 



Breathing increased 
even 40 to 60; cya- 
nosis and dyspnea 
without adequate 
physical findings. 
Fine and localized 
rales heard above 
and in front. Tym- 
panitic percussion 
note from lung relax- 
ation. Evidences of 
pleural adhesions, 
apical changes, fresh 
pleural rub. 



Meningitis tubercu- 
losa very frequent; 
optic neuritis; cho- 
roidal tubercles. 



Tubercle bacilli 
sometimes found 
in sputum, urine 
and feces, but 
indicate old tu- 
berculous lesions, 
not of miliary tu- 
berculosis. Diazo 
test less frequent. 



If lung congestion 
(severe forms), it is 
variable, recurrent, 
shifting from lobe to 
lobe. 



Headache at onset 
is rare; later is of- 
ten pulsating or 
neuralgic. Delir- 
ium from begin- 
ning in estivo- 
autumnal forms is 
frequent. Restless- 
ness, anxiousness. 
In pernicious forms 
may have convul- 
sions, coma, etc. 



Hemoglobinuria in 
pernicious ma- 
laria. Diazo test 
fairly frequent, 
though much less 
than in typhoid. 



Bronchitis frequent. 
Pulmonary infarcts 
and pleurisy. 



Dependent on cause. 
Septic meningitis 
(with arthritis, 
pleurisy, etc.), cer- 
ebral embolism ; re- 
tinal hemorrhages 
or embolism. 



Acute embolic ne- 
phritis. Pepto- 
nuria. 



Variable breathing; 
Biot's breathing. 



Early triad, head- 
ache, retracted 
neck and hyper- 
esthesia. Head- 
ache violent 
throughout the 
disease, convul- 
sions, paralysis, 
Kernig's sign, etc. 
Optic neuritis, ret- 
inal hemorrhage, 
tubercles in cho- 
roid. 



Mouse-like breath, 
semi-character- 
istic tongue, 
ochre yellow 
stools, tympany, 
diarrhea, bowel 
hemorrhage, per- 
foration, bacilli 
in stools. Re- 
tracted abdomen 
or early vomiting 
rare. 



Diarrhea not com- 
mon, but may 
rarely occur, as 
indeed may hem- 
orrhages; both 
result from tuber- 
culous ulceration 
of bowels. 



Nauseating breath. 
Sometimes ab- 
dominal pain even 
in mild types ; 
may rarely have 
diarrhea, even 

hemorrhage in ali- 
mentary pernic- 
ious types. Liver 
congestion fre- 
quent, also icterus. 



Septic diarrhea. 



Early cerebral 
vomiting. Re- 

tracted, scaphoid 
abdomen.' 



pain and edema in the striped muscles, trichinae in the muscles, and by 
eosinophilia. Three cases of double infection are reported. 

Prognosis. — The death-rate was 20 per cent, in 50,000 cases collected 
by Jaccoud. At present it is 5 to 10 per cent, because of more accurate 
diagnosis (thus including lighter cases), decreasing virulence and better 
hygiene and treatment. 



48 BACTERIAL DISEASES 

The prognostic factors are : 

1. Age: The mortality is least between the second and tenth years, 
higher after the twenty-fifth, and highest in babes. 

2. Constitution: Meagre and muscular patients are more likely to 
recover than the plethoric or adipose. 

3. Sex is immaterial, aside from pregnancy. 

4. Acute diseases modify the prognosis, e. g., scarlatina, measles, 
variola, diphtheria, malaria, erysipelas, etc. 

5. Chronic diseases, such as gout, cardiac, pulmonary and renal disease 
darken the outlook; in alcoholism, 34 per cent, mortality results from 
weak heart or hemorrhagic diathesis; convulsive affections, such as 
epilepsy or chorea, may cease; in diabetics the fever is low and the 
glycosuria may disappear. 

The prognosis is better in relapses and worse in recrudescences. In 
war times the prognosis is usually less favorable; the Spanish- American 
war was an exception, the death-rate being but 7 per cent., as against 
21 per cent, in the Boer war. 

Death usually occurs between the eighteenth and twenty-eighth days, 
and is caused by — 

1. Toxemia, the most frequent cause of death (40 per cent.), including 
hyperpyrexia, hemorrhagic types, heart weakness, vasomotor paralysis 
and cerebral toxemia. 

2. Local typhoid lesions, as meteor ism, diarrhea, peritonitis (in 16 per 
cent, of fatal cases), or hemorrhage (in 20 per cent.). 

3. Complications, as lung inflammations (in 15 per cent.), nephritis 
(4.5 per cent.), etc. In septicemia (' ( forme septicemique generalisee"), 
the symptoms are high fever, chills, sweats, enlarged glands and spleen. 
Pyemia may result from acute osteomyelitis, suppurative parotitis, 
adenitis, phlebitis, etc. 

4. Collapse. Dieulafoy estimates that sudden death occurs in 2 per 
cent, of typhoid cases (see page 31). The pulse is always more important 
than the fever, and early rapidity is unfavorable. Bradycardia and 
marked agglutination are favorable prognostics. 

5. We have already considered the ominous significance of pseudo- 
collapse, the typhoid state, early delirium, diarrhea and meteorism; 
of the various severe complications, such as noma, gangrene, laryngeal 
perichondritis and pneumonia; and of the more severe types, such 
as the hyperpyretic and hemorrhagic and of the ambulatory variety. 
Typhoid beginning suddenly entails a high mortality. 

Treatment. — Dujardin-Beaumetz said: "The best treatment for 
typhoid is a good physician." Treatment concerns (A) prophylaxis; 
(B) hygiene; (C) intestinal antisepsis; (D) antipyretic measures; (E) 
diet; (F) symptomatic treatment; and (G) convalescence. 

(A) Prophylaxis. — 1. Prophylaxis has as wide a scope in medicine 
as asepsis and antisepsis in surgery. In Chicago, during the years 1889 
to 18Q2, inclusive, there were 4747 deaths from typhoid. In the four 
years after the drainage-canal was opened there were 2235 cases, that 
is, the mortality was reduced 75 per cent. In 1905 typhoid was rare. 



TYPHOID FEVER 49 

General prevention is difficult, because of the ubiquity of the germ and 
the carelessness of individuals. Systematic cooperation regarding 
sewage regulation, water supply and typhoid-carriers could efface typhoid. 
Koch particularly emphasized this point and abolished certain typhoid 
foci. The difficulties are the infrequent recognition of the particularly 
dangerous light cases, light forms notably in children (Koch) , carelessness 
and the bacilli-carriers. It is easy to boil water for home use, and yet 
it is done in but few families, even in those of physicians. The traveller 
should avoid unboiled water and milk. In communities where sewers 
exist, sewer connections should be compulsory; if privies are inevitable, 
they should be water- and fly-tight. Private and public cisterns should 
be periodically tested. Work camps, country resorts and fair grounds 
demand careful inspection. The dairies and depots for milk distribution 
require closest scrutiny. 

2. In the treatment of a developed case everything with which the germ 
may come in contact must be sterilized. Next to the feces, the urine 
is the most important conveyer of the bacillus; these are the usual 
means of dissemination, and their proper disinfection in every case 
would obliterate typhoid. The bacilli may persist for years in the feces, 
five to seventeen years in the bile and five years in the urine. Chloride 
of lime should be placed in the bottom of the urinal or bed-pan before 
and after use. Acidulated sublimate (1 to 500) may also be used for 
the urine and 10 per cent, crude carbolic solution for the stools; but 
neither disinfects at once, for which reason the dejections should stand 
an hour in a quart of the disinfectant. Both the pans and urinals must 
then be sterilized. The same disinfection is indicated for thermometers 
and rectal tubes. The perineum, after each movement, should be sponged 
with a 1 to 2000 bichloride solution, and also the back and thighs, when 
there are involuntary evacuations. The rubber draw-sheets and linen 
should be sterilized regularly with carbolic acid or bichloride of mercury, 
and the blankets, pillows and mattresses, steamed when taken off the bed. 
The bath-tub should be carefully cleaned with carbolic solution, and one- 
half pound of chloride of lime added to the water after bathing, as the 
patient's soiled skin and the urine voided during the bath are obvious 
sources of danger. Cleansing the hands after examination or tubbing 
prevents direct transmission of the disease to nurses, orderlies and phy- 
sicians; 2 per cent, of hospital typhoid is acquired by direct contact in 
the care of the disease. Rubber gloves are the safest protection. In the 
Spanish- American war 20 per cent, of our soldiers were directly infected 
by flies, and in the Boer war more died of typhoid than were killed 
by bullets, infection being carried by flies and sand. The few cases 
among the Japanese is one of the many lessons they taught us. Flies 
should be carefully excluded from the house by screens. Quarantine 
should be enforced. 

3. Typhoid Bacillus-carriers. — Since 2 to 4 per cent, of typhoid con- 
valescents become chronic carriers, and one person in every 500 well 
people becomes a carrier (Park), special care in convalescence is indicated. 
Hexamethylenamine (urotropin) and salol, given in the disease, are help- 
ful, but they are useless later. Segregation, draining the gall-bladder and 

4 



50 BACTERIAL DISEASES 

washing the urinary bladder are ineffectual. Vaccination (v. i.) offers 
the greatest promise. 

4. Typhoid Vaccination (Pfeiffer, Ivolle and Wright, 1896). — In the 
Spanish-American war 10,729 troops were quartered at Jacksonville, 
Florida; among them 2693 probable cases (1729 certain cases) of typhoid 
developed, with 248 deaths and in contrast with these figures: in our 
army of 12,659 men during the 1911 maneuvers in Texas, not one 
typhoid death and but one mild case developed (here vaccination had 
not been completed). The vaccines are given as follows: the first 
inoculation of 500, and the second and third each of 1000 million bacilli 
at ten-day intervals, into the subcutaneous tissue. Local reactive 
erythema develops with some pain and a small percentage suffer a rigor, 
generalized erythema, herpes, fever (101° to 102°), vertigo or diarrhea; 
reaction is less after the second and third injections. An immunity of 
from under one year to two and a half years is conferred. The agglutina- 
tive power of the blood is increased, the opsonic index rises and the 
white cells increase. Vaccination is indicated in "carriers," soldiers and 
hospital attendants, as internes, nurses or laundry-women; it is also 
advisable in children, who leave home for schooling, vacation or travel. 
Against paratyphoid infections, a similar vaccine is employed. Typhoid 
vaccines are clearly indicated in prophylaxis, but their value in the 
developed disease is not established. 

(B) Hygienic Treatment. — Absolute physical and psychical rest is 
imperative, and the best results are obtained in cases which have been 
put to bed early. Ambulatory cases never fare as well. The invariable 
use of the bed-pan and urinal is insisted upon. The furniture, carpets 
and hangings should be removed from the room, which should be freely 
ventilated — fever patients do not catch cold. The nurse should have 
written instructions. The baths should be supervised by the physician, 
especially at the onset. The single bed should be low, should have a 
firm mattress, rubber draw sheet and perfectly smooth cotton or linen 
sheets. A second bed is desirable for change and convenience. 

(C) Antiseptic Therapy. — Antiseptic therapy is largely of historical 
interest, as typhoid is not a local enteric disease but a bacillemia. Calomel 
given early in typhoid was thought to reduce the virulence of the attack 
and lessen bowel complications; it is harmful. Salol (phenylis salicylas) 
in doses of grs. x, t. i. d., is the least objectionable, since it is mild. The 
urine should be closely watched for signs of renal irritation. Dilute 
hydrochloric acid, 3 ss after each feeding, prevents diarrhea and tympany. 
No one of this group of agents essentially influences the clinical course, 
and at the most, only decreases fermentation. 

(D) Antipyresls. — 1. Drugs are seldom indicated, for they merely 
reduce fever and do not eliminate its cause, the toxins. Quinine in 
one or two doses of fifteen to twenty grains has little influence on the 
fever. Coal-tar products, in full repeated doses, depress the brain, cir- 
culation, respiration and metabolism; cause vomiting and eruptions; 
increase the danger of collapse; and are not indicated in typhoid as 
they are in the fugitive fevers. In all cases drug antipyresis is far 
inferior to — 



TYPHOID FEVER 



51 



2. Hydrotherapy, the only logical febrifuge, since it alone eliminates 
the fever-exciting toxins. 1 Nature's method of reducing temperature by 
sweating, evaporation from the moist skin, should be helped by removal 
of the bedclothing. (a) The full cold bath of Currie (1787) and Brand 
is given with water at 64° to 68° F. ; it lasts fifteen to twenty minutes 
and is repeated every three hours for temperature of over 102° or for 
toxemia. Chilling is averted by vigorous friction, which must not 
abrade the skin; by cold affusions to the head; or by administration 
of alcohol. The apparent brutality of the Brand method excited popular 
and professional prejudice, but it is a most valuable measure. Early 
resort to hydrotherapy gives the best results. When the portable bath- 
tub is not available, A. H. Burr uses a wooden frame, shaped like a 
large box; the base fits over any bed; its upper part sustains a heavy 
rubber sheet, which passes under the patient and constitutes the sides 





Fig. 6. — Burr's bed-tub. 

and bottom of the tub (Fig. 6). Its use obviates the necessity of lifting 
the patient and saves excitement. Water is poured over the patient from 
pails and is removed with a siphon. The advantages of Brand's method 
are: (i) The mortality is lowered 6 to 8 per cent.; (ii) toxemia is lessened, 
and therefore nervous and digestive symptoms, heart weakness, and 
pulmonary complications are relieved; fever is successfully reduced 
and there is less visceral degeneration; (iii) renal secretion is stimulated, 
thereby washing the toxins out of the blood; (iv) the skin becomes more 
active and bed-sores less frequent; (v) the clinical course is shorter 
and fewer complications occur. Contra-indicaiions to Brand's method 
are hemorrhage, perforation, great prostration, alcoholism, phlebitis 
and advanced arteriosclerosis. Pregnancy, nephritis and pneumonia 

1 Toxemia disturbs the heat centre, located in the corpus striatum and connected with 
various parts of the brain, notably the vasomotor and other vital centres in the medulla. 
Though views differ, it seems that in fever there is a great increase in the production of 
heat, without a corresponding increase in its elimination. 



52 BACTERIAL DISEASES 

are no contra-indications. Various substitutes may be indicated for 
special reasons: (b) In the gradually cooled bath the temperature of 
the water is gradually reduced from 90° to 75° or 65°. It is adapted to 
cases coming under treatment late and to those with tendency to collapse, 
(c) The protracted tepid bath, (d) Cold sponging, first with warm water 
to dilate the skin vessels and then with cold water; equal parts of alcohol 
aid evaporation. One part of the body after another is exposed and 
sponged. It is a refreshing and quieting placebo, but inferior as an anti- 
pyretic, (e) The cold pack is also much less successful. In sthenic cases, 
ice applications to the head, axilla, spine, etc., may be used, or the body 
may even be ironed with ice. Ice- water enemas are never used in typhoid. 

(E) Diet. — The mouth and pharynx should be carefully cleansed of 
sordes and food particles lest infection travel to the ears, salivary or 
lymphatic glands. Vaseline keeps the lips soft. A boric acid solution, with 
tincture of myrrh or tincture of hydrastis, meets every requirement. The 
liquor antisepticus, U. S. P., contains 2 per cent, boric acid and antiseptic 
oils. The cleansing must be gentle lest fresh abrasions be inflicted. Fifty 
ounces of water should be given daily at definite intervals. It flushes the 
kidneys, lowers temperature by increasing the sweat production, and 
lessens parenchymatous degeneration of the viscera . Pure water is superior 
to barley- or albumin-water, lemonade, etc., which dull the appetite. 

In the diet no reference is made to individual symptoms, as there is no 
correspondence between the clinical symptoms and the anatomical ulcera- 
tion of the intestines. Graves was the first to feed fever patients, who up 
to that time had been starved, but at the present time there is some risk 
of overfeeding. Milk is the standard diet. Six to eight ounces should be 
sipped at intervals of three hours, day and night, as the patient, after 
being wakened, readily falls to sleep again. It may be diluted with half 
an ounce of lime-water or a little carbonated water, which should not be 
cold, since the gas expands at body heat. The physician himself should 
inspect the stools for curds. As in infant feeding, curds indicate reduction 
of the cream. Very few patients cannot take milk. Recalcitrant patients 
may be given koumyss, matzoon, buttermilk, whey or certain baby 
foods. If digestion is weak, peptonized milk may be given with thin, 
strained gruels or egg. Carbohydrates are indicated to lessen nitrogenous 
waste (Kendall), and well-boiled cornstarch, strained vegetable soups 
and tapioca are allowed if no tympany results; taka-diastase aids their 
assimilation. Meat-juice is obtained from freshly slaughtered beef, by a 
meat-press. It may also be given frozen (meat-juice, 5iij; sugar, 5ij; 
lemon-juice, 3 j; yolk of one egg; cognac, 5j). Yolk of egg in soup or 
wine, and white of egg with twice its weight of water afford some variety. 
Gelatin conserves metabolism but may irritate the bowels. Beef-tea 
contains only stimulating substances, less than 1 per cent, albumin, 
and no fat or carbohydrates and may irritate the kidneys and intestines. 
In stupid patients with anesthetic throats, food may enter the larynx 
and cause aspiration pneumonia. In these cases the nasal catheter is indi- 
cated. To its outer end a funnel is attached through which food, drink, 
and medicines are given. A safety-pin across its outer end prevents its 
escape downward. The catheter should be long enough to pass into the 
esophagus beyond the larynx. Rectal feeding is sometimes indicated. 



TYPHOID FEVER 



53 



High Calory Feeding. — Years ago Shattuck, Hare, von Miiller and 
others advocated more generous feeding, and lately Coleman and Schaffer, 
especially, have popularized high calorie feeding. At the height of the 
infection, the pyrexia (fever and toxemia), the alimentary disturbance 
and the starvation increase metabolism about 34 per cent., as regards 
the protein and fat of the body, somewhat as in simple starvation, 
although more extensively. Magnus-Levy demonstrated that metabolism 
is qualitatively the same in the febrile as in the well individual. To 
compensate the increased nitrogenous waste, a diet more ample than 
is usually given, is desirable. Coleman and Schaffer hold that theoretic- 
ally 5000 calories are demanded; 3000 are accepted as a compromise. 
The approximate values of available foods in calories are as follows: 
One quart milk, 700 (plus 6 per cent, milk-sugar, 900) ; 1 pint cream, 900; 
5 ounces oatmeal or hominy, with 2 ounces cream and 3 teaspoonfuls 
sugar, 300; eggs, each 80; cup of custard, 100; 1 slice of well-buttered 
bread, 200; 8 ounces milk-sugar, 1000. Absorption in fever is 90 per cent, 
of normal. The protein and fat loss is about 6 per cent, each, whereas 
carbohydrates are perfectly assimilated. Two quarts of milk give but 
1400 calories of the 3000 or more needed. Coleman believes that the 
ampler diet decreases indigestion. Eggs supply 'protein (6 eggs = 7 gm. 
N. = 480 calories) and are of higher food value in a mixed diet; Coleman 
discards meat, except for its extractives in soup to stimulate appetite, 
though v. Miiller advocates brains, hash, etc.; 100 gm. protein (=16 gm. 
N.) is the upper limit. Carbohydrates should constitute half the calories 
and are supplied by bread, toast, crackers, mashed potatoes, milk-sugar, 
and gruels (oatmeal and cream of wheat) ; cellulose is shunned (in 
vegetables and fruits). Fats include cream, butter and cocoa; in excess 
they disturb digestion, but as much as 200 to 250 gm. are sometimes 
tolerated. If the milk-sugar is too sweet in milk, it may be taken in 
lemonade, ice-cream or custard. In high feeding, two to four bowel 
movements a day are usual. In every instance this diet must be indi- 
vidualized, regarding the weight, appetite and digestion, and increasing 
slowly. It is difficult to give 3000 calories in the severest types, who 
most need the diet. Appended are caloric values, borrowed from White. 



DAILY FOOD DEMANDS. 



Adult. 



At rest in bed 
Slight activity . 
Light work . 
Moderately hard work 
Very hard work . 



Body 


Calories 


Total 


weight. 


pound. 


calories. 


150 lbs. 


12 


1800 


u 


15 


2200 


a 


17 


2600 


u 


20 


3000 




23-30 


3500-4500 



Child. 



Age 0-6 months. 


7-15 lbs. 


42-40 


1 
300-600 


6-12 " . . 


15-20 " 


40 


500-800 ! 


2 years . 


25 " 


36 


900 


4 " ... 


35 " 


34 


1200 


8 " ... 


50 " 


28 


1400 


12 " ... 


75 " 


22 


1600 



Total 

grams 

proteid. 



72 

88 

115 

120 

140-180 



1 gram 
per lb. 
35-40 

42 

55 

60 



Calories. 
1 gram proteid =4.1 

1 " carbohydrate = 4.1 
1 " fat = 9.3 

1 " alcohol =7.0 



54 



BACTERIAL DISEASES 



FOOD VALUES IN HOUSEHOLD MEASURES. 



Foods as eaten. 



Actual 
amount. 



Household measure. 



Approximate. 



Calories. 



Proteid, 


Fat, 


grams. 


grams. 


7.5 


9.5 


7.5 


1.0 


0.5 


3.0 


0.5 


6.0 


2.0 


2.0 


2.0 


2.0 




8.5 


4.0 


5.0 


4.5 


2.5 


4.0 


5.5 


6.5 


5.0 


2.5 


. 5.0 


1-4.5 




8.5 




11.0 


6.5 


11.5 


2.5 


11.5 


9.0 


8.5 


18.0 


1.0 


0.2 


2.3 


0.5 


3.5 


1.0 


0.5 


0.5 


1.0 




0.3 




3.0 


0.5 


2.5 


1.0 


5.5 


4.5 


1.0 


0.5 


2.0 




1.0 


1.0 


1.0 




1.0 


0.5 


2.5 


1.0 


1.0 




0.5 




0.5 


0.5 




0.5 


1.5 


0.5 


1.0 




1.0 


6.5 


2.5 


3.0 


0.5 




2.5 


0.5 


1.5 


9.0 


1.5 


2.0 


2.0 


2.0 




"4!6 




1.5 


5.0 


13.5 


2.0 


3.0 



Carbo- 
hydrate, 
grams. 



Dairy: 

Milk _. 

Skimmed milk and buttermilk 

p rpflm /thin (20 per cent.) . 
oream [ thick (40 per cent ) 

Condensed m il k {-^- d ned 

Butter ....... 

[Cream .... 

Cheese \ Skim milk . 
[American 

Eggs, whole 

Eggs, yolk 

Meat and Fish (cooked) : 

Beef-tea, clear soups . 

T?ic=v. /lean (cod, flounder) . 

■ blsn \fat (shad, salmon) . 
(lean 

Meat \ medium fat 

[fat . _ 

Oysters, medium size (raw) . 
Cereals andVegetables (cooked) 

Bread, white or Graham . 

Vienna roll 

Crackers (Uneeda) 

Cereals, cooked, moist 

Cereals, e.aten dry. 

Shredded wheat .... 

Gruels (cereal) 

Thickened or cream soups 

Macaroni 

Potato, boiled or baked . 

Potato, mashed .... 

Rice, boiled 

Corn, canned 

Peas, fresh 

Lima beans, canned . 

Squash 

Fruits: 

Apple, pear . . 

Apple sauce 

Banana 

Orange 

Strawberries 

Dried figs, dates, raisins . 

Fruit jelly, sweetened 
Desserts: 

Custard 

Ice-cream 

Sponge cake 

Pudding (rice, tapioca, bread) 
Alcohol 

Whisky, brandy, etc. (50 p. c.) 

Wines (8-45 per cent.) 
Miscellaneous : 

Sugar 

Honey 

Olive oil 

Olives 

Almonds, shelled .... 

Cocoa powders .... 



8 ozs. 
8 ozs. 

16 gms. 

20 gms. 
10 gms. 

15 gms. 

50 gms. 

15 gms. 

5 ozs. 
50 gms. 

50 gms. 

16 gms. 

25 gms. 
40 gms. 

7 gms. 
40 gms. 

5 gms. 
30 gms. 

8 ozs. 
8 ozs. 

25 gms. 
95 gms. 
35 gms. 
30 gms. 
35 gms. 
35 gms. 
25 gms. 
35 gms. 

120 gms. 

45 gms. 
100 gms. 
130 gms. 
100 gms. 
100 gms. 

50 gms. 

40 gms. 
40 gms. 
20 gms. 
45 gms. 
12 gms. 

1 oz. 

1 oz. 

8 gms. 
10 gms. 

4 gms. 

7 gms. 
25 gms. 
10 gms. 



A glass 

A glass 

A tablespoon 

A tablespoon 

A heaping teaspoon 

A heaping teaspoon 

A pat or ball 

One-inch cube 

One-inch cube 

One-inch cube 

One 

One 

A teacup 

A heaping tablespoon 
A heaping tablespoon 
A medium slice 
5 x 3 x | inch 

One 

One slice, 4 x 4 x | inch 

One 

One 

A heaping tablespoon 

A heaping tablespoon 

One 

A soup plate 

A soup plate 

A heaping tablespoon 

One medium size 

A heaping tablespoon 

A heaping tablespoon 

A heaping tablespoon 

A heaping tablespoon 

A heaping tablespoon 

A heaping tablespoon 

One medium size 
A heaping tablespoon 
One medium size 
One medium size 
A medium saucerful 
A medium saucerful 
A heaping tablespoon 

A heaping tablespoon 
A heaping tablespoon 
A slice 2 x 4 x ^ inch 
A heaping tablespoon 
A tablespoon 
A small wineglass 
A small wineglass 

A heaping teaspoon 
A heaping teaspoon 
A teaspoon 
One medium size 
A heaping tablespoon 
A heaping teaspoon 



160 
80 
30 
60 
70 
35 
80 
65 
45 
70 
75 
55 

5-20 
/ 35 
\105 
70 
U50 
[200 



70 
115 
30 
35 
20 
110 
75 
160 
25 
90 
40 
35 
35 
40 
20 
20 

75 

70 

100 

70 

40 

350 

160 

55 
135 
75 
80 
85 
85 
15-50 

33 
33 
37 
15 
165 
50 



12.0 

11.5 

0.5 

0.5 

11.5 

2.5 

0.5 
0.5 



0.5 



0.5 

13.0 

22.5 

5.0 

7.0 

4.0 

23.0 

14.0 

24.0 

4.0 

20.0 

6.0 

7.0 

6.5 

5.0 

3.5 

3.5 

17.0 

16.5 
22.0 
15.0 
7.5 
76.0 
38.5 

9.0 
11.0 
13.0 
13.0 



8.0 
8.0 

0.5 
4.5 
3.5 



(F) Symptomatic or Expectant Treatment.— 1. Digestive System. 
(a) Vomiting.— It must be ascertained that the patient has received 
no solid food from friends and that perforation has not taken place. 
Rectal feeding, warm carbonated water, cocaine gr. J, or tincture iodine 
THJ, for several doses, sinapisms or an ice-bag to the epigastrium, are 
indicated. 



TYPHOID FEVER 55 

]$ — Phenolis gr. iv 

Bismuthi subnitratis . . . 3iss 

Sacchari albi \ 

. > aa q. s. 

Acaciae J 

Aquae menthae piperita? q. s. ad. gij 

M. et fac emulsum. 

S. — One teaspoonful. undiluted, every fifteen to thirty minutes. 

(b) Constipation indicates enemas of water or oil every other day. 
Typhoid cases with constipation fare better than those with diarrhea, 
and cathartics cause meteorism. 

(c) Diarrhea is most frequently due to toxemia and is therefore most 
efficaciously treated with the cold bath ; curds (prevented by diluting or 
skimming the milk), beef -tea or impure milk, may be its cause. Treat- 
ment is indicated by more than four movements daily, colic, tenesmus, 
unrest or weakness. Cold tea with whisky and pulv. aromaticus, gr. xv; 
or paregoric and bismuth, each 3 j after each movement; extr. opii., gr. i; 
or the starch-and-laudanum enema usually give relief at once. 

1$ — Bismuthi subnitratis 5iij 

Extracti opii gr. ij 

M. et div. in pulv. xij. 
S. — One to four a day. (Since absorption from the alimentary tract is slow and uncertain, 
the effects of powerful drugs given by mouth should be watched carefully.) 

1$ — Acidi tannici 3J 

Tincturae opii Tfl,xl 

Emulsi terebinthinae q. s. ad. §j 

M. et S. — One teaspoonful every three hours for 3 or 4 doses. 

1$ — Plumbi acetatis . . gr. iss ad iij 

Opii pulveris gr. i ad iiss 

Sacchari albi gr. lx 

M. et divide in pulv. vj. 

S. — A powder every three hours (note caution under first formula). 

(d) Tympany. — In severe cases albumin-water must be substituted 
for milk. The cold bath often gives relief, since meteorism is generally 
toxemic. Hydrochloric acid after feeding may lessen the tympany. 
The turpentine stupe of Jenner should be applied to the abdomen, 
flannel cloths being dipped in warm water and 3ss ol. terebinthinae and 
slapped hard together to spread the oil evenly and thus avoid blistering. 
The ice-coil is also beneficial. The old turpentine emulsion (emulsum olei 
terebinthinae, 3j) is excellent, though the urine must be watched for 
renal irritation. Whisky, spices, and perhaps eserine sulphate or sali- 
cylate gr. -^V are effective. Emulsum asafetidae, Oj; spiritus chloroformi, 
3ij; and ol. terebinthinae, 3ss, as a warm enema, often give relief. 

(e) Hemorrhage necessitates absolute quiet, mental, physical and ali- 
mentary. The patient should not be moved for any reason. In severe 
cases he should lie in the voided blood, with cotton tucked around the 
hips and between the legs to catch the urine and feces, which should pass 
into it without his being lifted on the bed-pan. No food, no water, no 
enema, no bath, should be given. Morphine quiets the excitement 
attending hemorrhage, lessens peristalsis and enforces bodily quiet; 
gr. J is injected every hour for three doses, or enough to produce its 



56 BACTERIAL DISEASES 

full physiological effect. The sole objection to morphine is that it may 
mask coincident perforation, which occurs once in every five cases of 
hemorrhage; close circumspection invalidates this objection. Opium 
or styptics by the mouth are dangerous and uncertain. The lead- or 
iron-salts probably never reach the bowel. An ice-coil on the abdomen 
may be beneficial. Gelatin may be injected as in aneurysm, but 10 c.c. 
of horse serum or diphtheria antitoxin work better results; the latter 
should be fresh and not of the concentrated type, which largely contains 
globulins. Schreiber employs an intravenous infusion of 5 to 10 per 
cent, grape-sugar solution. The question of stimulation is perplexing. 
There is the risk of forcing blood through the leak by stimulation; on 
the other hand, the volume of blood must not sink too low; but first 
the heart must be allowed to run down — nature's most certain method 
of hemostasis. At a later time only, should strychnine or digitalis be 
administered hypodermically, or saline transfusions be given; delay 
in their use is better than haste. 

(/) Perforation necessitates an early diagnosis and immediate opera- 
tion. Most reported recoveries were operated on in the first twenty- 
four hours. Recovery occurred in 30 per cent, of 358 operations 
(Cazin). In twenty cases operated on at Johns Hopkins Hospital, 35 
per cent, recovered. 

(g) Quenu tabulates 67 operations on the gall-bladder; 82 per cent, 
of recoveries occurred in the cholecystostomies and 80 per cent, in the 
cholecystectomies . 

2. Circulatory System. — Heart weakness is best prevented by absolute 
rest and hydrotherapy. An ice-bag placed over the heart tends to regulate 
and calm its action. Strychnine is the best vasomotor tonic; gr. -§-$■ 
may be given three times a day in cases which do not show signs of 
circulatory failure, but it is best to await definite indications for stimula- 
tion. Digitalis is rarely beneficial in fever cases, and may produce 
signs of cumulative action; the author saw a case in which, with sudden 
defervescence, the pulse dropped from 140 to 40. Camphor, gr. ij, 
should be given under the skin in 1 to 10 parts of sterilized olive oil. 
Other cardiants are considered under Valvular Disease and Pneumonia. 
In typhoid alcohol may be indicated (a) as a food, with milk and eggs, 
thus aiding digestion; 3j _ iv of whisky may be given every two to 
four hours in hot milk. Stokes's mixture contained cognac, §ij — ovi 
vitellus 1, syr. aurantii 5v, and water q. s. ad. §v. (6) As a cardiant 
(though pharmacologists hold that pure alcohol is not a cardiant); 
Meltzer states that it equalizes the circulation. Cognac may be given 
by the mouth, in coffee; or by rectum, in peptonized milk with two 
drachms of tincture of valerian, (c) As a nervine in debility or old age, 
as whisky, champagne (especially for vomiting), sherry or port, (d) 
To a less degree as an antipyretic, since it increases the sweat production . 
Its use must be suspended when the pulse becomes bounding, the res- 
piration hurried, the skin or tongue dry, when there is restlessness, or 
the odor of alcohol appears on the breath. Alcohol has been abused, 
and the recent reaction against its use is in part sound. With discretion 
alcohol is invaluable in severe cases and in alcoholics. 



TYPHOID FEVER 57 

Thrombophlebitis is treated by quiet, elevation, warmth and ban- 
daging from the toes upward. 

3. Respiratory System. — Epistaxis usually ceases spontaneously. If 
the blood runs into the throat a tampon should be introduced. Laryn- 
geal complications may necessitate early tracheotomy; only 2 per cent, 
of severe complications recover without operation. Bronchitis is treated 
by hydrotherapy, rarely by codeine. Expectorants are avoided since 
they disorder digestion. Hypostasis is best treated by hydrotherapy, 
cardiants and explicit written orders for change of posture every two 
hours. 

4. Nervous System. — The initial headache may be relieved by hydro- 
therapy, the ice-cap, ergotin and acetphenetidinum (phenacetin), each 
gr. v (in extreme cases lumbar puncture may be considered). De- 
pression is relieved by valerian and whisky. For delirium and insomnia, 
hydrotherapy is the most useful measure; veronal, gr. v-vij, produces a 
natural sleep; alcohol; morphine, gr. J; codeine, gr. J; heroine, gr. y T ; 
sodium bromide, 5ss-j; or hyoscinse hydrobromidum, gr. T ^- may be 
indicated. 

1$ — Morphinse hydrochloridi gr. J 

Sodii bromidi gr. xxx 

Syrupi aurantii q. s. ad. 3iij 

M. et S. — To be taken at bed- time in water. 

Typhoid patients should never be left alone, lest they leave the 
bed or leap from the window. Restlessness may suggest a full 
bladder. 

5. The Skin. — Massage with alcohol or olive oil is useful. The skin 
functions are helped by the full bath. In the formation of bed-sores, 
local heat, pressure, moisture, maceration and filth are factors. These 
are generally avoided by frequent change of posture, thick pads or rubber 
rings and cleanliness. The least erythema, papule, abrasion or pustule 
on dependent parts is a matter of solicitude; skin infections may cause 
ward epidemics (Edsall). If bed-sores develop, the simplest treatment 
is the best, since antiseptics and powders may aggravate. Balsam 
of Peru is excellent. Scarlet-red ointment (8 per cent.) is often curative; 
it should not be used in deep ulcerations, as poisoning may occur — 
faintness, collapse, cramps, etc., as in anilin poisoning. Collodion and 
adhesive straps are always to be avoided. 

6. Bacilluria. — Bacilluria is met by phenylis salicylas and hexa- 
methylenamina, each gr. x, t. i. d. Urotropin operates best when the 
urine is acid or made so, by acid sodium phosphate; urotropin may 
induce alimentary or vesical irritation and possibly albuminuria. If 
bacilluria persists, irrigations with silver nitrate or bichloride solutions 
are indicated. Special care is necessary in the use of catheters. 

(6r) Treatment in Convalescence. — The convalescence must be 
actual and relapse excluded before the patient can have substantial 
food. It is best to err on the safe side, as embolism and collapse are not 
unknown in convalescence. The patient should not leave his bed for 
two weeks. Irregular fever lingers in some cases until solid food is given 



58 BACTERIAL DISEASES 

and the patient sits up. In other cases, meat causes a higher temperature 
(febris carnis). An excellent tonic is the following: 

1$ — Strychninae sulphatis gr. j 

Acidi nitrohydrochlorici 5J 

Tr. gentianse co q. s. ad. §v 

M. et S. — One teaspoonful after meals in half a glass of water. 

ERYSIPELAS. 

Synonym. — St. Anthony's Fire. 

Definition. — An acute, febrile, contagion caused by Fehleisen's Strepto- 
coccus erysipelatis; characterized by a circumscribed inflammation of 
the skin and adjacent mucosae, which tends to rapid and broad extension; 
and self -limited in its course. 

History. — Erysipelas was known to Hippocrates and Galen. Trousseau 
(1848), in France, held it was a wound infection; Werner, in England, 
maintained that it was infectious; and Koch (1880) found the streptococcus 
which was more fully described by Fehleisen (1881) and bears his name. 

Etiology. — Sporadic cases are seen in every centre of population. 
It occasionally breaks out epidemically. Sixty per cent, of cases occur 
between January and May. In the pre-antiseptic era it was the dread 
of hospital physicians, and even at this day it occasionally visits the most 
sanitary institutions. It is conveyed by a third person, fomites and, 
infrequently, by unclean instruments and vaccine. Cases of placental 
transmission to the fetus are known. The virus is not penetrative but 
adheres to clothing and furniture with great tenacity. Many persons 
exhibit a natural, perhaps an hereditary, susceptibility. In its recurrence, 
it resembles rheumatism. It occurs mostly in the female sex (73 per cent, 
of cases). Alcoholism, debility and chronic nephritis are predisposing 
factors. Any distinction between " idiopathic" and "wound" erysipelas 
is artificial, for in every instance, some abrasion, perhaps too small for 
the eye to detect, occurs in the skin or mucosae. 

Bacteriology. — The Streptococcus erysipelatos was found in the lymph 
vessels by Fehleisen, who first drew the distinction between erysipelas 
and phlegmon. Its absolute differentiation from the Streptococcus 
pyogenes is impracticable. Inoculations from cases of erysipelas some- 
times produce suppuration, pus has caused erysipelas and erysipelas 
and suppuration have developed simultaneously, which facts give weight 
to the theory of the bacteriological unity of erysipelas and suppuration. 

Symptoms. — 1. Incubation lasts three to seven days. 

2. Eruption. — (a) Usually preceded by a few hours of general dis- 
comfort, this stage begins with vomiting, fever, chill and the eruption. 
The fever rises rapidly to 103°. The chill occurs in 75 per cent, of cases 
and is chiefly absent in erysipelas secondary to other diseases, (b) The 
eruption first appears on the face (95 per cent.), near the inner canthus, 
nose or cheek. It consists of a hard, bright red, slightly elevated, and 
painful area which pits but little on pressure, though its color may 
disappear. Pathologically, erysipelas (literally, red skin) is simple 
inflammation; in the skin are found edema, hyperemia, white- and red- 



ERYSIPELAS 59 

cell extravasation, and streptococci which advance in the lymph clefts 
and are most abundant in the spreading edge, and in the lymph vessels 
beyond it. Its elevated red edge is sharply marked or "wall-like." As 
the area spreads, the skin becomes much swollen, edematous, smooth, tense, 
red and hot, causing a shapeless swelling of the face and obliterating its 
lines and expression. The extent is indicated more accurately by tender- 
ness than with the eye. The shin blisters and under the lens small 
vesicles are always found. The prong-like advance of the eruption is similar 
to that of spilled alcohol or burning paper, i. e., it disappears behind as 
it advances forward. Its extension is irregular, because the streptococci 
follow the lines of least resistance. If obstructed by dense tissue, deep 
attachments or the so-called ligamenta cutis, its course becomes cir- 
cuitous, asymmetrical and tardy in one area, though rapid in another. 
It rarely affects the chin, or passes over it to the opposite side. The 
neck resists its advance, often successfully, but erysipelas may course 
over the entire body. The sternum, condyles, ilium and Poupart's 
ligament check or divert its progress. When apparently obstructed, 
new islets of eruption appear near by, which may be seen to be consecutive 
by the faint lymphatic involvement between the foci. The scalp is 
often unaffected, but if invaded it becomes swollen, and pale or blue 
rather than red, and the hair falls out. The first area pales, and a coarse 
desquamation results, while the eruption at more remote points advances. 
The lymph glands are constantly swollen, tender and palpable, unless 
hidden by edema. They enlarge proportionately to the dermatitis. 
The eruption presents few variations: Erysipelas vesiculosum; E. 
bullosum; E. squamosum, or, in old or cachectic subjects, E. hemor- 
rhagicum. (c) The fever rises suddenly, and is 103° to 104° by the fourth 
day and continuous, then remittent, and after seven to nine days resolves 
by crisis. In attenuated erysipelas there is little fever and few general 
symptoms, though the rash may be well developed. In general the 
intensity and progress of the infection are marked by the degree of fever. 
The pulse is soft and ranges between 100 and 120. 

Course. — When limited to the face and head its usual duration is 
eight to ten days, rarely longer than two weeks. Erysipelas migrans may 
travel from limb to limb, and recur repeatedly. In one of the author's 
cases it lasted six months. 

Complications and Sequels. — 1. Nekvous. — Toxemic symptoms are 
infrequent except in aged, debilitated or alcoholic subjects. Delirium 
is an unfavorable toxemic development and occurs especially when the 
scalp is invaded. Meningitis, formerly confused with toxemia, in- 
frequently follows orbital cellulitis or extension along the fifth nerve. 
Postfebrile psychoses, multiple neuritis, degeneration of the cord and 
eye inflammation are exceptional. 

2. Circulatory. — Endocarditis, pericarditis, myocarditis, acute dila- 
tation, and arterial or venous thrombosis are infrequent. High leukocyte 
counts indicate concomitant suppuration. Streptococci in the blood 
are usually ominous. 

3. Respiratory. — Erysipelatous coryza and otitis are infrequent 
and difficult of recognition. Erysipelatous angina is characterized by 



60 BACTERIAL DISEASES 

much pain, sharply marked lividity, a glazed, varnished surface, marked 
edema of the uvula and epiglottis, the formation of vesicles or bullae, 
and sometimes a wall-like margin. Gangrene may develop in severe 
infections. The cervical glands may be swollen. Laryngeal, secondary 
to pharyngeal erysipelas, is rare, severe, easily or necessarily confused 
with glottis edema, and marked by great turgescence and rapid swelling. 
Without tracheotomy, fatal stenosis and extension to the lower air- 
passages may occur. The rare so-called "erysipelas pneumonia" is 
probably a septic localization; in streptococcus pneumonia, the spleen 
is enlarged more frequently than in ordinary pneumonia. The advance 
is rapid, the extension wide, the gray hepatization great, and fibrin 
formation scant or lacking. In pneumococcic infection the same " wander- 
ing pneumonia" may be seen. Pleurisy is usually metastatic 

4. Alimentaky. — Vomiting is toxemic. Exceptional complications 
are parotitis, esophagitis, gastritis, enteritis, intestinal ulceration, hemor- 
rhage, pain, icterus and pylethrombosis. 

5. Genitourinary. — Albuminuria is the most constant visceral 
finding (50 per cent.). Nephritis (4 per cent.) is often of the acute 
glomerular type. Streptococci have been found in the urine and kidneys, 
especially in septic types. Erysipelas may begin in the external genitalia, 
especially in puerperal (page 22). 

6. Septic. — Subcutaneous abscesses, which resemble cold abscesses, 
appear in 6 per cent, of cases, especially in alcoholic, nephritic, diabetic, 
aged or debilitated patients. Phlegmons may develop, usually on the 
legs. Gangrene is fortunately rare (y of 1 per cent.) ; it develops early 
over the eyelids, genitalia or joints, or later in the extremities. Herpes 
is not infrequent. Baldness may also result. The joints may be painful; 
suppurative arthritis or adenitis is metastatic. Generalized fatal sepsis, 
aside from the puerperal form, is infrequent. It bears the same relation 
to local erysipelas as does miliary tuberculosis to a local tuberculous 
focus. 

Diagnosis. — Diagnosis is easy, when the area is the size of a dollar, 
(a) because of its very location; (b) the early involvement of the lym- 
phatics; (c) often the atrium can be found; (d) the redness, smoothness, 
swelling and edema ; (e) the elevated, wall-like margin ; and (/) the prong- 
like, irregular progression. 

In weeping eczema, the edges are not raised, the skin is not smooth, 
there is less fever, the development is slower and itching is present. 
Malignant pustule causes redness and swelling, but anthrax bacilli are 
found under the primary papule and crust. Dermatitis venenata or 
medicamentosa, and pemphigus, are unlike erysipelas. Erythema nodosum 
is discrete and does not spread. Diffuse simple erythema is a febrile 
affection, and of short duration. Dermatitis exfoliativa in the newborn 
is afebrile, develops first about the mouth and chin, and reaches the body 
and limbs later. Its diffuseness and redness are characteristic. In 
lymphangitis the swelling of the lymphatics advances centripetally and 
presents cord-like areas, which are not confluent, vesiculated, uniformly 
red or evenly edged. In phlegmon and deep cellulitis, the process is 
deeper and harder, and the blisters and margin of erysipelas are lacking. 



ERYSIPELAS 61 

Erysipelatous angina may not be diagnosed without coincident facial 
erysipelas. The local findings are not pathognomonic. 

Erysipeloid, a zoonotic affection described first by Rosenbach (1884), 
occurs especially in persons who handle meat; the bacillus is identical 
with that of mouse sepsis and hog cholera. It is recognized by the 
"butterfly" eruption on the cheeks or finger-ends, and is unaccompanied 
by fever or general symptoms. The edge of the eruption is clear-cut, 
its advancement slow, its color a dark livid-red, and its course lasts one 
to three weeks with spontaneous recovery. Gilchrist reported 329 cases, 
of which 323 were caused by crab-bites. 

Prognosis. — (a) In uncomplicated facial erysipelas, the mortality is 
3 per cent, in private practice, and double that figure in hospitals. (6) 
In erysipelas migrans the outlook is less favorable, (c) Erysipelas neo- 
natorum is fatal within a week. It begins on the navel, and less often 
on the vulva or circumcision wounds. Vomiting, diarrhea, peritonitis, 
icterus, pneumonia, necrosis, gangrene, suppuration and sepsis are much 
more common than in adult forms. Fortunately, like puerperal fever, 
this form is now infrequent, (d) Erysipelas secondary to other infections 
is serious, especially in chronic maladies, such as alcoholism, diabetes, 
nephritis and tuberculosis, and also in bed-ridden or senile subjects, 
in whom the asthenic, hemorrhagic and gangrenous types are chiefly 
observed. In acute diseases such as typhoid, diphtheria and pneumonia, 
erysipelas is dreaded, (e) Puerperal forms or involvement of the larynx 
are unfavorable (Hippocrates). (/) Recurrence is more frequent than 
in any other infection, and no permanent immunity is conferred. Re- 
lapses (10 per cent.) are attacks recurring within a few days. Recurrence 
(35 per cent.) suggests the possibility of a bacterial latency and develops 
after months or years; in some individuals, erysipelas may be called 
habitual. It is observed most frequently in the young and in women 
(75 per cent.), and mostly on the face. Five to fifteen attacks are not 
uncommon, and Roger saw forty in one person. 

Treatment. — 1. Prophylaxis. — In this bacteriological era, the disease 
has decreased by asepsis and isolation, though in the latter regard 
many physicians are still remiss. Chronic rhinitis, rhagades, decayed 
teeth and neglected ulcers, must be considered in habitual erysipelas. 
(See Smallpox; Disinfection.) 

2. Mechanical Means. — Mechanical efforts to limit extension of 
the disease are always futile. These consist of binding with elastic 
strips, elastic constriction or massive applications of collodion. 

3. Local Applications. — Iodine, creolin, bichloride of mercury, mag- 
nesium sulphate (saturated solution), phenol, alcohol, iodoform, boric 
acid and other topical applications, are recommended, but the water 
they contain is their most potent ingredient, and was recommended 
by Hippocrates. No application can reach the deeply situated cocci. 
Cold compresses afford a certain relief for pain and tension. Ichthyol 
ointment, 10 per cent., is soothing but not curative. 

P* — Creolin 1 part 

Iodoformi 4 parts 

Adipis lanae hydrosi (lanolin) 10 parts 

M. et f. ung. (Koch.) 



62 BACTERIAL DISEASES 

4. Drugs. — Erysipelas is a self-limited disease. Iron (Hamilton 
Bell, 1851) is well tolerated in large doses, but neither shortens nor miti- 
gates the disease. 

R- — Tincturse ferri chJoridi 3iiss 

Quininse sulphatis gr. xxiv 

Spiritus chloroformi 3ij 

Aquae q. s. ,ad. §vj 

M. et f. mist. 

S. — Two tablespoonfuls every three or four hours. (J. Burney Yeo.) 

5. General? Treatment. — The symptoms are managed expectantly, 
i. e., as they arise. Headache, delirium, pain, vomiting and cardiac 
weakness are treated as in typhoid. Rest in bed and as generous nourish- 
ment as the stomach will tolerate are indicated. 

6. Serum. — Chantemesse reduced the death-rate to 2.5 per cent, by 
serum treatment (a figure often reached by more simple measures). 
Vaccines have not proven successful. 

Erysipelas as a curative agent {erysipelas salutare) : Permanent cure 
of lupus has followed a complicating erysipelas. Syphilitic manifesta- 
tions quickly subside after this infection, and its beneficial effects have 
been observed in leukemia, Hodgkin's disease, carcinoma, sarcoma, 
chronic arthritis, tuberculous adenitis, diphtheria and tuberculosis. 

PNEUMONIA. 

Synonyms. — Fibrinous, croupous or lobar pneumonia, pleuropneumonia, 
pneumonitis, lung fever. 

Definition. — An acute, specific, self-limited infection caused by the 
pneumococcus, characterized by fibrinous inflammation of the lung, 
toxemia, pneumococcemia, and solution of the fever by crisis. 

Frequency. — Pneumonia constitutes 6.5 per cent, of all internal diseases, 
4 per cent, of all diseases, 6.6 per cent, of all medical deaths, and 8 per 
cent, of all deaths. 

Bacteriology. — 1. The pneumococcus or Diplococcus pneumoniae (Plate 
II) was recognized by Frankel (1884), and Weichselbaum (1886) first 
demonstrated its frequency and importance. It is a lanceolate, encap- 
sulated diplococcus; it is easily seen in cover slips, it readily stains by 
the Gram method, and presents many cultural variations. Its atrium 
in pneumonia is the respiratory tract, although it may enter the blood 
by other avenues in sepsis (q. v.). From the lung it may spread diffusely, 
chiefly through the bloodvessels. It is found in dust, saliva, and in 30 
per cent, of healthy noses and throats, though usually with attenuated 
virulence. Experimental inoculation has produced pericarditis, endo- 
carditis and empyema. In lobar pneumonia or apart from this acute 
bacteriemia the pneumococcus has been found in the blood, joints, brain, 
bone-marrow, etc.; in otitis media, endocarditis, peritonitis, cholangitis 
and endometritis; in the urine and feces; in the nasal sinuses; and it 
may pass from the mother to the fetus. It may be a terminal septic 
infection. Until recently it was thought that typhoid and pneumonia 
were local infections and that bacteriemia was a serious complication; 



PLATE II 




L. SCHMIDT, FEC. 



The Diploeoeeus Pneumoniae, Stained With Methylene Blue 
and Fuehsin as a Counterstain. Taken from the Sputum of a 
Case of Acute Croupous Pneumonia. (Simon.; 



PNEUMONIA 63 

the typhoid bacillus is found in the blood in 100 per cent, of early typhoids 
and the pneumococcus in from 90 to 100 per cent, of pneumonics (v. i.). 
It is assumed that a pneumotoxin exists producing the toxemia; when an 
antitoxin develops, the crisis occurs, but the factors of resistance to, 
and recovery from, pneumonia are not known. Immunity does not 
result from one attack; recurrence is likely in 23 per cent.; ten, even 
twenty-eight recurrences are known. The pneumococcus is the sole 
cause of typical pneumonia, but other microorganisms are sometimes 
found, as the pneumobacillus (Friedlander), and the typhoid, colon, 
diphtheria, proteus, influenza, plague, and pyogenic organisms. 

Indirect Causes. — (a) Age. — Pneumonia may develop even in the new- 
born. Predisposition to infection is great up to the sixth year, then 
much less until the fifteenth year, when its frequency increases with 
each decade. Over half the cases of pneumonia occur between the 
twentieth and fortieth years, and over 80 per cent, between the tenth 
and fiftieth years. 

(6) Sex. — Eighty per cent, of cases are males. The relation to trauma 
is in doubt. 

(c) Cold. — Three-quarters of all cases of pneumonia occur in cold 
months (February, March and April) when the weather varies, the tem- 
perature is low, the moisture is great and the winds are high. Dust 
disseminates the dried sputum. Pneumonia is half again as frequent 
in the cities as in the country. In the winter of 1903-4, when 4000 
died of pneumonia in Chicago, practitioners in towns not one hundred 
miles distant did not see a case. 

(d) Individual predisposition is a more important factor than in any 
other infection. Susceptibility is increased by debility, overwork and 
alcoholism. 

General Clinical Course. — After a short incubation of some hours the 
disease begins suddenly. In infants it often begins with convulsions — 
in the young with vomiting, and in older subjects with a severe chill, 
often brusquely in persons of robust health. On the first day there is a 
sudden rise of temperature; the face becomes red, even livid; the eyes 
are injected; the pulse and respiration are accelerated; the patient lies 
characteristically flat in bed; there is much depression; headache and 
sudden sharp pain in the side develop, accompanied by cough. On the 
second day the cough, pain, respiration-rate and headache increase; 
the expiration is short and grunting, with dilatation of the alse nasi, 
and speaking is difficult; leukocytosis develops. The bloody sputum 
appears, which with the above symptoms establishes the diagnosis before 
consolidation appears. On the second or third day there are evidences 
of lung consolidation, such as tympany, soon followed by dulness, the 
crepitant rale, and bronchial breathing; there is an increase in the 
pulse and respiration; herpes, anorexia, coated tongue, constipation, 
moderate delirium and febrile urine develop. The coughing is frequent 
but short in duration, voids a viscid red sputum, and causes catching 
respiration, pain and broken sleep. The clinical course may be unfavor- 
ably modified (a) especially by collapse due to myocardial or vosomotor 
paralysis, or to pulmonary embolism; (b) by profound toxemia; (c) 



64 



BACTERIAL DISEASES 



by delirium tremens; or (d) by death, though at this stage it is rare. 
In favorable cases, when the toxemia is spent, the crisis occurs, usually 
on the fifth, seventh or ninth day with gradual disappearance of the 
local findings. A "critical" fall of temperature, pulse- and respiration- 
rate, sweating and relief of nervous symptoms result. Lysis is less 
frequent. Toxemia is the dominant feature of pneumonia, and the con- 
solidation is secondary. The degree of toxemia has no constant relation 
to the amount of consolidation, just as the toxemia of typhoid does not 
depend on the presence or degree of the intestinal changes. 

Analysis of Individual Symptoms. — 1. Onset. — In over 75 per cent. 
the onset of -pneumonia is sudden. Chill, convulsions, vomiting and 
fever, after a short incubation, usually mark the brusque onset. Repeated 

chilly sensations do not as accurately 
designate the onset as does an initial 
rigor. In no other acute disease except 
malaria is the chill so severe and con- 
stant (in 75 per cent.). The onset is 
atypical in senile pneumonia and in 
pneumonia secondary to other diseases 
— e. g., delirium tremens, typhoid and 
psychoses — the chill, cough, dyspnea, 
pain and sputum are often absent, so 
that the existence of pneumonia may 
not be suspected. Prodromes occur in 
25 per cent, of cases, mostly in men 
between thirty and forty years, and 
rarely last over five days; depression, 
headache, bronchitis, backache and low 
fever may be noticed. In one of the 
author's cases a pneumococcus infection 
began in the throat, then invaded the 
larynx, and only after three weeks in- 
vaded the lung. In four cases, low 
fever and hemoptysis for several days 
suggested tuberculosis. 
2. Fever. — Its usual course is, first, 
very sudden rise; the fever is then 



Day 


1 


2 


a 


4 


5 


6 


7 


TEMP. 

105 
















104 




/ 


/i 


1 


7 


,/ 


Vj 


103 




v 


VI 


J 


V 


V 




102 




V 












101 
















100 








I 








99 


(A 












c 




1 














98 

































Fig. 7. — Fever curve of typical case 
of pneumonia: A, sudden rise; B, 
pseudocrisis; C, crisis. 



continuous, often with not 



a 
more 



than 1° or 2° variation; in three- 



quarters of the cases the maximum fever averages 102° to 105°. It may 
then remit, which is of good prognostic import and then at the end of a 
week's illness follows the crisis (v. i.). Remittent fever throughout 
the disease occurs in some cases. Recrudescences occur when consolida- 
tion passes from one lobe to another. The fever is lower or even absent in 
the aged, alcoholics, and in secondary pneumonia; the writer saw a total 
pneumonia, with normal rectal temperature in a man aged forty-eight. 
Fever causes a loss of weight of even twenty to thirty pounds. The rise 
preceding the crisis (perturbatio critica) may be mistaken for an ante- 
mortem rise; in both conditions there may be delirium, chill or an 
alarmingly irregular pulse. A pseudocrisis may deceive the physician, 



PNEUMONIA 



65 



the fever resuming its original elevation. Crisis occurs in 80 per cent, 
of cases, usually on uneven days, as noted by Hippocrates — the fifth 
seventh, ninth or eleventh day — usually between evening and early 
morning. It very rarely occurs on or before the third day. It marks 
the end of the toxemia but not of the consolidation which lasts several 
days more. In six to ten hours the temperature falls to or below normal, 



Days 




Fig. 8. — Pneumonia; remittent (subcontinuous) fever. 

accompanied by sleep, euphoria, lessened pulse and respiration, lateritious 
deposits, reappearance of the chlorides in the more abundant, limpid 
urine, and "critical" sweating or even diarrhea. The fall may measure 
even 10° or 11° and the pulse may reach 30. Lysis occurs in 20 per cent, 
of cases. It is likely to occur when the fever lasts more than ten days, 
but lingering fever may indicate progression in other lobes or compli- 
cations, as empyema or endocarditis. 

3. Respiratoky Findings. — (1) Pain in the side is generally pleural 
and its presence in 90 per cent, of cases gives it a diagnostic value; this 

March 



Dnys 28 1 2 3 4 1 


5 C 7 8 9 1 10 111 12 13 1 


4 15 1G 17 18119 2 


21 22 23 24 25 2G 27 28 29 30 


105 


1 






104 




. 




103 


■ I 


A 1 i 




102 


■ J A Mil 


i\ Hi \ K li 




101 




WW 


.. 1A 


100 A 


A. /*M \ l\l ^ 11 


ffi-A-^ 


99 AsA / v r\ k . 


/\/V^' V |V y 


vTvri \ 


J 1 \ A A /\ a ^ /~\ 


98 / V \| ^r* 


V 


V 


1 V v V/ \A A *> / v ^- 


97 f V 1 




r 1 


1 V » | V 


1 


1 







Fig. 9. — Pneumonia fever curve; exceptionally protracted though uncomplicated fever. 



most frequent respiratory symptom appears early, is increased by cough- 
ing or motion, and is sharp or even agonizing. It is usually localized 
over the consolidated focus, but in 8 per cent, is referred along the lower 
intercostal nerves to the abdomen, in children especially, and sometimes 
in adults. Appendicitis or cholecystitis may be thus simulated. Some- 
times the pain is radiated to the opposite side of the chest. Pain is 
5 



66 



BACTERIAL DISEASES 



absent in central, secondary and upper-lobe pneumonias; often in the 
aged and in children; and in cases with great delirium. 

(2) Dyspnea is frequent; it is caused especially by toxemia, but also 
by pain, cardiac weakness and bronchitis. 

(3) The Respiration-rate. — Because of cerebral toxemia, or pleuritic 
pain, the respiration-rate is increased to 24 or 40 (or more in children); 
and in two-thirds of all cases, it ranges between 30 and 50; it almost 
never rises to 60 or 80 except in the death agony. The author saw a 
rate of 96 with recovery; the pulse was 90. Dilatation of the nares is 
said to be ominous, but to the author seems common in ordinary cases. 
Alteration of the pulse and respiration ratio was first noted by von Jurgen- 
sen; the normal ratio of 1 to 4 becomes 1 to 3 or 2. In a personal 

observation with the entire right 
lung consolidated, the respiration- 
rate was 18. 

(4) The Cough. — The cough always 
irritates, and seldom relieves the 
patient. It is present from the 
onset to the crisis, is due to the 
bronchitis and almost invariably 
occurs in lower-lobe pneumonia; it 
is often absent in upper-lobe, term- 
inal or secondary pneumonia, in very 
delirious subjects, in the aged and 
young. 

(5) The Sputum. — The sputum, 
at first transparent, mucous and 
scanty, soon becomes viscid, and 
difficult to raise and to expectorate, 
as it adheres to the mouth and lips. 
It is so viscid that the sputum-cup 
may be inverted without spilling the 
sputum. In two days it becomes 
red and rusty (80 per cent, of cases). 
Later it becomes more abundant. 
Increased fluidity may rarely result 
from weak heart. Rusty sputum 

is often absent in children who swallow sputum; in upper-lobe pneu- 
monia, in which there is less hemorrhage, less consolidation and less 
cough to dislodge exudation; and finally in the senile and secondary 
pneumonias, because of weakness or toxemia. The cause of unusual 
color in the sputum, such as lemon- or brick-color, is unknown; it is 
sometimes observed in pulmonary edema or incipient gangrene and 
obscures the prognosis. Safranin color {sputum croceum) indicates 
resolution. The rusty sputum is of great diagnostic value — e. g., 
in the beginning of the disease or in central pneumonia — and gener- 
ally is of good import. Fibrin threads or "casts" of the bronchioles are 
usually seen between the third and seventh days. On shaking the 
sputum in water and catching the shreds on a slide, they appear clubbed 




Fig. 10. — Fibrinous coagulum from a case 
of croupous pneumonia (Bizzozero). 



PNEUMONIA 67 

at their alveolar ends; they are also found in tuberculosis and fibrinous 
bronchitis. They consist of fibrin, white cells, fatty cells and epithelium. 
The sputum contains blood cells, epithelia and pneumococci, found 
first by Wolff in sputum and by Weichselbaum in the lung. 

(6) Lung Pathology. — Laennec, the first to differentiate pneumonia 
from pleurisy (1819), described three stages: (a) The stage of hyper- 
emia is very exceptionally observed unless the subject dies in twenty- 
four to thirty-six hours, although hyperemia may be seen at the 
edges of the consolidation where the pneumonia is beginning to 
extend. The lung crepitates less and floats; it is red, tears readily, 
since it has lost its elasticity, and on section exudes a serosanguineous 
fluid. Under the microscope, congestion, serum and diplococci in the 
alveoli are observed. The alveolar epithelial cells swell and desquamate, 
which, according to some observers, are the primary changes. (6) In 
the stage of red hepatization, the lung is evenly red, friable, airless (not 
wholly so in penumonia of an upper lobe), and sinks when put into water. 
Its weight is increased ten to fifty ounces. The lung has marks of the 
ribs on its fibrin-coated surface and is enlarged to the size of deepest 
inspiration (Rokitansky, who developed the gross anatomy of pneumonia). 
On scraping the cut surface, fibrinous plugs or casts of the bronchioles 
are observed. The lung is granular on section (Laennec), from fibrinous 
exudation into the alveoli; these granulations are seen best by oblique 
illumination. Under the microscope, coagulated blood and exudate, 
alveolar epithelium, injected bloodvessels, emigration of leukocytes, 
diplococci and meshes of fibrin are noted, (c) In the stage of gray hepati- 
zation, the granulations are grayish-yellow — not red, because the blood 
is absorbed; they are larger and looser than in the second stage. The 
connective tissue is grayer than the granulations, and is sharply defined 
by the lung pigment. It has been claimed that death always occurs 
if this stage is reached. If the patient lives, the granulations disappear; 
the lung exudate becomes semifluid (purulent infiltration) and can be 
washed out; resorption of this fatty emulsion occurs by the lymphatic 
vessels and not by evacuation through the sputum. Proteolytic ferments, 
probably derived from the leukocytes, dissolve the exudate; the products 
of this autolysis are excreted by the kidneys. 

Seat of Pneumonia. — The process begins at the hilum and extends to 
the pleura, as proved by the arrays. If it remains at the hilum it is central 
pneumonia (1.7 per cent.); if the entire lung is involved, it is pneumonia 
totalis or, if the bronchi are plugged, massiva; the terms "double pneu- 
monia" and "crossed pneumonia" are self-explanatory. The lobes are 
involved in the following order of frequency: (a) Right lower lobe; (6) 
left lower; (c) right middle; (d) right upper; (e) left upper lobe. Jiir- 
gensen's 15,614 cases of pneumonia show that the right lung is affected 
in 53 per cent., the left in 37, and both lungs in 10 per cent. The upper 
lobes are involved in 16 per cent, and the lower in 84 per cent. 

(7) Physical Signs. — The physical signs develop in the lungs, at the 
earliest, only after twelve to twenty-four hours. 

(a) Inspection.- — The decubitus is often dorsal in lower-lobe, and erect 
in upper-lobe pneumonia; the patient at first lies on the sound side to 



68 BACTERIAL DISEASES 

avoid pain; on the diseased side later, for better expansion of the sound 
lung. The spinal column is concave toward the diseased lung for its 
better immobilization. The excursion is less on the diseased side because 
of pleuritic pain. Litten's sign is absent and the sound lung is vicariously 
active. The diseased side is larger, by one inch or so. The accessory 
muscles of respiration are active and dilatation of the nares is seen. 
Systolic pulsation of the lung occurs when the lingual lobe is consolidated, 
or, in the first stage, when the heart beats against semifluid exudation. 

(b) Palpation. — Lessened excursion is detected more readily than by 
inspection; vocal fremitus is usually increased because of better sound 
propagation, fremitus being normally greater on the right side. It is 
decreased by (i) bronchial occlusion by fibrinous plugs, usually dislodged, 
however, by having the patient cough; (ii) coincident pleural effusion; 
and (iii) great consolidation rendering the chest wall tense. Pleural 
friction may be felt. 

(c) Percussion. — (i) A tympanitic note (Skoda' s resonance) is obtained 
in the first stage, caused by decreased elasticity of the lung and therefore 
decreased amplitude of vibration, due to the swelling of the alveolar 
epithelium and turgescent capillaries. This condition lasts one or two 
days, and may cause doubt as to the side involved. Tympany may 
denote new pneumonic extension (relaxation of the lung tissue contiguous 
to areas already consolidated). Tympany in the later stages is not 
uncommon in upper-lobe pneumonia where exudation is usually incomplete 
or in moderate compression, e. g., of a right upper lobe when the right 
middle and lower are consolidated. It is rare in lower-lobe pneumonias. 
Tympany may persist days after the crisis, (ii) Dulness usually develops 
on the second day and is the percussion sign of the second stage. When 
complete it corresponds to the lobe confines. The dulness is not 
absolute. It is usually first detected in the posterior axillary line in 
lower-lobe pneumonia, and generally is more complete behind than in 
front, and more in lower- than in upper-lobe involvement. Dulness 
is difficult to detect if the area is not at least 1 by 2 inches, or if it is 
deeper than 2 inches from the surface. It is absent in central pneumonia. 
With resolution it is replaced by tympany. 

(d) Auscultation. — Decreased breathing, or sudden local puerile breath- 
ing is often noticed at first. 

First Stage. — The crepitant rale of Laennec remains the auscultatory 
sign of the first stage ; but, as he stated, it is not specific, because it also 
occurs in tuberculosis, lung edema, infarct, hypostasis and bronchiolitis. 
It originates in the viscid exudate in the finest tubules and alveoli. 
It is coarser in the aged and in children because the large tubes are 
more involved. It is heard at the height of inspiration as a succession 
or shower of delicate crackles; when not heard, a coughing effort may 
elicit it; it often disappears after a number of deep inspirations, e. g., 
when demonstrated to a class, only the first students hear it. The crepi- 
tant rale disappears during the second, and reappears in the third 
stage. 

Second Stage. — The intense bronchial breathing is due to increased 
transmission of the breath sounds through the solidified lung. It sounds 



PNEUMONIA 69 

as though nothing intervened between the lung and the stethoscope 
and is especially near when the ear is applied directly to the chest. It 
is absent or partial, especially anteriorly, in central pneumonia, coincident 
pleurisy, and obstruction of the bronchi by fibrinous casts. In the latter 
case, several coughs usually loosen the obstruction and restore the 
bronchial breathing. Bronchophony, also explained by increased con- 
duction, is heard when the patient counts or speaks, but especially after 
each involuntary expiratory grunt. Egophony is occasionally heard, 
as well as Baccelli's phenomenon (auscultatory whispering). The 
crepitant rale disappears in this stage, except at the edges of the hepati- 
zation where extension occurs. 

Third Stage. — The crepitant rale reappears — the rale redux. 

4. Circulation. — (a) The pulse-rate is usually 100 to 120, or higher 
in children, the aged, and severe toxemia. In adults, a rate of 130 to 
140 or a slow pulse, indicating grave heart or brain complications, irreg- 
ularity and gallop-rhythm make the prognosis less favorable. Ante- 
critical irregularity frequently occurs. The pulse is deceptive and its 
fulness is of no value in prognosis. Extensive pneumonias may compress 
one subclavian artery, making the corresponding radial smaller, (b) 
In the right heart, dilatation from toxemia frequently occurs; the second 
pulmonic tone is accentuated unless the right ventricle becomes greatly 
weakened. There may be functional bruits. In very rapid cardiac action, 
the two heart tones sound alike, resembling the fetal tones (embryocardia) . 
(c) Collapse, usually due to myocardial or to central vasomotor paralysis, 
may occur at any stage, (d) The blood shows anemia. The fibrin increase 
is readily noted in fresh blood preparations. A polymorphonuclear 
leukocytosis appears early, and slightly survives the fever. The leuko- 
cytosis ran between 15,000 and 30,000 in 75 per cent, of Cabot's counts; 
it may reach 100,000. The eosinophiles are decreased or absent until 
the acme whence the favorable significance of their reappearance. The 
lymphocytes are decreased. During convalescence many myelocytes 
appear. The white count remains high in delayed resolution or complica- 
tions. A low count generally is unfavorable. Pneumococcemia, until 
recently considered of bad import, is of no prognostic value, since it occurs 
in 90 to 100 per cent, of cases, perhaps even before hepatization. The 
agglutinative power of the serum increases until the crisis occurs. 

5. Digestive System. — There is the febrile thirst and anorexia. 
Vomiting occurs in 25 per cent, of cases, from toxemia or coughing. 
The distressing tympanites occurs in the severer cases — and invariably 
in alcoholic subjects — from toxemic paresis of the intestinal muscularis. 
The occasional diarrhea is toxemic; constipation is the rule. There is 
often intumescence of the liver and spleen (in 15 per cent, of all 
cases) . 

6. Skin. — The red cheek on the affected side was known to Aretseus. 
The skin is Usually dry, but miliaria and sweating may be seen. Herpes 
is found more often than in any other disease (40 per cent.), from the 
third to fifth day, chiefly on the face; Howard found causal changes 
in the Gasserian ganglion; herpes may develop on the body, limbs, 
genitalia, etc. It is of diagnostic and generally of favorable import. 



70 BACTERIAL DISEASES 

Rarer eruptions are erythema, roseolas and purpura. The lymph glands 
are enlarged in 25 per cent, of cases. 

7. Urine. — Characteristic fever urine is found, and the urea is increased 
threefold after the crisis from overproduction and accumulation during 
the fever; from the resolving exudate, uric acid and xanthin result. 
The chlorides are decreased (from 225 grains daily to 30 grains) or 
absent until the crisis, when they reappear in increased quantities (Rotten- 
bacher); no satisfactory explanation for the chloride retention is known; 
The urine often becomes neutral or alkaline two days after the crisis. 
Albuminuria and cylindruria appear in 50 per cent, of cases; peptonuria 
and acetonuria are not uncommon; and the diazo reaction appears in 
20 per cent., hematuria in 1.6 per cent., nephritis in 1 per cent., and 
uremia very uncommonly. 

8. Nervous System. — Headache is constant. There may be insomnia, 
restlessness, or stupor which is always ominous. Delirium (22 per cent.) 
occurs with upper-lobe pneumonia, alcoholism or marked toxemia; 
nervous symptoms resulting from exhaustion may occur even a week 
after the crisis (2.5 per cent.). The patellar reflexes are often absent and 
the pupils may be dilated or sluggish. Convulsions, coma and rigid 
neck, in children, result from toxemia, brain edema or meningitis. 
Hemiplegia may result from brain edema or anemia, or arteriosclerosis 
plus a weakened heart. 

Mechanism of Death in Pneumonia. — Death is rare in the first three 
days, except from some antecedent malady, as nephritis. (1) Toxemia 
is all-important in its action on the heart, brain and vasomotor nerves. 
Death ensues with rapid pulse and respiration, algid extremities and ob- 
tunded sensorium. (2) Pulmonary edema is cardiac, or inflammatory, 
from an extending pneumonia. (3) The extent of pneumonia is the least 
important factor. A massive pneumonia in a robust person causes less 
disturbance than a small patch in a nephritic. There is no parallelism 
between the area hepatized and the resulting toxemia. (4) Pneumococci 
in other tissues cause pneumococcic meningitis, endocarditis, etc. 

Complications. — These are few but severe. 

1. Pleurisy. — Dry pleurisy is so constant as to justify the name of 
pleuropneumonia, the pleura being covered with a thick, tenacious, 
exudate, usually pneumococcic; if due to the streptococcus, it is a 
complication of great danger. Frankel saw serofibrinous pleurisy in but 
1 per cent, of 1000 cases, yet Maragliano aspirated some fluid in 66 per 
cent, of his pneumonic patients. The writer has seen three cases of 
pneumonia on one side and pleurisy on the other. Pneumococcic empyema 
occurs in 2 per cent, of pneumonias and is notable since the pneumococcus 
seldom provokes suppuration in the lung (v. Pleurisy). Recovery is 
possible even without operation. Interlobar empyema is most serious, 
because it so often escapes detection. 

2. Endocarditis. — Acute endocarditis complicates pneumonia in 
1 per cent, of all cases and 5 per cent, of fatal cases. Endocarditis is 
malignant in 80 per cent, of cases; 25 per cent, of all ulcerative endo- 
carditides are pneumococcic. The pneumococcus is found in the vegeta- 
tions. The valvular exudate is voluminous, though ulceration, valvular 



PNEUMONIA 71 

• 

aneurysm and perforation are less common than in staphylo- and strepto- 
coccic forms. Endocarditis develops especially on old valvular lesions 
in the left heart, most frequently on the aortic valves. The right heart 
is involved three or four times as frequently as in endocarditis due to 
other bacteria. Sixty per cent, of cases are associated with meningitis. 
Middle-aged adults are most often affected. Endocarditis is probable 
when a murmur, systolic or particularly diastolic, occurs with irregular 
protracted fever, chills, sweats, positive blood cultures and embolism 
(50 per cent.). Symptoms may directly follow the pneumonia or develop 
after one-half to one week of normal temperature. Fever is sometimes, 
and leukocytosis frequently, absent. Symptoms may be absent (v. Septic 
Infections and Ulcerative Endocarditis). 

3. Pericarditis. — Its frequency is 1 per cent., and the pericardial 
rub is absent in 60 per cent, of cases. Dry pericarditis occurs more 
often in children, at the height of the disease and when the left lung is 
involved. Effusive pericarditis is less common than the fibrinous 
form. 

4. Arteritis and Phlebitis are less frequent than in typhoid. Steiner 
collected forty-eight cases of venous thrombosis (1903) ; it develops 
in convalescence and heals usually (75 per cent.), though embolism 
or permanent venous obstruction may develop. 

5. Nervous Complications. — Delirium tremens may develop in an 
alcoholic from the shock of the pneumonia onset; or, during the course 
of delirium tremens, pneumonia may develop insidiously and is easily 
overlooked and remarkably fatal (v. Prognosis). Meningitis occurs in 
5 per cent, of autopsies, and in 0.3 per cent, of clinical cases, in asthenic 
patients, in upper-lobe pneumonia, and often accompanies endocarditis. 
One of the author's cases died a week after apparent convalescence, and 
the autopsy showed a quarter inch of pus over the convexity. The 
usual meningitic symptoms develop if infection reaches the base of the 
brain, but this is not usual (see Meningitis). The mortality is 93 per 
cent. ; the author has seen recoveries. 

6. Alimentary Complications. — Parotitis and peritonitis occur, each 
0.3 per cent. Dieulafoy described an ulcerative gastritis caused by 
pneumococcic embolism and attended by gastrorrhagia. Fussell col- 
lected 12 cases of acute dilatation of the stomach. Icterus averages 1 per 
cent. ; its causes are hepatic stasis, duodenal catarrh, and hematogenous 
jaundice from toxemic hemolysis. (See Pneumococcic Peritonitis.) 

7. Lung Complications. — Suppurative mediastinitis was regarded 
as the connecting link between pneumonia, meningitis and pericarditis. 
Pulmonary induration may follow incomplete resolution. Abscess 
develops in 5 per cent. ; pus and elastic fibers in the sputum, less frequently 
cholesterin and hematoidin crystals may be the sole signs, and continual 
coughing the chief symptom. Gangrene occurs in 1 to 2 per cent, of the 
cases. Clinically it is recognized by the horribly fetid sputum. 

8. Arthritis.— Hematogenous pneumococcic arthritis may be serous 
or purulent; its incidence is 0.5 per cent, and its mortality 28 per cent. 
In 62 per cent, it is monarticular, and the knee is involved in 30 per 
cent.; 158 cases are reported. 



72 BACTERIAL DISEASES 

Clinical Types and Variations. — These are as follows: 

1. Abortive Pneumonia is recognized by the sputum, fever and 
respiratory disturbance, but produces no hepatization. 

2. Ephemeral Pneumonia is characterized by one day of fever, and 
very rapid resolution. The onset is brusque and severe but the symptoms 
speedily abate. 

3. Relapsing Type. — After the crisis, the entire cycle recurs (in 0.3 
per cent.). Recurrent type (v. s.). 

4. Local Variations. — Apex pneumonia is often more severe, atypical, 
adynamic and complicated. Migratory pneumonia travels from one 
part to another (so-called erysipelas-pneumonia). Central, total and 
massive pneumonia (v. page 67) . 

5. In Children. — An abrupt onset occurs without chill before the 
seventh year, but with vomiting (50 per cent.), convulsions (7 per cent.), 
and other cerebral symptoms. Cough is often absent, no sputum appears, 
and the pain is referred to the abdomen (third to fifth year). Pain is 
more important than increased respiration, which occurs in any fever; the 
respirations may number eighty under two years of age; in older children, 
fifty. Crepitant rales are usually absent because of the superficial 
breathing caused by pain. Latency of physical signs, such as absence of 
bronchial breathing, bronchophony or dulness is sometimes noted. 
Localization is more often central, apical or migratory. Lysis is more 
frequent than in adults. 

6. In the Aged. — Pneumonia is frequently latent, insidious and 
asthenic, with ill-marked signs, without chill, even without fever, and 
often without cough, pain or sputum. It is remarkable that so severe an 
infection can exist with so few of its usual symptoms. In this type, 
pneumonia is declared by the physical findings only. 

7. In Alcoholics. — (See page 71). 

8. Asthenic Pneumonia. — In asthenic or "typhoid" pneumonia, 
toxemia is dominant, with high fever, enlarged spleen, albuminuria, 
icterus, severe complications and high mortality. In contrast to these 
cases, the author had two patients who worked throughout the disease. 

9. Secondary Pneumonia. — Pneumonia may be secondary to emphy- 
sema, arteriosclerosis, hepatic cirrhosis, nephritis, diabetes, tuberculosis, 
typhoid or other conditions. The frequency of ether pneumonia in 
abdominal operations suggests the possibility of embolism as a factor; 
ether predisposes to pneumonia by irritation of the respiratory tract. 
The nose and mouth should be cleansed before anesthetization to remove 
native germs. 

This type is atypical, ill developed, or masked by the primary disease ; 
the hepatization is rarely typical and is more lobular than lobar; the lung 
section is smooth and moist, and the exudation is more cellular than 
fibrinous. 

10. Delayed Resolution.— Resolution is effected by lymphatic 
absorption, (a) Resolution may require weeks or even months, especially 
in apical involvement, and more often after a lysis than crisis ; the toxemia 
disappears but dulness and bronchial breathing persist, (b) Imperfect 
resolution may be caused by abscess formation, or inflammatory involve- 



PNEUMONIA 73 

ment of the connective tissue and lymphatic vessels. Induration of 
the lung by organization of the exudate is usually febrile. 

Diagnosis. — Mistakes are rare in the diagnosis of frank pneumonia 
in adults — they occur mostly in aged individuals, alcoholics, children 
and secondary pneumonia. All subjects with chronic disease must be 
closely examined when the respiration, pulse and temperature rise, or 
when the subject is not doing well. 

1. Onset Symptoms. — The chill in adults, or convulsions and vomiting 
in children, suggest the possibility of pneumonia. Chill, pain in the 
side, sudden high fever and rusty sputum, are almost final, because 
practically the only other disease in which they occur is infarct of the 
lung — in which the sputum is reddish, not viscid, usually darker, and 
more abundant. In 25 per cent, of cases the onset of pneumonia is 
not brusque and the physical findings of pneumonia are present without 
a typical history; indeed it may rather be suggestive of simple pleurisy, 
etc. Pneumococcemia without lung involvement may simulate influenza 
{q. v.). 

The occasional reference of the initial pain to the abdomen may 
simulate appendicitis. As a rule the abdominal pain exists without 
tenderness or with superficial tenderness only. Consideration of the 
toxemia and respiration-rate generally prevents errors in diagnosis; 
collapse, intense abdominal tenderness and rigidity may simulate per- 
foration. 

2. Physical Findings in the typical case appear within two days after 
the onset: lessened expansion, increased vocal fremitus, dulness, bronchial 
breathing, the crepitant rale, the grunting, short expiratory "huh," 
and a bronchial tone to the whispered or louder voice sounds. These 
findings are modified by many conditions; thus the fremitus is decreased 
in massive consolidations, in coincident pleural effusions or in fibrinous 
plugging of the bronchi; usually the plugs are dislodged by repeated 
coughing. The dulness is preceded and followed by a tympanitic note. 
The crepitant rale is found only in the first and third stages, but in 
almost every case can be found in some part of the affected lung. 
Bronchial breathing is rudimentary or absent in incomplete hepatization, 
is often so in upper-lobe pneumonias, in complicating effusive pleurisy, 
and in obstructed bronchi. The physical signs are pathognomonic only 
in connection with the cyclic course, disturbed pulse and respiration 
ratio, pneumococcemia, herpes and leukocytosis. 

3. Localization. — Massive pneumonia not infrequently simulates 
pleurisy, because fibrinous plugging of the bronchi abolishes bronchial 
breathing, bronchophony, the crepitant rale and vocal fremitus; there 
may be slight luxation of neighboring viscera. Consideration of the 
onset, cyclic course and the dislodging of the plugs by forcible coughing 
almost invariably determines the diagnosis. Conservatism is necessary 
in the diagnosis of central pneumonia; all pneumonias are central in 
their incipiency; in two personal cases the local findings did not appear 
for a week. 

4. In Children. — Pneumonia may be mistaken for abdominal disease 
or pleurisy. "Cerebral pneumonia" may be (a) convulsive, occurring 



74 



BACTERIAL DISEASES 



under two years, with fever and vomiting, but the evenly high fever is 
suggestive even if the cough and dyspnea are obscured by the brain 
symptoms; or (b) meningeal, occurring between the second and sixth 
years; but the pulse is not slow, and there is no other sign of meningitis. 
5. Differentiation, — Differentiation from pleurisy is usually easy 
(v. i.). In lung tumors, bronchial breathing, bronchophony, dulness, 
red or green sputum, are also noted, but the history and course differen- 
tiate. The course differentiates acute tuberculous infiltration from an 
upper-lobe pneumonia in which cough, sputum and typical physical 
findings are absent. Mistakes in both directions are made, by forgetting 
that in apical pneumonia the incomplete exudation may impart a tym- 
panitic note, and that the breath sounds are not always bronchial, at 
least anteriorly. Some tuberculous pneumonias may commence like 
lobar pneumonia (see Course of Pulmonary Tuberculosis). 



Pneumonia vs- 

Onset sudden, with rigor, herpes. 
Friction less common; may be present. 
Cyclical short course; high fever, crisis. 

Sputum rusty. 
Leukocytosis. 

Ectasia absent. 

Fremitus increased (coughing usually dis- 
lodging bronchial plugs). 



Dulness, preceded and succeeded by tym- 
pany (tympany or partial dulness in upper 
lobe pneumonia is not uncommon). 

Crepitant rales, bronchial breathing, and 
bronchophony (unless bronchus is 
plugged) . 

No essential luxation of heart, liver or 

spleen. 
Paracentesis negative. 



-Pleuritic Effusion. 



Gradual; chilly sensations commoner. 

Usual at some time in its course. 

Longer duration, lower fever, lysis. Often 
tuberculous foci at apex, etc. 

Mucous, if any. 

Usually absent, unless purulent or com- 
plicating a pneumonia. 

Present. 

Absent over effusion (unless adhesions 
bind the lung to the chest wall; in- 
creased above, over compressed lung 
or in the interscapular region). 

Flatness, increased downward; entering 
Traube's space on the left side. Level 
seldom shifts with change of position. 

Decreased or absent respiratory murmur 
(bronchial breathing in interscapular 
region from compression, or even through 
the fluid ; egophony) . 

Luxation of viscera usual in large effusions. 

Tapping nearly always decides doubtful 
cases ; fluid found beneath the flat area. 



Prognosis. — Pneumonia is the most fatal acute disease and has even 
a greater death-rate than tuberculosis. In 1903, 4629 persons died of 
pneumonia in Chicago, and in 1904, 8360 in New York City. From 
1851 to 1860 the mortality in Chicago from tuberculosis was 35 per 
cent, more than from pneumonia; from 1891 to 1901, the pneumonia 
death-rate was 9 per cent. more. 

There are various prognostic factors: 1. The Virulence of the pneu- 
mococcus, which varies from year to year (5 to 31 per cent, mortality). 
The mortality of 85,000 cases in the German army was 3.6 per cent. 
In 465,400 collected cases, E. F. Wells found the death-rate 20 per cent. 

2. Age.— The mortality is: one to five years, 30 per cent.; five to 
ten years, 3; ten to twenty years, 5; twenty to thirty years, 8; thirty 
to forty years, 25; forty to fifty years, 39; fifty to sixty years, 43; sixty 
to seventy years, 53; seventy to eighty years, 87 per cent. Cruveilhier 



PNEUMONIA 75 

spoke of pneumonia as the most formidable scourge of the aged, and 
Peter characterized pneumonia as the natural end of old people. 

3. Sex. — The mortality is over 50 per cent, higher in women. 

4. Location. — Right-sided is more fatal than left-sided pneumonia, 
and upper- is more fatal than lower-lobe involvement. 

5. Unfavorable conditions include cirrhosis and nephritis (almost 
100 per cent, mortality); delirium tremens and inveterate alcoholism 
(50 per cent.); cardiovascular disease, etc. 

6. Unfavorable symptoms are long prodromata, hyperpyrexia, 
enteritis, jaundice, albuminuria, severe pain, marked cyanosis, pul- 
monary edema, diffuse bronchitis, and a white cell count under 10,000. 
"When the blood-pressure, expressed in millimeters of mercury, does 
not fall below the pulse-rate expressed in beats per minute, the fact may 
be taken as an excellent augury; the converse is equally true" (C. A. 
Gibson). The mortality is 60 per cent, with the respirations constantly 
over 60 per minute, and 50 per cent, with the pulse over 130. Over 50 
per cent, of delirious subjects die. 

7. Unfavorable Complications. — Endocarditis and meningitis are 
almost always fatal; abscess, gangrene and arthritis are always serious; 
pericarditis is fatal in 75 per cent, of the cases. 

Death is due to cardiac toxemia. Mechanical overwork of the heart 
or diminished respiratory space is of small importance. 

Treatment. — 1. Prophylaxis concerns disinfection of the sputum, 
cleansing of the room (page 258), isolation and maintenance of the 
physiological resistance. 

2. Serotherapy. — Serotherapy and vaccines have not proved suc- 
cessful and pneumonia remains a self-limited disease. 

3. Hygiene is the same as in typhoid; quiet, frequent change of pos- 
ture, etc.; the patient should be clothed with a light flannel jacket 
open down the back. The fresh air treatment works wonders in pneu- 
monia; the bed should be placed out of doors or the windows widely 
opened. Aretseus spoke of the pneumonic's desire for cold air. Cold air 
often raises the blood-pressures 10 to 20 mm. and allays delirium. 

4. Diet. — The diet consists of milk, eggs, beef-juice and cereals (v. 
page 53) . Plenty of water is indicated ; some is retained in connection with 
the chloride retention and much voided by the increased respiratory effort. 

5. Symptomatic Therapy. — (a) The chill, which is rarely seen by 
the physician, is managed as in malaria. 

(6) Cough. — Expectorants are unnecessary; codeine gr. J to quiet 
irritation and carbonate of ammonium gr. iij to stimulate secretion, 
may be given every four hours; morphine may be indicated (v. L). 

(c) Pain. — The chest should be firmly strapped with adhesive plaster, 
applied in several oblique directions so that the pieces cross each other. 
Morphine lessens the irritability of the respiratory centre and relieves 
pain. Ice, blisters, leeches, and the cautery are superfluous; heavy 
poultices impede respiratory movement. In pneumonia, general is 
more important than local treatment. 

(d) Care of the heart is the main objective in treatment. Constant 
watching is imperative lest the patient leave his bed; it is a safe rule to 



76 BACTERIAL DISEASES 

consider all pneumonics delirious. Sitting up to drink, defecate or 
urinate is never permissible in a disease of sudden and alarming changes, 
with constant danger of collapse. No measure which depresses the heart 
should be employed, and acetanilide, antimony and aconite are always 
to be avoided. 

Cardiac Stimulation. — Strychnine is the best vasomotor tonic, and should 
be given in every case because vasomotor paralysis and collapse develop 
without warning, attended by accumulation of blood in the abdominal 
vessels. Strychnine is here indicated, because it constricts the deep 
abdominal vessels; the peripheral vascular tonus is not increased, but 
the brain vessels are flushed and the bulbar vasomotor centre is stimu- 
lated. The drug stimulates the central nervous system; the digestive 
tract, its secretions and musculature; the circulation, the tonicity of the 
heart, but chiefly the vasomotor centre ; and the respiratory centre. 

The dose is gr. -^ to ^V> every two to four hours. (For dosage in 
children see page 269.) Some strychnine remains in the system over three 
days, some is destroyed at once by the liver, and some is quickly elimi- 
nated by the kidneys. If the kidneys or liver are diseased as in old age, 
the drug may accumulate. Full doses produce twitching, nervousness, 
palpitation or renal-vessel spasm. Hypodermic administration gives 
less chance for the liver to destroy the drug. 

Caffeine is of great value, particularly when morphine is indicated, 
supporting its tonic effect and neutralizing its somnifacient action. 
Rhomberg ranks caffeine above strychnine and camphor, (v. Therapy 
of Valvular Heart Disease). 

Ammonia is of great clinical importance. It stimulates the heart- 
muscle, increases its frequency, and raises arterial tension. Its super- 
ficial effects are flushing, warmth, exhilaration and increased secretion 
of urine, sweat and mucus. Its prime indication is sudden functional car- 
diac adynamia, e. g., at the crisis. It is a local irritant to the skin, and 
respiratory and alimentary mucosae, and therein lie its therapeutic value 
and its clinical disadvantages. Its application to the upper respira- 
tory passages or its ingestion by mouth causes a sudden reflex stimula- 
tion of the respiratory and circulatory centres before the drug is absorbed. 
Gastric, intestinal, renal and bronchial irritation from overdosage, and 
irritation following subcutaneous administration may be observed. The 
corrosiveness and fugitive action of ammonium carbonate are obviated 
by small, frequent doses, gr. iij, every two hours. 

Digitalis was once exhibited in enormous doses, which simply proves 
that the drug is not absorbed; Thomas, in 1865, remarked its inac- 
tion in fevers. The author considers digitalis far inferior to camphor, 
and has repeatedly noticed toxic symptoms at the crisis when the repeated 
doses of digitalis were absorbed together. Digitalis is a last resort 
(TTlij-v of the fluidextract hypodermically ) . Strophanthin should not 
be used if digitalis has been administered, as it may cause sudden 
death. (See Treatment of Valvular Heart Disease.) 

Alcohol was first recommended by Todd for fevers. The chief interest 
centres in its action upon the circulation. Formerly called a heart stimu- 
lant, pharmacologists now hold that alcohol does not stimulate the 



PNEUMONIA 77 

heart, except by preparations like champagne which contain other ingre- 
dients. The heart's frequency is increased, but the drug acts as a vaso- 
dilator or as a blood distributor. Some clinicians reject it because it is 
narcotic to the respiratory, circulatory and vasomotor centres in the 
lower brain, or because it is a vasodilator. Alcohol is effective in all 
varieties of sepsis and it protects the tissues from excessive waste. 
Alcohol is indicated by collapse or cardiac toxemia, in which hot 
whisky and water unquestionably stimulate by reflex action on the 
throat and stomach; cognac, or whisky in hot water, and coffee can 
also be given by rectum. Alcohol may not be used in any routine 
fashion; within limits, it is valuable. 

Opiates. — The cardiovascular value of morphine is not sufficiently 
appreciated. Many withhold opiates even when the drug is indicated by 
maniacal outbursts, active delirium, and harrassing coughing or pain, 
lest it depress respiration and the heart. However, it decreases the 
irritability of the respiratory centres, lessens cough, dyspnea, headache, 
and insomnia. Its renal effects are negligible, as little morphine is 
eliminated by the urine. Morphine of itself helps to sustain life, and in 
critical cases its hypodermic use strengthens and regulates respiration. 
It is a most valuable adjunct to strychnine, camphor, or caffeine, which 
latter has an excellent effect, given by rectum, in neutralizing its nar- 
cotic action. 

Camphor is an excellent diffusive stimulant, grain ij hypodermically 
in 10 parts of sterilized almond oil, every two to four hours. 

Saline infusions are indicated in profound toxemia with weak heart 
— two drams of salt in one quart of water. They "lavage the blood." 
Continuous use of the salt solution by rectum, by the drop method, is 
valuable. Although once abused, venesection, employed by Hippocrates, 
has again come more into vogue. It is valuable at the onset in the robust 
for severe pain, active delirium and urgent dyspnea, and later when 
great engorgement of the right heart occurs. Heart stimulants must be 
used with phlebotomy. 

Oxygen, said to relieve dyspnea, is often irritating and injurious. The 
mouth-piece should be held near, not over, the mouth. (An excess, 
experimentally, produces hepatization.) 

Atropine is valuable for collapse, low temperature and clammy skin, in 
a daily dosage of not over one-fiftieth of a grain. 

Adrenalin (1 to 1000), in 5-10 drop doses, is as efficacious given intra- 
muscularly as intravenously; acting on the nerve-endings of the sym- 
pathetic, it is a vasoconstrictor; small and repeated doses are better 
than larger doses which may induce pulmonary edema. 

(e) Antipyretics. — A high temperature is not per se injurious; patients 
with fever between 103° and 105° progress most favorably and those 
with temperature above or below these limits run a more severe course. 
All measures which suddenly reduce the temperature must be avoided, 
especially at the crisis, when the heart sometimes staggers under the 
sudden fall of the fever. 

Hydrotherapy is opposed by many clinicans; by others the tonic vaso^ 
motor effects are thought to outweigh the shock. It is contra-indicated 



78 BACTERIAL DISEASES 

in the obese, the weak and the aged. Cool sponging with water and 
alcohol is the safest method. Quinine has no effect except in large doses; 
so-called specific action is a phantasy. 

(/) Nervous symptoms are toxemic, but may be considered with regard 
to: (i) fever; the greater the temperature variation, the more marked 
are the nervous symptoms, which are most efficaciously treated by baths 
or cool affusions; (ii) deficient oxygenation, in which cardiants and 
oxygen are indicated; (iii) insomnia, which is treated by morphine, 
hyoscine hydrobromide, sulphonal, and cool sponging, but rarely by 
chloral; and (iv) delirium tremens (q. v.). 

(g) Iodides are indicated in delayed resolution. 

DIPHTHERIA. 

Definition. — An acute specific infective disease, usually of the throat 
or upper air-passages, and characterized by a membrane formed by the 
Klebs-Loefner bacillus, and by toxemia. 

History. — Diphtheria was known to Hippocrates. Asclepiades, 100 
B.C., performed the first tracheotomy. The first full account was 
Aretseus', in the first century, a.d. Diphtheria literally means mem- 
brane and originated with Bretonneau (1821). 

Terms. — True diphtheria implies a membrane formed by the Klebs- 
Loefner bacillus whose absorbed toxins produce toxemia. Membrane, 
however, may be due to the scarlatinal virus, strep to-, pneumo-, staphylo- 
cocci, etc.; while these are diphtheritic membranes in the old anatomical 
sense, they are not diphtheritic in the bacteriological sense, and we 
term them pseudodiphtheritic, or diphtheroid. Therefore, clinically, 
there are some discrepancies: (a) what seems diphtheria, anatomically, 
may not be due to the Klebs-Loeffier bacillus; (b) what apparently is 
angina or tonsillitis, may show no membrane or an atypical membrane, 
but bacteriologically is due to the Klebs-Loeffier bacillus; (c) the 
diphtheria bacillus is found in 1 per cent, of perfectly healthy throats; 
(d) there are bacilli which closely simulate the diphtheria bacillus. The 
pseudodiphtheritic membrane is most often due to the streptococcus 
and is seen oftenest in scarlatina, but also in typhoid, measles, Vincent's 
angina, syphilis and pertussis. It develops wherever the true diphtheritic 
membrane may occur, e. g., the throat, larynx, bronchi, eyes, skin, etc. 
Most cases (72 per cent.) clinically resembling diphtheria are proved 
diphtheria by repeated bacteriological tests. 

Bacteriology. — The diphtheria bacillus (described by Klebs, 1883, 
and cultivated by Loeffler, 1884) is 1.2 to 2/jl long and 0.3 to 0.5m wide, 
with small round or slightly enlarged ends. It stains readily by Gram's 
method, Loeffler's methylene blue and carbol fuchsin. There are many 
variations in form, but the serum culture always reveals the wedge- or 
mallet-like forms. Their grouping is characteristic, like Chinese letters, in 
lines set asymmetrically at various irregular or slight angles. They are 
immotile and sporeless. The bacillus overgrows other associated bac- 
teria on blood serum mixed with glucose bouillon; the culture is visible 
in ten hours as yellow streaks, whose surface is slightly granulated and 



PLATE III 



■'-« — x 



*+f^JtJ$JL££ 



A 



B 






3&k* 



< y/ ->&L? 



<4W 



/ 






V 



^A 









**v 



^ 



A. Cu.ltu.re of diphtheria bacillus. 

B. Same magnified. 

C. Diphtheria bacilli. 



DIPHTHERIA 79 

edges somewhat thick. In twenty-four hours the growths diffuse, with 
a wave-like surface, undulating edges, and a succulent appearance. The 
diphtheria bacillus is very resistant, and though it usually disappears 
three weeks after the patient has shed the membrane, it may live for 
weeks in the throat (even fifteen months) or for a long period in clothing. 
It is found chiefly in the membrane, and is less frequently detected in 
the submucosa, heart (endocarditis), blood (diphtheriemia), lungs 
(bronchopneumonic foci), spleen, liver, brain, cord, kidney or urine. 
In one report, it was found in the blood and viscera eleven times in four- 
teen cases. Symbiosis with the streptococcus, the most common of all 
secondary infections, increases the virulence of the diphtheria toxin 
(Roux and Yersin); the streptococcus is found in septic types, broncho- 
pneumonia and glandular suppuration. Less important are the staphylo- 
cocci — which rarely enter through the throat, but then with increased 
virulence — the proteus, colon bacillus and pneumococcus. 

The action of the bacillus is (a) local; when inoculated in animals, 
local necrosis develops, whereon fibrin exudes and forms a membrane in 
which the bacillus is found; and (6) general, forming toxins, absorbed 
by the blood and lymph vessels. Roux and Yersin found that the toxins 
injected alone, after killing the bacillus, produce no membrane or necrosis, 
but toxemia and paralysis similar to the postdiphtheritic paralysis. 
Ehrlich distinguishes two toxins : the toxin producing the ordinary pheno- 
mena of diphtheria, and the toxon producing the later anemia and paraly- 
sis. The chief receptors of the virus are the nervous and lymphatic 
tissues. 

The virulence of the germ varies. This is tested by inoculating a 
guinea-pig with ytto of its body-weight of a forty-eight-hour bouillon 
culture, and noting the results; (a) death in three days or less results 
from fully virulent cultures; (b) death in three to five days from one 
of medium virulence; (c) death after a longer time, or only local changes, 
from weak cultures. 

Bacilli, known as the pseudodiphtheria bacillus, Bacillus xerosis, etc., 
resemble the Klebs-Loeffler bacillus, and may become virulent; they 
are not antagonized by the diphtheria serum but only by the pseudo- 
diphtheria serum. 

Dissemination. — Diphtheria is disseminated (1) by patients acutely ill 
with the disease; the secretion or membrane may be coughed into the 
mouth of one of the family, nurse or attending physician. Children 
going to school may impart to others a most virulent diphtheria, though 
the same bacilli have produced in them little constitutional reaction. (2) 
By healthy individuals, in 1 per cent, of whom the germ is found without 
causing diphtheria; these carriers may or may not have been in contact 
with the disease. (3) By fomites, especially damp cloths, in which 
the germ may live for five months. (4) The germ probably may be 
spread by dust, cheese, milk and eating utensils. It is not demonstrated 
that domestic animals convey the disease. Diphtheria is endemic in 
all thickly populated districts, from which epidemics develop. 

Age. — Most infections occur between the second and fifteenth years, 
and most deaths occur between the second and fourth vears. Jacobi 



80 BACTERIAL DISEASES 

observed three cases in the newborn, but infants at the breast are less 
exposed than creeping children who come into close contact with dirt. 
Adults are frequently affected. 

Hypertrophied tonsils, nasopharyngeal and bronchial catarrh, measles, 
nervous affections and cold weather are predisposing factors. Some 
individuals are temporarily, and some permanently, immune. One 
attack confers no immunity, wherein diphtheria resembles erysipelas, 
pneumonia and rheumatism. 

Symptoms. — There are three major localizations of diphtheria: the throat, 
the nose and the larynx. 

1. Pharyngeal Diphtheria. — The typical case is pharyngeal. 

(a) The simple localized diphtheria after an incubation of two to seven 
days begins with fatigue, pallor, coated tongue, anorexia, dysphagia, 
vomiting, and pain beneath the angle of the jaw. Chilly sensations, 
fever and thirst and pharyngeal voice ensue. 

The pharynx is glistening and characteristically purple-red, with, later, 
areas of gray, yellowish or dirty green color, as small white bands or 
irregular, gelatinous masses, located on the tonsils, palate, pillars or 
pharynx. Except in their very incipiency, they are adherent, and on 
removal leave red, bleeding spots which are rapidly covered again with 
membrane. 

Wagner, Weigert and Oertel showed that the diphtheritic membrane 
is composed: (i) Of necrobiotic tissue; the superficial and, later, the 
deeper structures are necrosed; bacilli are found in the superficial layers 
and streptococci and staphylococci may be found more deeply situated; 
the necrobiosis may be noticed also in the connected lymph glands and 
internal organs (Weigert's coagulation necrosis), (ii) Somewhat deeper 
the membrane is composed of fibrin exudation, which is a conservative, 
walling-off process, (iii) In the deepest part of the membrane emigra- 
tion of leukocytes occurs. In most adults the membrane is thrown off 
by the fourth or fifth day; in children by the seventh or eighth day. 

The breath is septic in odor. Some nasal discharge is the rule. The 
glands at the angle of the jaw are tender. Fever may be irregular or 
absent; in 90 per cent, of patients who recover it does not exceed 102°. 
The patient usually recovers in seven to ten days, and seldom exhibits 
marked toxemia. 

The form described is the classical type of mild local infection; the bacilli 
may be virulent but the tissues and blood resist the infection. Several 
deviations from this type may be misinterpreted: (1) In " catarrhal 
diphtheria" the membrane is absent or atypical and pultaceous; this 
type is common in families where the more typical forms are seen. (2) 
Diphtheria may resemble follicular pharyngitis; between them there is 
no absolute distinction except bacteriologically, although in diphtheria 
the red is brighter, the tendency to fuse is greater, and the spots are more 
yellow, gray or green. (3) Follicular tonsillitis may be very closely simu- 
lated, and then is only distinguished bacteriologically. (4) In chronic 
diphtheria, there is a deposit upon a red, edematous pharynx. The 
glands may be swollen, but usually there are no toxemic symptoms. 
(5) The latent diphtheria in marantic subjects may easily escape detection. 



DIPHTHERIA 81 

(b) The diphtheritic general infection begins with high fever and toxemic 
symptoms as headache, prostration, increasing anemia, dysphagia and 
vomiting. The heart movement follows the fever, the tones being dull 
and often accompanied by a systolic murmur. The pharynx is dark red, 
swollen and a thin gray membrane is seen on the tonsils or pharynx; 
it begins as streaks, or a thin veil over the pharynx and spreads rapidly. 
The secretion is offensive. The hard palate and upper soft palate 
are usually normal. The neck is tender from glandular intumescence. 
The nose is often closed by a purulent secretion and diffuse membrane, 
and oral breathing results, of great moment in nurslings. There is a 
type peculiar to young children who, with initial nasal symptoms and 
without throat symptoms, suddenly develop laryngeal stenosis, and in 
the pre-antitoxin days, almost invariably died. In severe cases the heart 
is irregular; there are throat paralysis, neck infiltration, dyspnea, albu- 
minous urine, tympany, swollen liver and spleen, antemortem fall of 
temperature, and death from pneumonia, cardiac insufficiency, toxemia, 
paralysis or nephritis. 

(c) • In septic diphtheria the exudate becomes dirty green or brown, is 
horribly fetid, and may reach the nose or larynx, causing necrosis and 
stenosis. It excites lymphadenitis and periadenitis. The respiration 
is difficult; and nephritis, generalized hemorrhage or local arterial ulcera- 
tion, failing pulse, low temperature, and intumescence of the abdomen, 
liver and spleen, usually result fatally. In 1881, 94 per cent, of cases 
of this type died. According to Baginsky, it is due to the diphtheria 
toxin, and is seldom observed since the introduction of antitoxin. Others 
maintain that symbiotic streptococcus infection determines this septic 
type. 

The initial fever in diphtheria may be maintained by otitis, pneumonia, 
adenitis and other complications in the severer types. Septic tempera- 
ture may prevail. A pre-agonal rise may be observed, or an antemortem 
collapse. These developments relate chiefly to cases untreated with 
antitoxin. 

Leukocytosis of the polymorphonuclear type develops in 90 per cent, 
of cases. It does not correspond to the severity of the disease. When 
absent the infection is either very severe or light. 

2. Nasal diphtheria may usher in the disease or accompany the 
benign, or more usually, the severe forms. The serous and often sanious 
or bloody nasal discharge excoriates the ala? nasi, lips and cheeks (every 
"coryza" in which this occurs, must excite alarm);- membrane often 
protrudes. Cervical adenitis is suggestively frequent. The prognosis 
is grave, and convalescence very tardy. In contrast with this severe 
form there is a fibrinous rhinitis usually subacute or chronic, which is 
due to the Klebs-Loeffler bacillus (82 per cent.), or the streptococcus 
(18 per cent.); it is obviously dangerous to other children, since the 
remarkable absence of constitutional reaction, despite the menacing 
discharge, does not prevent play or school-going. 

3. Laryngeal Diphtheria or Croup.— Most cases are diphtheritic 
(85 per cent.), though some are streptococcic. Diphtheria involves the 
throat in 84 per cent, and the lar}mx in 16 per cent, of cases. Forms: 

6 



82 BACTERIAL DISEASES 

(a) Catarrhal laryngitis, due to the diphtheria bacillus, produces symp- 
toms of two or three days' duration; they may be severe, even stenotic. 

(b) Diphtheritic laryngitis (croup) is descending in 97 per cent, of cases, 
i. e., secondary to pharyngeal or nasal diphtheria; even in seemingly 
primary cases there is usually some pharyngeal involvement. The child 
becomes hoarse in the night or early morning, coughs the hoarse, croupy 
cough, and after twelve to twenty-four hours is dyspneic. Aphonia is 
the rule. The stridor becomes menacing and then the enduring croup is 
surely diphtheritic. The stenosis is due to membrane in the epiglottis, 
true cords, trachea or even in the bronchi. The accessory muscles of 
respiration come into play, with inspiratory retraction of the thorax and 
epigastrium, especially in rhachitic children, up-and-down excursion of 
the larynx, extreme restlessness, and temporary improvement after 
expectorating the membrane. The stenosis is accentuated by the central, 
immovable position of the vocal cords, swelling in the subchordal tissue 
and muscular spasm. The cough may disappear because of decreased 
reflex bronchial excitability. Fever is usually absent. The pulse increases 
with augmentation of the stenosis. The respite following the raising 
of the membrane is usually transient; exacerbations occur and finally, 
without intubation or tracheotomy, dyspnea becomes continuous, with 
stagnation of secretion and membrane in the tubes, absence of the 
vesicular murmur, stridor, increasing rapidity and weakness of the 
pulse, cold, clammy skin — in short, the complete picture of carbon 
dioxide poisoning and total asphyxia develops. 

4. Other Localizations. — (a) Diphtheria of skin is usually asso- 
ciated with pharyngeal diphtheria. The skin is hard and infiltrated, 
the secretion corrosive, the contiguous lymphatics involved, and cellu- 
litis or phlegmon may result. Most instances of "wound diphtheria" 
and the membrane which forms in tracheotomy wounds are usually 
streptococcic. 

(b) Diphtheritic vulvovaginitis (under 1 per cent.) is dangerous, and 
usually follows severe pharyngeal diphtheria; it consists of diffuse 
membrane, painful rhagades, ulcers and foul secretion. A streptococcic 
form is also encountered. 

(c) Diphtheritic ophthalmia is (i) false or diphtheroid (due to pus 
cocci) or (ii) genuine or diphtheritic, which occurs in 3 per cent, of cases, 
chiefly in young children. It may be primary in the eye, or secondary 
to nasopharyngeal diphtheria. 

(d) Diphtheritic otitis occurs in 6 per cent, of cases (as against 33 per 
cent, of otitis in scarlatina and nearly 100 per cent, in measles). The 
diphtheria bacillus travels from the throat to the Eustachian tube or 
middle ear. 

Complications and Sequels. — The most important are heart weakness, 
nephritis, and paralysis. 

1. Cardiac Complications. — Anatomically, the heart muscle is 
altered early. It is soft, friable, light brown or yellow, and fatty; it is 
the occasional seat of endocardial and myocardial hemorrhages, acute 
interstitial myocarditis and fragmentation or myolysis, which Eppinger, 
in describing eighteen cases of sudden death, considers the usual cause 



DIPHTHERIA 83 

of death; degeneration may be found in the bundle of His. Pericarditis, 
with septic or hemorrhagic effusion, or permanent changes due to endo- 
carditis (in 2 per cent, of fatal cases) or myocarditis are uncommon. 

Clinically, the first tone is impure or obscured by a systolic murmur 
in one-half the cases; the second pulmonic is accentuated, the rhythm 
is disturbed (60 per cent.) and sometimes there is gallop-rhythm and 
embryocardia. The pulse is rapid and soft but it may be ominously 
slow, even 14. Heart-failure is more frequent than in any other infection, 
and occurs early in severe or gangrenous types, or only after three to six 
weeks (in 20 per cent.). It is marked by copious vomiting from vagus 
neuritis, pain in the chest and epigastrium, cardiac dilatation, pallor, 
dyspnea, cyanosis and convulsions. Heart failure is explained in various 
ways (a) acute interstitial myocarditis; (b) myolysis; (c) centric vaso- 
motor paralysis; (d) neuritis of the vagus; (e) degeneration of the bundle 
of His; 33 per cent. die. 

2. Diphtheritic Nephritis. — (a) Albuminuria ocours in 33 per cent, 
of all and in 100 per cent, of severe cases, (b) In light forms of neph- 
ritis there is some albumin, the specific gravity and quantity of urine 
are about normal, and there are leukocytes or epithelial cells with 
indistinct nuclei, the cells being highly refractive and coarsely granular. 
Blood is rarely found. There are some hyaline and granular casts. 
These toxemic findings correspond in time and degree to the diphtheritic 
process in the pharynx, (c) The severe forms of nephritis occur in severe 
or septic types and are characterized anatomically by diffuse parenchy- 
matous changes, necrosis, hemorrhage and exudation. Albumin, epithe- 
lium, casts and cylindroids are abundant. Hematuria is rare; aceto- 
nuria occurs in 65 per cent, of cases. Nephritis rarely produces hydrops 
or uremia as in scarlatina. It rarely becomes chronic. 

3. Diphtheritic paralysis occurs clinically (and experimentally) 
from toxemia in 20 per cent, of cases. Paralysis rarely develops in patients 
receiving antitoxin on the first day but most often develops in those in- 
jected after the third day, or with insufficient doses. Its frequency and 
intensity is directly proportional to the severity of the diphtheria. 

(a) Early paralysis occurs in septic cases at the acme. Dysphagia 
is its most common form. There is danger of inhalation pneumonia, 
especially in stupid cases. Most cases die. 

(6) Postdiphtheritic Paralysis.- — This, the typical variety, occurs after 
two or three weeks and usually follows throat lesions since laryngeal 
cases are likely to die early; all throat infections leading to paralysis 
are probably diphtheritic. The most common paralysis is that of the 
palate, which was described by iEtius in the sixth century, and causes 
dysphagia, anesthesia of the throat and nasal speech. The pupils widen, 
and react to light but not to accommodation. The arms frequently 
escape. Ataxia may be the first symptom. The reflexes disappear early 
and the muscles react slowly, if at all, to the faradic current, although 
the reaction of degeneration by no means runs parallel to the degree 
of loss of voluntary motion. The muscles waste, the palsied limbs are 
sometimes painful and the muscles and nerve trunks are often tender. 
The trunk, bladder, and rectum are sometimes involved. The sensory 



84 BACTERIAL DISEASES 

nerves suffer less, sensation being largely retained above the knees. 
Sensory disturbance may be noted in the rectal, genital and vesical 
twigs. The cranial nerves (strabismus, ptosis, diplopia), the phrenic 
nerve and vagus may be involved; fearful abdominal pains with threaten- 
ing collapse attributable to sympathetic involvement may be noted. 
Anatomically, disintegration of the medullary substance, multiplication 
of nuclei in Schwann's sheath, granular degeneration, and even total 
loss of the axis-cylinder are present, the changes being almost totally 
parenchymatous; neuritis (actual nerve inflammation) is seen almost 
wholly in the palate, due to local invasion from the inflamed throat. 
The patient recovers in two or three weeks if the pharynx alone is 
involved, and in three to eight months if the limbs are affected. Death 
results in 18 per cent, of cases, chiefly from vagus involvement. 

(c) Organic Central Changes. — Accidental findings are cerebral hemor- 
rhage, embolism and acute encephalitis. The literature contains 85 
instances of hemiplegia (Rolleston, 1905). The Babinski reflex, found 
in 20 per cent, of severer cases, is due to toxemic action on the pyramidal 
tracts. Degenerative cerebrospinal lesions not infrequently occur with 
multiple neuritis. 

4. Respiratory Complications. — The bronchi and trachea exhibit 
membrane in 50 per cent, of fatal cases. Bronchopneumonia is present 
in 65 per cent, of fatal cases, caused by the Klebs-Loeffler bacillus alone, 
or by the pus or pneumonia cocci, etc. Anatomically, some cases are 
due to downward extension of the bronchitis; some are hematogenous; 
others are due to inhalation, and still others, seen after intubation or 
tracheotomy, are elevated and granular. Increase of pulse and respira- 
tion-rate, local consolidation and accession of fever are observed. Serous, 
hemorrhagic or purulent pleurisy is seldom encountered. 

5. Alimentary Tract. — Fissures, sordes, membrane or ulcers on the 
lips, suppuration in the tonsils or retropharyngeal space and gangrene 
sometimes occur. In septic cases the esophagus may be occluded by mem- 
brane. Epigastric pain and vomiting are chiefly cardiac; death is usual 
when vomiting develops late in the disease; the rare hemorrhage and 
membrane formation escape clinical recognition. Constipation is usual; 
in septic forms, thick, foul or dysenteric evacuations may be exceptionally 
observed ; there may be membrane formation and swelling of Peyer's 
patches. The liver is swollen from fatty or cloudy degeneration or from 
congestion, in which latter case it also becomes painful. Splenic tumor 
is found in septic types especially. 

6. Skin. — The skin is usually normal, except for the febrile hyperemia, 
cardiac pallor, croup-cyanosis or septic grayness. Herpes, in 4 per cent., 
petechia?, symmetrical gangrene (of which 9 cases exist in the literature), 
and septic dermatomyositis usually occur with adenitis, nephritis 
or ulcerative endocarditis. Scarlatina or measles may complicate 
diphtheria. 

7. Glands. — The anterior cervical glands are swollen and painful. In 
the severest forms periadenitis follows, with diffuse cellulitis (angina 
Ludovici), section of which evacuates serum, seldom pus. Glandular 
and articular changes are less frequent than in scarlatina. Muscular 



DIPHTHERIA 85 

degeneration, interstitial infiltration and fragmentation are observed 
in the heart and diaphragm. 

Diagnosis. — A thick, adherent membrane, which is not removable without 
hemorrhage, with subjacent ulceration (Bretonneau) and enlarged glands, 
is characteristic. A positive bacteriological diagnosis is important in 
cases with membrane, diffuse reddening and tonsillitis, yet four negative 
examinations are necessary to exclude diphtheria positively. Statistics 
show positive findings in 92 to 98 per cent, of cases in which the clinical 
diagnosis of diphtheria has been made. The nose, nasopharynx and 
pharynx must be examined in every sick child and adult. In suspicious 
cases antitoxin should be given at once. 

The health departments in large cities provide cultures, stations at 
which cultures and antitoxin may be obtained, and central and subsidiary 
laboratories for diagnosis. In smaller towns communal laboratories can 
be maintained easily. The Chicago Health Department has an able 
corps of physicians for free treatment, consultation and intubation. It 
is easy to obtain a smear from the suspicious focus, to rub it on the 
serum without breaking its surface, and to put the tin box containing it 
under the axilla until the brood-oven can be reached. In half a day 
characteristic cultures are obtained. Direct smears very often show 
the bacillus. In laryngeal diphtheria the bacillus is usually found on 
the pharynx, but not on the tonsils. Repeatedly negative findings are of 
value in the pseudodiphtheritic pharyngitis, rhinitis and laryngitis, e. g., 
membranes due to strepto-, staphylo-, and pneumococci, aphthous growth, 
syphilis, etc. The scarlatinal membrane (q. v.). In Vincenfs angina 
(q. v.) described by Vincent (1898), the whitish-yellow or grayish-brown 
membrane may be confused with diphtheria and syphilis and is caused 
by the symbiosis of two otherwise innocuous parasites, the Bacillus fusi- 
formis, and the Spirocheta darticola. 

Course and Prognosis. — Aside from complications, the average course 
is one or two weeks. It is more favorable in diphtheria of the tonsils 
than of the nose. The prognosis concerns the toxemia, mechanical 
obstructions, as of the larynx, mixed infection, and the therapy, (a) 
Without serotherapy the danger is great, since light infections may 
intensify or extend, (b) Epidemics vary in virulence, 30 to 50 per cent, 
mortality having been observed twenty years ago. (c) In the first year 
the mortality is 77 per cent., and sinks with each year until it is, at ten 
years, 20 per cent.; after ten, 3 per cent.; after thirty and forty, 2.5 per 
cent, (d) Other factors are debility, adenitis and croup; the general 
diphtheritic infection or septic forms; renal complications; rapid and 
weak or slow pulse; ecchymoses and late vomiting; and paralysis, (e) In 
946 fatalities studied by White and Smith, about 50 per cent, died of 
bronchopneumonia, usually after intubation or tracheotomy; 25 per 
cent, died of cardiac complications, and 25 per cent, of early severe 
toxemia, though some succumbed to asphyxia or late paralysis. (/) 
Coincidence with other infections is ominous, such as measles, in 
which the exanthem may become hemorrhagic, and a lethal res- 
piratory catarrh usually results. Diphtheria belongs to the recurrent 
infections. 



86 BACTERIAL DISEASES 

Treatment. — 1. Prophylaxis begins with the case in hand. In Boston 
the isolation hospital has reduced the mortality of diphtheria to one- 
sixth of its former rate. All suspicious throat cases should be isolated 
pending their cultural evolution; other children in the family should be 
kept from playmates and school. The patient is isolated until the throat 
gives two negative cultures, successively, requiring three weeks. The 
physician may protect himself by examining the throat through a piece 
of glass, and avoid carrying the germs, by a surgical gown and washing 
face and hands with bichloride solution. In fatal cases the body should 
be wrapped in a sheet saturated with bichloride, and buried privately 
in a tightly closed casket. Those exposed to infection may receive 
antitoxin, and should gargle the throat often with bichloride (s-qVo)- 
The clothing, blankets, rugs, etc., must be steamed. After convales- 
cence, the walls of the room should be rubbed with bread which is then 
burned, the woodwork washed with 2 per cent, phenol solution or bichlo- 
ride and the room fumigated (page 258). Under prophylaxis may be 
included the building up of the physiological resistance and the treatment 
of chronic catarrh of the nose, throat and bronchi. "Carriers" must 
be isolated; Hewlett reports success from vaccines. Schiotz advocated 
the use of a staphylococcus spray; a fresh bouillon culture is sprayed 
into the nose and throat, until they are moist; recent reports are encour- 
aging. V. Behring recently reports a new prophylactic against diphtheria 
— a mixture of very strong diphtheria toxin and antitoxin combined in 
such a proportion that the mixture shows only a slight surplus of the 
toxin; the method is a result of experiments which shows that it is impos- 
sible to produce in a test-tube complete neutralization of the diphtheria 
toxin. 

2. Local Treatment. — Though local treatment of the throat is less 
important than before the days of serotherapy, the antitoxin does not 
always kill the bacilli, and does not affect the associated streptococci. 
Caustics are never indicated. In children such mild antiseptics as 
3 per cent, boric solution and 3 to 10 per cent, potassium permanganate 
solution, should be used lest they be swallowed. The child is held in 
the nurse's arms with its arms and body firmly wrapped in a sheet. 
The mouth is opened by closing the nostrils, and a piece of cork is inserted 
between the teeth. The throat is then swabbed. It is a harsh procedure 
and the benefit is apparently more than offset by the resultant exhaus- 
tion. In adults 1 to 1000 bichloride, 25 per cent, hydrogen peroxide, 
1 per cent, carbolic solution, or iodoform salve, may be used, or the 
somewhat irritating Loeffler's solution, which is as follows: 

1$ — Mentholis 10 parts 

Toluolis 30 parts 

Liq. ferri chloridi 4 parts 

Alcoholis absoluti 60 parts 

It should be kept corked in a dark bottle. Local injury, opening up new 
wound surfaces for infection, must be avoided. In nasal irrigation the 
tube is held horizontally, so that fluid may return by the other nostril. 
A kettle should be kept steaming in the room. 



DIPHTHERIA 87 

3. Serotherapy. — Behring (1890) borrowed Ehrlich's results with 
ricin and abrin to establish the units of immunization, and used the 
diphtheria antitoxin on diphtheria patients (1893). Antitoxin is obtained 
from horses which have been rendered immune by the injection of pro- 
gressively increasing doses of diphtheria bacilli. According to Ehrlich's 
" side-chain" theory, toxins combine chemically with the cells of the 
body, just as food unites with cells in ordinary metabolism. Parts of 
the cells, which combine with toxins, are called receptors. The stimula- 
tion or injury excited by toxins causes in the process of repair, an over- 
production of receptors, which are thrown free as antibodies, into the 
circulation. Thus the horse serum unites with toxins and spares the 
cells in human diphtheritic toxemia. Immunity may result from the 
body cells being devoid of receptors or an excess of receptors in the blood 
may unite with the toxins and spare the cells. 

1. Technique. — The glass syringe is the best; it should be cleaned after 
each injection, with water to remove the serum, and then washed with 
alcohol, which should be thoroughly removed lest it coagulate the anti- 
toxin at the next injection. With ordinary surgical antisepsis, inject 
the antitoxin into the muscular tissue of the thigh in adults, and into 
the interscapular region in children. Intravenous injections act in 16 
hours, intramuscular in 24 hours, and subcutaneous in 72 hours. 

2. As we cannot measure the toxins the dosage is empirical, depending 
on the localization, age, severity of the disease and the results obtained 
(the discharge should lessen, the membrane exfoliate, the fever fall, and 
toxemia decrease). After eight hours, three times as much is necessary 
as at the beginning; after twenty-four to thirty-six hours, eight times 
as much. The author prefers an initial dosage of 5,000 units to insure 
results and avoid frequent repetition. The unit is 1 c.c, which counter- 
acts ten times the minimum dose of diphtheria poison fatal to a 300 gm. 
guinea-pig. The decreased bulk of present preparations allows a larger 
dosage. In severe cases twice the above amount should be given. Mc- 
Callum emphasized the importance of full doses, 10,000, 30,000 or 50,000 
units in desperate cases. Sutherlin gave a total of 498,000 units in one 
case. The present practice reverts to smaller doses, 1200 to 2000 in 
mild, and 3000 to 6000 in severer infections. 

3. Effects. — (a) The mucosa becomes redder, and the membrane 
exfoliates in one to three days, with decrease in glandular swelling; (b) 
The fever falls; antitoxin is given until the fever falls, (c) The pulse 
and hyperleukocytosis decrease. Light cases rarely become severe, 
and non-septic rarely become septic. Paralysis and heart failure are 
less frequent with early serotherapy; many patients now live who pre- 
viously died before developing paralysis, (d) The mortality is reduced 
from 40 to 15 per cent. (Siegert's collection 42,000 cases); to 10 per 
cent. (Wenner, 9.8 per cent., 132,500 cases, American cities); or to 
6.7 per cent. (Chicago Health Department). According to Bayeux, 
the mortality in 230,000 diphtheria patients was 55 per cent, before, and 
16 per cent, after, the introduction of antitoxin. The fatal cases and 
severe complications are lessened in direct ratio as the antitoxin is given 
early; if on first day of disease, less than 1 per cent.; second day, 2 per 



88 BACTERIAL DISEASES 

cent.; third day, 8 to 10 per cent.; fourth day, 14 per cent. Failure to 
use antitoxin is criminal neglect, (e) Antitoxin is a prophylactic, and 
should be given in special instances, e. g., to weak or very young children 
(in smaller doses) ; this passive immunity lasted for two or three weeks 
in all but 0.7 per cent, of 1000 cases (Zuppinger). (J) The sequels are: 
(i) Abscess formation; (ii) nephritis, always due, however, to the diph- 
theria itself; (iii) serum disease and anaphylaxis. In one or two weeks 
fever and exanthems appear in 33 per cent, of cases— urticarial mostly, 
but also morbilliform, scarlatiniform and petechial. In 3 to 4 per cent, 
there is also acute pain and swelling in the joints or tendons. Another 
type comes on more rapidly (12 hours to 6 days), the ''accelerated 
reaction" — with the above symptoms plus vomiting, albuminuria, 
prostration, and weak heart. A third type appears at once, the " imme- 
diate reaction," with high fever, convulsions, dyspnea, cyanosis, vaso- 
motor paralysis, and rigors. In a fourth form, sudden death ensues, 
of which some 35 instances are on record (in all but 2 instances, 
death followed the first injection); most deaths occurred in persons of 
asthmatic tendencies or in those experiencing discomfort in the neigh- 
borhood of horses. This condition is termed serum disease, hypersus- 
ceptibility, anaphylaxis, allergy, etc. In its varying degrees it is due to 
hypersusceptibility of the tissues to a specific foreign proteid; thus, the 
first dose of antitoxin causes a gradual increase of the antibodies which 
have the properties of a ferment; if a second injection be given 8 to 10 
days later, the antibodies (now increased) acting like a ferment, produce 
a rapid disintegration of the proteids, with liberation of toxic substances, 
causing the anaphylaxis, which is closely related to the immunity problem. 
Auer and Lewis proved that the lungs, in fatal cases, are enormously 
distended, due to a tetanic muscular contraction of the finer bronchioles; 
the heart is also paralyzed. How may these disasters be avoided? First: 
There is greater danger of anaphylaxis in immunizing serotherapy than 
in its use for actual diphtheritic infection; the writer has seen high fever, 
renal suppression and the most alarming vasomotor instability (pallor, 
cyanosis and scarlet flushing occurring in succession). Immunizing 
serotherapy must not be indiscriminate. (Schick uses 0.1 c.c. of toxin 
solution intradermically and finds that subjects not immune to diph- 
theria develop a reaction similar to v. Pirquet's in tuberculosis). Second: 
One large dose is less dangerous than doses repeated at frequent intervals. 
Third: A small dose (0.5 c.c.) is given first and if there is no reaction, a 
second full injection is given. Fourth: The second or later injections 
should be from some other animal than the horse, e. g., sheep antitoxin, 
etc. Fifth: Give the smallest possible bulk of serum. Sixth: Use 
atropine before the second dose, and if anaphylactic symptoms have 
developed, use salt solution and adrenalin (1 to 40,000); digitalis is 
injurious, (iv) Seibert collected 18 cases of tetanus following antitoxin. 

4. Symptomatic Treatment. — A rich fluid diet of milk, eggs, etc., is 
given. In marked dysphagia, rectal feeding is indicated. Forced feeding 
by the nasal catheter injures the throat. 

Sepsis. — Alcohol, saline enemata, strychnine and iron should be given; 
all measures fail if tens of thousands of units do not give relief. 



CEREBROSPINAL FEVER 89 

Paralysis. — Electricity is of no avail; massage, baths and strychnine 
are useful in the later stages. 

Heart Failure. — The ice-bag is indicated for stormy heart action; 
strychnine, coffee and camphor should be given (dosage v. page 269) for 
severe abdominal pain and vomiting, usually evidences of cardiac failure, 
and champagne with menthol and carbolic acid, and twenty drops each 
of adrenalin and tr. belladonna? in nutrient enemata. The heart must 
be watched far into convalescence. 

Nephritis. — Alcohol, tincture of iron, beef -tea and eggs are avoided; 
milk diet, baths, laxatives and care of the skin are indicated. 

Local Diphtheria. — Two per cent, nitrate of silver in balsam of Peru 
affords relief in vaginitis; ice applications, atropine and silver in ophthal- 
mia; local diphtheria necessitates antitoxin. 

Croup. — Steam tents and ice locally are applied; the child's head may be 
held over a pail of water into which live coals are thrown; emetics may 
be administered. Retraction of the chest walls, suffocation and cyanosis 
necessitate intubation or tracheotomy. 

O'Dwyer's Intubation. — Advantages. — It is bloodless, easier and quicker 
than tracheotomy, and is less objectionable to the family. 

Disadvantages. — Membrane may rise beneath the tube and the tube 
sometimes produces false passages, necrosis, perichondritis and stricture. 
The tube is usually replaced two, three or four times, and rarely need 
remain more than five days when the serum is used. It is removed by 
the extubator or pressure. 

Tracheotomy is indicated by heart weakness, asphyxia, much secretion, 
or gangrenous, diffuse or septic infiltration. The after-treatment requires 
a moist atmosphere and daily cleaning of the tracheotomy tube. The 
tube is not permanently removed until all stenotic symptoms and all 
plaques disappear, which, with serotherapy, may be done on the fourth 
day. The prognosis depends upon possible wound-infection with erysipe- 
las or diphtheria, phlegmon, thrombophlebitis, mediastinal suppuration, 
ulceration of trachea and inhalation pneumonia. Rapid rise of tem- 
perature is ominous. Antitoxin reduced the mortality from 66 per cent, 
to 25 per cent. 

CEREBROSPINAL FEVER. 

Definition. — An acute infection, caused by the meningococcus, charac- 
terized anatomically by fibrinopurulent exudation in the meninges and 
marked clinically by headache, rigidity of the spine, hyperesthesia, 
vomiting, Kernig's sign and often by paralyses. 

In 1805 Vieusseux described epidemic meningitis; in 1806 Danielson 
and Mann, in New England, made the first autopsies. 

Bacteriology. — The Diplococcus intracellulars meningitidis of Weich- 
selbaum or meningococcus resembles the pneumococcus, though wider 
and less lanceolate. It lies in pairs or tetrads and resembles two coffee 
grains with their flat sides apposed. It is usually enclosed in the poly- 
morphonuclear leukocytes. Unlike the pneumococcus, it has no capsule, 
although one may develop in serum cultures. It decolorizes by Gram's 
method. It develops best on agar or blood serum as white, viscid, shin- 



90 BACTERIAL DISEASES 

ing colonies. Subcutaneous inoculations are usually negative, therein 
differing from the pneumococcus, but it produces inoculation-meningitis 
and peritonitis. The meningococcus is found in the nose, from which 
it is thought to invade the brain, in cases with and without meningitis. 
Von Lingelstein found it in the nasopharynx in 94 per cent, of cases in 
the Silesian epidemic and every time in 68 personal observations. He 
asserts that the disease is communicable only by direct contact with 
the mucus from the nasopharynx of patients or of those in contact with 
them. Its presence has been demonstrated in the blood in 25 per cent, 
of cases by Elser; kidneys, herpetic vesicles, conjunctiva, joints, spleen, 
ear, tonsils, lymphatic nodes, pleura, lung, heart and more rarely in 
the sputum and urine; it travels by way of the lymph or bloodvessels. 
Meningococcus septicemia without meningitis is recorded in four instances 
(Bovaird). 

Predisposing Etiology. — Fifteen per cent, occurs under two years of 
age and 60 per cent, between the second and fifteenth years; it is often 
epidemic in barracks, prisons and tenements or closely follows the move- 
ments of armies. Its contagiousness is proven. As many as seven members 
of a family have been successively stricken. Between epidemics, 1.7 
per cent, of persons are said to be "carriers," and during epidemics, 2.5 
per cent. ; Fliigge estimates that the healthy carriers outnumber by ten- 
fold those sick with the disease. Fortunately the coccus has little resist- 
ing powers outside the body. Most cases are seen in the late winter and 
early spring; 3455 deaths occurred in New York in 1904 and 1905. In 
a Silesian epidemic in 1905 there was a mortality of 57.6 per cent, in 3102 
cases. Councilman collected five instances of recurrence. The disease 
is also seen in the horse and goat. 

Pathology. — The findings are those of the suppurative form, viz., those 
of an acute fibrinopurulent, or less often a seropurulent leptomeningitis. 
The exudate is rich along the fissures, fossa of Sylvius and at the base 
about the chiasm or the surface of the pons and cerebellum. The inflam- 
mation follows the lymphatics and vessels penetrating the brain and 
cord, resulting in encephalitic or myelitic foci, small abscesses, paren- 
chymatous and interstitial changes. Flexner and Barker observed rows 
of cells "like miniature tubercles," two to eight times the size of the 
leukocytes. Hydrops ventriculorum is frequent in cases of long standing. 
The cerebral dura is seldom, and the spinal dura often, involved. In 
other organs the changes are those of acute infection; the muscles are 
brownish-red, dry and degenerated, there is parenchymatous degenera- 
tion in the heart and kidneys, and sometimes acute splenic tumor, 
arthritis, pneumonic foci or swollen glands in which the coccus may be 
found. 

Symptoms. — The incubation lasts from a few hours to three to eleven 
days. Prodromes are vague, as malaise, headache or coryza. The 
onset may be gradual or sudden, sometimes with a chill and usually with 
fever. The course is attended by fever and brain irritation; an almost 
constant triad of symptoms, headache, rigid neck and hyperesthesia; 
vomiting, mental, motor and sensory symptoms, and in fatal cases death 
results from paralysis, convulsions or coma. 



CEREBROSPINAL FEVER 



91 



1. General Nervous Symptoms. — (a) Headache is very rarely absent 
except in very young children. It is early, most severe and generalized. 
It is constant, with exacerbations, and in children provokes the short 
plaintive, clear meningeal cry, cri hydrencephalique (Coindet, 1817). 
The headache is throbbing or lancinating, even under narcotics, and 
persists even after delirium and coma have set in. Its cause may be 
compression of the dura, inflammation of the nerve trunks, or ventricu- 
lar exudation, (b) Hyperesthesia or hyperalgesia affects the special 
senses, causing intolerance of light and noise, or general sensation — affect- 
ing the arms most, the trunk less and the legs least. It is rarely absent, 
always suggestive, and due to root neuritis, (c) Rigidity of the neck 
and spine is caused by inflammation of the nerve roots. The head is 
retracted, sometimes so severely 
that the occiput lies between 
the shoulders, producing dys- 
phagia and decubitus; marked 
opisthotonos may be present. 
The entire body may be lifted 
by the head. The most com- 
mon attitude is the lateral, with 
the head * retracted, the arms 
flexed and the knees drawn up. 
Flexures in the ankles, knees 
and hips result when an attempt 
is made to flex the neck (Brud- 
zinski's "neck sign"). Closely 
associated and caused in the 
same way is severe spinal pain 
with tenderness, chiefly in the 
neck and loins. It may radiate 
to the trunk and in 33 per cent, 
of cases to the extremities, (d) 
Contractures of the limbs are 
caused by root inflammation, 
increased pressure, or lesions in 
the pyramidal tracts. Kernig's 
sign comes under this head ; when 

the patient sits or the thighs are at right angles with the trunk, in 85 per 
cent, of all meningitis cases it is impossible to extend the knees (Fig. 11). 
The legs and thighs are flexed (flexor contracture) and the knees 
cannot be pressed down when the patient is sitting, but this is possi- 
ble* when he is lying. It indicates involvement of the spinal meninges, 
pyramidal tracts or posterior sensory roots. It lasts well into convales- 
cence, whence, as Netter states, "a retrospective diagnosis may be made." 
It occurs in other conditions, but in infancy is generally meningitic. 
(e) Mental symptoms occur early, especially in children and include unrest, 
insomnia, delirium sometimes with periods of normal intelligence, and fol- 
lowed by incomplete coma. (/) Vomiting in the initial stage is due to 
vagus irritation ; later it results from ventricular hydrops or increased cere- 




Fig. 11. — Kernig's sign, showing retraction of 
head and back and prominence of knees in the 
erect posture, i. e., the impossibility of extension 
of knees. (Dieulafoy.) 



92 BACTERIAL DISEASES 

brospinal pressure. It is of the cerebral type, i. e., it occurs without nausea 
or relation to eating, is often projectile and is not amenable to gastric 
therapy. Vomiting is more typical and common in children, (g) The 
pulse at first is increased, perhaps disproportionately, considering the 
fever. Sometimes it slows later because of brain pressure, but ultimately 
it is fast again. It may be irregular in rhythm and oscillating in rate 
from 84 to 144 within a minute. Blood-pressure increases in proportion 
as the disease is severe, (h) Respiration is irregular in 20 per cent, of 
cases; Cheyne-Stokes breathing develops toward the end in 53 per cent. 
(Conner). Deep breathing with apneic pauses and undulatory respira- 
tion (Biot's breathing) are less common than in the tuberculous type. 
(i) Convulsions are most common in the young, but are ambiguous from 
their frequent occurrence in other diseases of childhood. 

2. Focal Nervous Symptoms. — These are partly irritative and partly 
paralytic, (a) The cranial nerves are most involved in basal localization, 
while the limbs are most affected in that of the convexity. Optic neuritis 
is frequent, if the disease lasts over four days. The disk is swollen and 
its margin is "washed"; hemorrhage and choking are uncommon. (See 
Plate IV, Fig. 4.) The pupils at first are usually small, often unequal, 
and sometimes variable. Later they widen spontaneously or on move- 
ment of the rigid neck and irritation of the skin, but do not react to 
light. Ptosis, diplopia, nystagmus and strabismus are frequent and may 
vary from time to time. Complete paralysis of the third nerve is not 
common. Involvement of the fifth nerve is unusual, although trismus, 
grinding of the teeth and trigeminal neuralgia have been noted. Involve- 
ment of the facial nerve ranks next to that of the third nerve; basal 
paralysis is usually total; cortical palsy is of the cerebral type, and its 
upper third escapes. The facial expression indicates suffering, the brows 
are slightly elevated and the forehead is corrugated. The auditory nerve 
is often bathed in pus, and extension may induce hemorrhagic inflam- 
mation in the labyrinth. The tongue on protrusion may deviate to one 
side; dysarthria or dysphagia is sometimes seen, (b) Paralysis of the 
limbs is not frequent. Hemiplegia is rarely complete, occurs with or 
without participation of the tongue and face, and is caused by involve- 
ment of the cortex or pyramidal tracts. It is frequently accompanied 
by rigidity of the limbs and aphasia. It is most frequent in children 
and may be temporary or permanent. The less frequent monoplegia 
most often concerns the face or arm. Choreiform or athetotic movements, 
twitchings and tremors are occasional. Convulsions are frequently 
Jacksonian in type. The tendon reflexes may be increased at first and 
are often decreased or abolished late in the disease. The skin reflexes 
are variable. 

3. General and Somatic Symptoms. — (a) The almost invariable 
fever is usually irregular or remittent, follows no definite cycle, and lysis 
is usual in cases which recover. A temperature of 107° may be registered 
before death, (b) The blood shows leukocytosis, which is early and 
constant; the white cells may number 25,000 to 40,000; the lympho- 
cytes increase during convalescence; the meningococcus is found in 25 
per cent, of cases, (c) The abdomen is often retracted and scaphoid, 



PLATE IV 








Retinal Findings in the More Important Diseases. 

1. Retinitis diabetica. 2. Atrophy (and pigmentation) of retina and optic 
nerve. 3. Choked disk in brain tumor. 4. Optic neuritis iri meningitis. 5. 
Medullated nerve fibers (normal). 



CEREBROSPINAL FEVER 93 

although less so than in the tuberculous type; it is due to retraction of 
the abdominal walls or possibly of the intestines from irritation of the 
vagus, (d) The spleen is often palpable, (e) The urine is febrile, albu- 
minous (33 per cent.) and may show peptonuria, hematuria in malignant 
cases, and rarely glycosuria or polyuria. (/) Skin: The tdche cerebrale 
has no differentiating value, for it occurs in many other conditions. 
Eruptions are more common in epidemic than in sporadic cases. Herpes 
varies with the epidemic (40 to even 90 per cent.); it is most frequent on 
the face, but may develop anywhere; it spreads more rapidly than in 
any other disease;. in one case the author saw it extend from the lip to 
the ear, neck, chest and shoulder. Purpura (" spotted fever") occurs in 
severe types. 

Clinical Forms. — (a) The ordinary acute type in which the general 
nervous symptoms enumerated are followed by focal nervous symptoms, 
somatic symptoms, death in coma, or slow recovery; (b) the foudroyant 
form, with violent onset, rapid course and death in three to thirty-six 
hours, with apoplectic symptoms, purpura, high fever and early coma; 
(c) the abortive form, with low fever and symptoms so mild that the 
disease is recognized only during an epidemic; and (d) Heubner's 
chronic form., which lasts two to six months, with marasmus and recur- 
rent fever. 

Complications and Sequels. — Pneumonia, tonsillitis, pleurisy, parotitis, 
endo- and pericarditis, arthritis and nephritis are the most common. 
Pneumonia is usually pneumococcic, but Councilman found the menin- 
gococcus in isolated foci in the lung. The arthritis is poly- or mono- 
articular, simple or suppurative, and may heal even when suppurative; 
it occurs in 25 per cent. Mental alteration, paralysis, contractures, 
obstinate headache, optic atrophy, deafness or Meniere's syndrome, 
chronic hydrocephalus, vomiting and convulsions may remain after 
recovery. In a Heidelberg epidemic, Moos found deaf-mutism in 60 
per cent., deafness in 31 per cent, and ataxia in 50 per cent, of the cases. 

Prognosis. — The mortality averages 37 per cent., but it varies with the 
epidemic, and may reach 75 per cent. Fifty per cent, of deaths occur 
in the first five days. Recovery is exceptional after deep coma, repeated 
convulsions, high fever or vagus paralysis. Obstinate vomiting, dis- 
turbed respiration, sudden drop of temperature and inanition are ominous 
signs. 

Diagnosis. — The first step is the diagnosis of meningitis, and the second, 
its variety, cause and localization. 

Cardinal Symptoms. — (a) The early triad of headache, retracted rigid 
neck and hyperesthesia and (6) general symptoms, as vomiting, abdomi- 
nal retraction, pulse and respiratory changes, fever or convulsions, are 
important in their grouping, (c) Lumbar puncture (Quincke, 1890) is 
of great diagnostic value. Its technique is as follows: The patient sits 
or lies on the side with the knees drawn up and the body bent as far 
forward as spinal rigidity allows; an aspirating needle is introduced in 
the median line in children, and a quarter to half an inch to one side in 
adults, between the third and fourth lumbar vertebrae and is pushed 
forward toward the median line and a little upward, 1.5 inches deep in 



94 



BACTERIAL DISEASES 



children and 1.5 to 2.5 inches in adults, until it passes into the canal; 
15 to 30 c.c. should be withdrawn. Results: (i) Normally the pressure 
with the patient in the lateral position, equals 100 to 150 mm. of water 
and the escaping fluid only trickles out. In meningitis, the pressure is 
greatly increased (200 to 700 mm.) and the fluid often spurts out. (ii) 
The normal fluid is clear, has a specific gravity of 1.007-09 and contains 
little albumin (J to 1 gm. per mille). Though the fluid may be clear in all 
forms of meningitis, it is usually clear in the serous form, but cloudy, 
flocculent or sometimes bloody in other forms; in the tuberculous variety 
it is usually clear or slightly yellow with a whitish clot forming on stand- 
ing; in the epidemic form, it may be turbid or clear, with a yellowish 
clot; in the purulent type it is opaque, and in rare cases pure pus. The 
specific gravity is about 1.010 in the serous, 1.011 in the tuberculous, and 
1 .015 in the purulent or epidemic type. The percentage of albumin is small 
in the serous, 2 per mille in the tuberculous, and 3 or even 9 gm. per mille 
in the suppurative forms. The Nonne, Noguchi and Ross- Jones globulin 
tests are positive, (iii) Bacteriologically in the purulent type the strep- 
tococcus, staphylococcus, pneumococcus, typhoid and colon bacilli are 
found; in the epidemic variety, the meningococcus was positive in 100 
per cent, in the last New York epidemic; in the tuberculous type, tu- 
bercle bacilli exist in 80 to 100 per cent, in the small clot, which forms 
after standing, (iv) The cellular morphology is a valuable aid. In 
purulent and epidemic forms the leukocytes are largely polymorphonu- 
clear; in the tuberculous form the lymphocytes predominate (see Cyto 
diagnosis, Pleurisy), (d) Local signs usually follow the general signs, 
and are more important, but their late development lessens their diag- 
nostic value. 

Diagnosis of the Variety (v. i.). — Cases of tuberculous meningitis 
sometimes increase when the epidemic form prevails. Sporadic cases 
may be indistinguishable from primary pneumococcic meningitis, save 
by lumbar puncture. 



EPIDEMIC FORM. 

Onset: Sudden, with few 
prodromes. 

Fever: Fairly high; pulse 
more rapid. 

Eruptions : Herpes and pur- 
pura very common. 

Leukocytosis: Regular and 
marked. 

Rigidity of neck: Most 
frequent. 

Other symptoms: Pepto- 
nuria. 

Course : Rapid — more re- 
coveries. 

Lumbar puncture: Menin- 
gococcus; leukocytes, 
polymorphonuclear. 



TUBERCULOUS. 

Longer prodromes; family 
history; other evidences 
of tuberculosis. 

Less; in versed type fre- 
quent. 

Rare. 

Exceptional. 

Spinal symptoms less fre- 
quent. 
Choroidal tubercles. 

Subacute, slower, fatal. 

Tubercle bacilli; mono- 
nuclear. 



SUPPURATIVE. 

Secondary to ear disease, 
acute infections, pneu- 
monia, etc. 

Especially high, with chills 
or pyemia. 

Rare — polymorphous septic 
rashes. 

Frequent. 

Sometimes absent (pneumo- 
coccic) . 
Peptonuria. 

More acute, very rarely re- 
cover. 
Pyogenic cocci, pneumo- 
coccus; polymorphonuclear. 



Diagnosis of Location. — (a) Convexity localization is characterized 
by delirium, Jacksonian convulsions, mono- or hemiplegia, less cranial 



CEREBROSPINAL FEVER 95 

nerve paralysis and less optic neuritis; (b) basal localization, by more 
frequent cranial nerve neuritis and optic neuritis; (c) the ventricular 
form rarely involves the cranial nerves. 

Differentiation. — 1. Fkom Nervous Toxemia. — Jenner pointed out 
that toxemic headache ceases when delirium begins in acute infections. 
Meningitis without focal symptoms may resemble uremia (q. v.), but 
the albuminuric retinitis, cardiovascular changes, albuminuria and 
cylindruria are usually distinctive. Acute inflammation of the labyrinth 
may mimic meningitis, for it sometimes produces headache, vomiting, 
fever, convulsions, stiff neck and even optic neuritis; if labyrinthitis 
involves the meninges, the facial nerve is likely to be affected. Such 
conditions resembling meningitis Dupre called meningismus, and Bou- 
chut pseudomeningitis (see pages 34, 46, 47). 

2. From Brain Disease. — See syphilitic and tuberculous meningitis, 
brain abscess, cerebral hemorrhage and encephalitis. 

3. From Hysteria. — Hysteria is marked by psychical alteration, 
limitation of the field of vision, anesthesia and other stigmata. Hys- 
terical strabismus is always spastic and convergent, and is often asso- 
ciated with small pupils; meningitic strabismus is often divergent (always 
a sign of organic disease), and the pupils are unequal. 

Treatment. — Prophylaxis; the nose should be douched with a weak 
resorcin solution. 

Flexner's and Jobling's Serum has given 70 per cent, of recoveries 
in 1300 cases; given on first to third day the mortality was 18 per 
cent.; fourth to seventh, 27 per cent.; after the seventh day, 37 per 
cent. The results are (a) the meningococci become more intracel- 
lular, and degenerate; (b) the exudate becomes less turbid or purulent; 
(c) leukocytosis decreases rapidly; and (d) complications are few and 
recovery is usually complete. The mortality under 1 year was 50 per 
cent.; 1-2 years, 31 per cent.; 2-5 years, 28 percent.; 5-10 years, 15 
per cent.; 10-20 years, 37 per cent. The serum is bactericidal rather 
than antitoxic, although some antibodies exist in the serum. In some 
failures, the parameningococcus should be considered; it was discovered 
by Dopter and is distinguished by the fact that it does not agglutinate 
in antimeningococcus serum. Technique: Lumbar puncture is performed 
and from the trickling fluid, cover slips, cultures and a leukocyte count 
are made. If possible, 30 to 45 c.c. are withdrawn; an aspirating syringe 
is then attached and injects an equal amount of serum, warmed to body 
temperature by standing in warm water. Injections are repeated daily 
for 4 days, and if improvement follows, injections are discontinued for 
4 days, and then repeated. Now and then, increased intradural pressure 
is evidenced by disturbed, even stertorous breathing, cyanosis, cold sweats 
and fall of blood-pressure. Sophian, who has given 1500 injections with- 
out accident, employs a gravity method rather than a syringe, which 
allows of more ready control of the amount of serum injected; he takes 
the blood-pressure during the injection. Anaphylactic death has been 
reported. When intraventricular effusions occur, the ventricles should 
be tapped and filled with the serum. 

The patient should be kept quiet in a dark room, the head elevated 



96 BACTERIAL DISEASES 

without flexion, an ice-bag applied to the head and spine, or an ice-pillow 
used. Nutrition is maintained by feeding with the nasal tube or by 
nutrient enemata, if retraction of the neck causes dysphagia. The bowels 
are mildly relaxed, and the bladder is watched. Vomiting is treated as 
in acute gastritis (q. v.), but therapy is usually unavailing, for the cause 
is cerebral irritation; of drugs the bromides are in general most service- 
able. Feeding by the rectum, sucking of ice, and the remedies indicated 
for the headache give the greatest relief. Counter-irritation by blisters 
or cautery is dangerous because the skin sloughs readily. Headache, 
restlessness and convulsions necessitate the hypodermic use of morphine 
or the tincture of deodorized opium by mouth with atropine; no other 
analgesic is equally potent. Chloral is used for convulsions and unrest. 
Warm baths are considered almost specific by Netter. Stimulation 
is indicated when the heart weakens. Resorbents, as iodides and mercurial 
inunctions, are inefficacious although they seem to modify serous menin- 
gitis. Crowe recommends urotropin, 5ss-j daily; formalin is found in 
the spinal fluid 30 minutes after ingestion. 



ACUTE POLIOMYELITIS. 

Definition. — An acute general infection, characterized by (i) diffuse 
cerebrospinal lesions, especially in the anterior horns (acute anterior 
poliomyelitis), with sequential acute, flaccid paralysis, wasting of the 
muscles, loss of reflexes, reaction of degeneration and contractures; 
(ii) lymphoid hyperplasia in the lymph glands, spleen and intestine; 
and (iii) parenchymatous changes in the lungs, liver and kidneys. 

History. — Infantile paralysis, acute poliomyelitis, atrophic paralysis, 
was first described clinically by Heine (1840). The famous contribution 
of Charcot and Joffroy (1870) referred the trophic relation of the special 
cells involved to the atrophy of the nerves and muscles supplied and 
stated that the disease was due to primary inflammation of the cells 
themselves. The first epidemic in America occurred in Louisiana, in 
1841. Medin described it definitely as an infectious disease, the epidemic 
character of which was fully considered by Wickman in his monograph. 
Among recent investigations are those of Landsteiner and Popper, who 
inoculated the disease into rabbits, followed by the brilliant work of 
Flexner and Lewis, Landsteiner and Levaditi, etc. In the United States, 
Boston and New York are the chief centres, probably invaded from 
Northeastern Europe. In New York there were 2500 cases in 1907, 
and in 1910 over 8000 in the United States. It exists epidemically 
and sporadically. In some statistics it constitutes even 8 per cent, of 
the diseases of childhood. 

Etiology. — I. The virus, which passes the finest filters, is found in the 
brain and cord, tonsils, nasopharynx, lymphatic and salivary glands, blood, 
cerebrospinal fluid, stomach and intestine. Flexner regards the naso- 
pharynx as the atrium to the nervous system and also as the point of exit; 
its ingressis along the lymph channels, around the filaments of the olfactory 
nerves, and its egress, in the reverse direction, along the same paths. 



ACUTE POLIOMYELITIS 97 

Mtiller holds that, as in rabies, infection progresses along the nerve 
sheaths, but Flexner maintains that it occurs by the cerebrospinal fluid. 
The virus was inoculated into monkeys, and from one to another through 
25 animals successively. Flexner and Noguchi cultivated the virus; it 
is anaerobic; small bodies are found, 0.15-0.3 microns, single, double, 
in chains or masses. The virus is extremely resistant to external influences, 
as freezing or drying, and persists in the nasopharynx from six weeks to 
six months after the disease, in monkeys, and after it had disappeared 
from the brain and cord. 

II. Dissemination. — The nasal, bronchial and intestinal secretions, 
the house- and stable-fly, and dust, may convey the disease. 

III. Carriers. — In epidemics a certain percentage of cases occur of 
the abortive type, in which few symptoms develop. Frost and Anderson 
proved that two-thirds of these cases were actually poliomyelitis, by the 
biological test (the serum of one who has had the disease, injected into 
monkeys, protects the latter from inoculation). This may explain the 
apparent immunity of children in households in which the frank form of 
the disease prevails; they may have a light infection, overlooked save 
for the presence of an epidemic, or may carry the virus without themselves 
contracting the disease. 

IV. Secondary Factors. — Sixty per cent, of cases occur in the first 
three years, and 87 per cent, in the first ten years, and 80 per cent, of 
cases occur in the summer months. 

Pathology. — The affection is called poliomyelitis (Kussmaul), because 
it is an inflammation of the anterior gray matter, supplied by the central 
arteries, branches of the anterior median artery of the anterior longitu- 
dinal fissure. A given vessel branches up and down, supplying a cylin- 
drical vertical area of two inches or more, the usual dimension of a polio- 
myelitic focus. Recent reports place equal emphasis on changes in the 
central vein and in other arteries. The cord changes are always accom- 
panied by a round-cell infiltration of the pia mater and the arach- 
noid, such as occurs in rabies and syphilis, but not in diseases of bacterial 
origin. The meningitis is most marked in the lumbar and sacral regions 
of the cord, next in the cervical; it is most intense over the anterior sur- 
face, whence it follows the pia into the depths of the anterior fossa, 
along the sheaths of the vessels, the posterior root fibers and the arach- 
noid covering the spinal ganglia. This inflammation of the pia, arachnoid 
and ganglia is responsible for the irritative symptoms of the disease. 
The inflammation may extend back of the anterior horns into the antero- 
lateral columns. The fresh focus is rarely seen, since death is unusual; 
to the naked eye it is red, soft, juts above the cut section and is mostly 
confined to the anterior horn, i. e., the beginning of the lower motor 
neurone. Microscopically, the lesion in the anterior roots is inflammation 
in and about the vessels above named, even before they enter the cord; 
the perivascular spaces are full of round cells and granule-cells; there is 
exudation of red and white cells, with actual hemorrhage in severe cases ; 
the ganglion cells in the anterior horn suffer secondary changes; their 
dendrites may shrink, their nuclei disappear, or the whole cell may disin- 
tegrate, while here and there some cells escape. The cells involved depend 
7 



98 BACTERIAL DISEASES 

solely on the vessel affected; involvement is sometimes bilateral and in 
severe cases is distributed through several segments, especially in the 
lumbar cord. 

An inflammatory edema is detected throughout the cord, macroscopi- 
cally, by the moist appearance of its cut surface; it explains the transitory 
nature of certain symptoms. As easily anticipated, disease of the trophic 
cells of the lower motor neurone must be followed by degeneration of 
their axis-cylinders, nerve roots, peripheral nerves and muscles (which 
become granular, fatty and later indurated). In old cases the unaided 
eye detects shrinking of the anterior horns, with lack of differentiation 
between the gray and white matter. Microscopically, the formerly 
inflamed vessels are thickened and pigmented; groups of ganglion cells 
have disappeared and their nerve fibers are degenerated or wholly wasted, 
which led Charcot to consider the process essentially in the ganglionic 
cells, but the thicker connective tissue is rich in cells and stains deeply 
with carmine. In severe cases, identical changes are found in the medulla, 
pons, centrum ovale, and even in the cortex or cerebellum. Acute polio- 
myelitis differs from acute myelitis and disseminated myelitis only in 
its localization. The visceral pathology, other than the nervous, consists 
of lymphoid hyperplasia of the lymph glands, spleen and intestinal fol- 
licles (which may be the atrium of the infection), changes similar to those 
of typhoid; the kidneys are cloudy, foci of necrosis appear in the liver, 
and there is bronchitis and often bronchopneumonia. 

Symptoms. — Wickman's classification of poliomyelitis includes eight 
types as follows : 

I. The Spinal Type. — There are three clinical periods after an incuba- 
tion of 5 to 10 days. (1) The acute stage. (2) The diffuse paralysis when 
degeneration appears and regeneration begins. (3) The stationary 
stage, with determination of the paralysis to given muscles. 

1. Acute Stage. — The typical onset is acute, appearing in a child 
previously well, with fever (75 per cent.), often with vomiting, headache, 
somnolence and sometimes with convulsions or coma, which are followed 
by a sudden complete and flaccid paralysis in one or more limbs ; it cor- 
responds to the acute inflammation in the anterior horn. The fever 
averages 101°, may reach 105° or more and lasts about twenty-four hours. 
Convulsions are not as common as in the cerebral type, and occiir mostly 
in younger subjects, are attributed perhaps to teething, once thought 
the cause of the paralysis. The motor paralysis usually reaches its 
maximum in twenty-four to forty-eight hours and is not progressive. 
In many cases prodromata exist, as tonsillitis or angina, coryza, bronchitis, 
swollen joints, malaise, pain in the back and limbs or diarrhea; Miiller 
anticipates poliomyelitis in a general infection beginning with profuse 
sweats, hyperesthesia and leukopenia; tympanites and weakness of the 
abdominal reflexes and abdominal muscles are also emphasized. Varia- 
tions -in onset; the fever may last one or two weeks before the paralysis 
develops, it may last a few hours only or may be absent. The paralysis 
may develop during the night; sometimes it is not noticed until, for 
example, the child fails to walk. Convulsions involve principally the 
extremities, sometimes as clonic muscular contractions. 



ACUTE POLIOMYELITIS 99 

2. Stage of Degeneration. — The localization in the anterior horn 
produces paralysis, disturbed nutrition, vasomotor changes and loss of 
reflexes, (a) The paralysis is motor only; it is sudden, complete, flaccid 
and non-progressive; at first diffuse, it usually regresses, although 
incompletely, leaving some permanent paralysis. General localization: 
(i) Paralysis, most frequently of one leg, then (ii) of both legs, and (iii) 
and (iv) of all four limbs or of one arm (with equal frequency), (v) of 
arm and leg of same side (spinal hemiplegia), (vi) of arm with opposite 
leg (crossed paralysis), (vii) of three limbs and least often (viii) of both 
armsl The back, abdomen, neck, face and eye may be involved in severe 
and diffuse foci. As to its special localization, the leg is paralyzed in 
75 per cent, of cases; in one form the lasting paralysis affects the quadri- 
ceps femoris with the adductors (upper lumbar lesion), but the sartorius 
is not involved; another form involves the muscles below the knee 
supplied by the peroneal nerve — the tibialis anticus, extensor digitorum 
communis, ext. longus or brevis, ext. hallucis longus, peronei (lower 
lumbar and upper sacral lesion), of which some muscles may escape, 
as the tibialis anticus. If both legs are involved the paralysis is rarely 
symmetrical. Poliomyelitis usually involves several segments because 
of the arterial distribution. The arm is paralyzed in 25 per cent., 
chiefly in the form of the combined shoulder paralysis of Remak, 
involving the deltoid (sometimes alone), biceps, brachialis, supinator 
longus with the supra- and infraspinatus and teretes (lesion in upper 
cervical enlargement, fifth to sixth segment); in some cases the forearm 
type may be seen, with involvement of the flexors, possibly the extensors, 
while the supinator longus often escapes (lower cervical lesion, seventh 
and eighth segments) . The trunk or neck muscles usually show improve- 
ment in this stage, (b) As to disturbed nutrition, the muscles and nerves 
corresponding to the level of the poliomyelitis rapidly degenerate, as 
shown by early reaction of degeneration and muscular atrophy. The 
reaction of degeneration consists of failure of the nerve and muscles to 
respond to the faradic current and usually appears in one or two weeks; 
it also includes a lack of response of the nerve to the galvanic current 
and finally a too prompt response of the muscles to the galvanic current 
and more quickly to the positive than to the negative pole; this latter 
reaction lasts for two, three or six months and then gradually disappears 
in a year or two. Muscular atrophy is more clearly seen in the arm 
than in the leg or trunk, where adipose deposit may obscure it. Fibrillary 
contractions are frequent. The wasted flaccid member hangs and swings 
in a lifeless fashion, (c) Vasomotor paralysis causes the low temperature 
(1° to even 10° below normal) and the livid, clammy skin, (d) The skin 
and tendon reflexes are abolished in the limb at first; the skin reflexes 
usually return later. The sphincters are almost always intact and sen- 
sation is very rarely affected. Trophic changes are almost unknown. 

3. Stationary, Chronic, Residual Stage. — This stage is marked 

(a) by accentuation of muscular atrophy, connective and sometimes 
adipose tissue replacing the contractile substance, especially in the legs. 

(b) The bones become flexible, friable, arrested m development and there- 
fore shorter; the bone cortex wastes and its medulla becomes more 



100 BACTERIAL DISEASES 

spongy; scoliosis may result, (c) There may be pronounced vasomotor 
lividity. (d) In the joints, nodules may appear as in cerebral hemi- 
plegia; the joint structures are relaxed and the "flail joint" may develop 
with luxation or subluxation, (e) Contractures are due principally to 
the mechanical influence of the unopposed antagonist muscles on the 
posture of the joint; if all the muscles are paralyzed they sometimes 
result from static causes, as from standing or attempting to walk; 
the arm, shoulder, wrist and fingers are flexed and the elbow usually 
escapes involvement. In the leg, deformity (pes equinovarus) is more 
common than in the arm. 

II. The Ascending or Descending Type. — This variety, more often 
ascending than descending, may exactly mimic Landry's paralysis. 
In one epidemic (1905), among 159 poliomyelitis deaths, 28 per cent, 
were of this form. 

III. Bulbar or Pontine Type. — Perivascular exudation may crowd 
closely around these vital nuclei, without injury to them, yet in all fatal 
cases they are affected; death is caused by disease of the respiratory 
centre. The third, fourth, fifth, sixth and seventh nerves are often 
affected. 

IV. Encephalitic Type. — This is identical with StrumpeH's polio- 
encephalitis (see Infantile Cerebral Paralysis). Convulsions may 
antedate paralysis by days; hemiplegia, epilepsy and mental deficiency 
may be its legacy. 

V. Ataxic Type. — Involvement of the tract between the dentate 
nucleus of the cerebellum and the contralateral red nucleus may occasion 
a coarse intention tremor, some paresis and rigidity and increased 
muscular tonus. 

VI. Polyneuritic Type. — While the sporadic forms are often painless, 
the epidemic forms are often exquisitely painful, not merely during the 
acute phase but for weeks afterward. 

VII. Meningitic Type. — Without spinal puncture, differentiation may 
be impracticable, because of the rigidity of the neck, Kernig's sign, 
twitchings, convulsions, and herpetic, petechial or other rashes. 

VIII. Abortive Types. — Positively proved to be poliomyelitic by inocu- 
lations (v. s.), many or most cases would be mistaken, in the absence 
of an epidemic. The subforms are (a) those evidencing only fever or 
toxemia; (b) those with symptoms of meningitis or meningismus; (c) 
the pseudo-influenzal (pains and hyperesthesia) ; and (d) gastro-enteric 
symptoms as diarrhea, which in some epidemics are the first symptoms, 
even in 90 per cent, of cases. 

Diagnosis. — The initial vomiting, fever and convulsions are usually 
misinterpreted until the diffuse motor paralysis appears and conse- 
quently the physician is unjustly blamed for what no one can anticipate. 
The rapid atrophy, reaction of degeneration and loss of reflexes are 
positive diagnostics. 

Differentiation. — (a) The various forms of muscular atrophy in chil- 
dren are gradual in onset, progressive, symmetrical and often familial. 
The atrophy precedes and exceeds paralysis and there is no arrest in 
development. The neural progressive muscular atrophy of Hoffmann 



ACUTE POLIOMYELITIS 101 

is progressive, familial and involves sensation, (b) Multiple neuritis 
(q. v.) has several distinctive features. Poliomyelitis is due to a local 
inflammation, is unilateral and spinal in type — or if bilateral, it is asym- 
metrical. Multiple neuritis is hematogenous and toxic, and therefore 
affects the spinal, and often the cranial nerves symmetrically and bi- 
laterally and usually involves the arms and legs; ataxia, sensory dis- 
turbance and local tenderness over the nerve trunks are common; 
its onset is more subacute, the reaction of degeneration less intense 
and the issue more favorable, (c) The cerebral palsies of children 
(q. v.) never produce marked degenerative atrophy or loss of faradic 
irritability. The hemiplegic form involves the face and the paraplegic 
form is spastic. Disturbance of the intellect, convulsions and hemichorea 
are common, (d) Myelitis also begins acutely, but usually in older sub- 
jects. Poliomyelitis may be confused only when it is bilateral, located 
in the cervical or lumbar enlargement, when sensory changes occur 
(2 per cent.) or the sphincters are involved, producing a flaccid atrophic 
paralysis of an arm and a transitory spastic paresis of the leg. Bed-sores 
so common in myelitis, are almost unknown in poliomyelitis, (e) Painful 
affections causing immobility of a joint, hip-joint disease, Parrot's syphil- 
itic pseudoparalysis and infantile scurvy but superficially resemble polio- 
myelitis. (/) Meningitis shows its appropriate microorganism (tubercle 
bacillus, meningococcus, etc.). Lumbar puncture of the poliomyelitic 
shows a clear, possibly slightly opalescent fluid, under increased pressure, 
exhibiting a mononucleosis, a slight fibrinous clot and positive globulin 
reactions. 

Prognosis. — (1) Regarding life; there is little danger after the fever 
subsides; life is rarely threatened from extension to the medulla ob- 
longata. In epidemics the mortality may reach 15 to 33 per cent., but 
averages 7 per cent. (2) Regarding recovery, improvement is the rule 
and recovery is due to the recession of the congestion and edema; in 
some epidemics abortive cases number 33 to 50 per cent. (Trethowan, 5298 
cases, 1912). A localized initial paralysis may show little improvement, 
or an extensive initial paralysis may diminish greatly. A definite prog- 
nosis cannot be made for two weeks and then only by the electrical 
examination. Muscles which show no reaction of degeneration after 
fourteen days will probably recover; those showing slight loss of faradic 
irritability will recover in great part; after six weeks only those muscles 
are paralyzed which will remain paralyzed; if there is no recovery in three 
months there will be none or it will be slight. 

Treatment. — In prophylaxis, isolation should be practised, and carriers 
should be quarantined. The nose and throat require special care in 
those ill of the disease, in carriers and in those exposed to infection; 
two parts water to one of hydrogen peroxide, and urotropin are advised 
(v. i.). In the acute stage rest, a light diet, laxatives and diaphoretics are 
indicated. After administration of urotropin, Cushing found formalde- 
hyde in the spinal fluid; Starr recommends urotropin, gr. v, every four 
hours; Flexner and Lewis found that urotropin given to monkeys, in- 
oculated with the virus, prolongs the incubation and often prevents 
paralysis. After the fever the patient should be kept in bed for weeks; 



102 BACTERIAL DISEASES 

immobilizing the limb lessens spinal irritability. Electricity is contra- 
indicated. As the paralysis recedes a fuller diet and careful passive 
movements are beneficial. Hot baths are quieting and repeated lumbar 
punctures apparently are beneficial. In the chronic stationary stage, 
with its inevitable and permanent paralysis, fresh air and liberal nourish- 
ment are important. Strychnine is valuable because of its general tonic 
action and its effect on the motor side of the cord. It is given for three 
weeks after the paralysis becomes stationary. Full doses may induce 
muscular spasm, pain and irritating paresthesia, and of late its use is 
far less popular. Electricity cannot restore destroyed tissue, but it 
hastens recovery in partial lesions; if applied to the spine it is useless, 
but the constant stream to the muscles and the faradic current to the 
skin are helpful. Contractures and deformities due to neglect may be 
modified by gymnastic movements, massage and orthopedic apparatus. 
The child should be kept in bed for a long period. In some cases teno- 
tomy, arthrodesis and tendon transplantation (by attaching the tendons 
of sound muscles to those of paralyzed muscles) and nerve transplan- 
tation are indicated. 



INFLUENZA (LA GRIPPE). 

Definition. — A specific infection, caused by the Bacillus influenzae, and 
characterized by its protean symptomatology and particular affinity for 
the respiratory tract. 

Varieties. — (1) Influenza vera, pandemic, endemic or epidemic, due to 
Pfeiffer's bacillus. (2) Influenza notha s. nostras, pseudogrippe, catarrhal 
fever, of variable bacteriology. 

Pandemics originate in Asiatic Russia. No other pandemic is so widely 
or rapidly distributed as influenza, which is due to the enormous virulence 
of the virus; to the universal susceptibility; and to the fact that many 
moderately sick individuals frequent public places. Epidemics usually 
follow pandemics; they occur every few years whereas pandemics are 
separated by decades. The first epidemic occurred in 1173 and the 
first pandemic in 1510. 

Etiology. — Most cases occur between the twentieth and fortieth years. 
The immunity conferred by one attack is less enduring and absolute 
than in other infections. The organism discovered by Pfeiffer (1891-2) 
is the smallest bacillus cultivated. Its ends are rounded and it resembles 
a diplococcus when two bacilli lie end to end. It has no capsule, is non- 
motile, it lies free in the sputum in the early stages and later within the 
leukocytes, but often disappears early from the sputum. The bacilli 
lie in lines " like schools of fish." It is best stained by Gram's method and 
then ten minutes' staining with carbol f uchsin ; if pneumococci and strepto- 
cocci are present, they are stained deep purple, and the influenza organism 
red. The bacillus is aerobic, short-lived and very susceptible to drying. 
It grows characteristically on blood serum as closely compressed yet 
discrete colonies, clear as water and almost microscopic in size; it is 
easily overgrown by saprophytes. The germ has also been found in rare 



INFLUENZA 103 

instances in the blood, cerebrospinal fluid, gall-bladder, joints, pneumonic 
and encephalitic foci, peritoneum (puerperal sepsis) and other parts, 
and possesses rather marked pyogenic characters. Its atrium is probably 
respiratory. 

Symptoms. — There is scarcely another acute infection with such 
varied symptoms, sequels and complications. 

After a short incubation of one to three days, the grippe begins suddenly 
with chill and fever, headache, general pains, respiratory catarrh and 
intense nervous and sometimes digestive symptoms. 

Types. — In the simple toxemic type there are coryza, moderate soreness 
of the throat, possibly some cough and toxemia, evidenced by fever, 
depression, and pains in the head, back and limbs. In the severer toxemic 
forms, these symptoms obtain, but the patient suffers profound depression 
both with the fever, and after it. The intensely respiratory variety 
(75 per cent, of all influenzas) is attended by fever and toxemia, the 
bronchitis is severe, perhaps intractable and not uncommonly followed 
by pneumonia. The g astro-intestinal grippe is attended by gastric 
intolerance and diarrhea. Of the septicopyemic type, only seven in- 
stances are reported. 

The duration is one to three days and the diagnosis is usually easy 
without the detection of the bacillus. Recurrences are frequent; most 
frequently, an initial respiratory catarrh is seen with nervous mani- 
festations in the recrudescence but the order may be reversed. In rare 
instances influenza may cause chronic symptoms. Convalescence is 
marked by great nervous depression, neuralgias, possibly cardiovascular 
atonicity, and tardy return of vigor. 

Special Symptoms. — 1. Fever. — The rise is usually sudden to 103° 
or 104°. It is entirely atypical. Remittent fever is more common than 
continuous fever, which may suggest typhoid. It is occasionally inter- 
mittent, resembling malaria. Hyperpyrexia is observed particularly 
in encephalitis. Certain nervous forms are afebrile. The fever runs 
one to four days, or longer as a result of complications. 

2. Nervous System. — The nervous system is second in importance 
only to the respiratory tract. The most frequent disturbances are 
functional and psychical. Headache is observed in nearly all cases, and 
often is very severe. Influenza comatosa results from very acute intoxi- 
cation, which also may cause epileptiform seizures, or severe delirium. 
The postinfluenzal psychoses, due to toxemic exhaustion, are observed 
eight times as frequently as in any other acute disease, and most cases 
are seen in the young. They usually follow the attack and chiefly are 
of the hypochondriacal type. Suicides in Paris increased 25 per cent, 
during the last pandemic. In encephalitis grippalis, acute foci of inflam- 
mation, usually discrete and multiple, occur in the gray substance of the 
cortex or ganglia and vary in size from the "flea-bite" spots of inflam- 
matory hemorrhage with surrounding softening to the size of a cherry 
or pigeon's egg — due to embolism by the Bacillus influenza? (Pfuhl and 
Nauwerk). Mono- and hemiplegia or sudden apoplectiform onset may 
mark the process, or there may be diffuse cerebral symptoms without 
definite focal localization. Encephalitis is usually fatal. Meningitis 



104 BACTERIAL DISEASES 

grippalis generally develops early, the virus reaching the brain by the 
blood stream or through the basis cranii. Slawyk first found the organism 
in the cerebrospinal fluid. Nearly all are under ten years of age; of 
Flexner's 58 cases (1911), all but six died. Transverse myelitis has 
been observed. Neuritis is usually postinfluenzal; neuralgia affects 
most often the fifth, sciatic and intercostal nerves. 

3. The respiratory tract is the atrium of the bacillus and is in- 
volved in 75 per cent, of cases; coryza is seen in 70 per cent, of cases, 
angina in 33 per cent, and tonsillitis in 60 per cent. Laryngitis (10 per 
cent.) occurs with hoarseness. Tracheitis (65 per cent.) causes pain, 
tenderness and severe paroxysmal cough, induced by irritation at the 
tracheal bifurcation. 

Bronchitis is diffuse or more characteristically occurs over one lung 
or lobe. At autopsy are found great congestion, hemorrhage, round-cell 
infiltration into the mucosa, and thrombosis of the smaller vessels, which 
causes necrosis of the mucosa. The sputum is characteristically num- 
mular and greenish-yellow. It is often blood-stained, viscid and contains 
the bacillus. Rales abound near the liver and lingual lobe. We may 
observe dyspnea without physical findings. Cyanosis is inauspicious 
in the young, aged and decrepit. Acute bronchiectasis is not uncommon, 
but usually escapes clinical recognition. 

Influenzal pneumonia (in 6 per cent, of cases) is the most important 
complication. Pfeiffer's bacillus is its most frequent cause, alone or 
combined with the pneumococcus, streptococcus and staphylococcus. 
Influenzal pneumonia, strictly speaking, shows no fibrinous exudation 
or granulations, but is catarrhal, with infiltration of cells about the 
bronchi as discrete foci. Clinically, the pneumonia is atypical and begins 
without a chill, but with insidious increase of the prior cough and dyspnea. 
It usually develops during or after the influenzal attack, although pneu- 
monia may be the first sign of influenza. Its symptoms are more pro- 
nounced than its physical signs, and the disproportionate cyanosis and 
dyspnea sometimes suggest miliary tuberculosis. Foci of dulness may be 
found but distinct bronchial breathing is rare; bronchophony is a much 
more reliable symptom. There may be oligopnea (slow breathing) 
with difficult, prolonged expiration. The heart is often weak and a peculiar 
redness of the face and head, profuse sweats at the beginning, and char- 
acteristic paroxysmal coughing are symptoms not seen in ordinary 
pneumonia. The foci are bilateral or multiple in 60 per cent, of cases 
and the apices are involved frequently. The sputum is purulent or bloody. 
Issues: (1) solution by lysis; (2) death from early edema pulmonum; 
the patient may die later, with early gray hepatization; the mortality 
is 20 to 30 per cent.; (3) chronic influenza-pneumonia, with hectic 
fever and suppuration, simulating tuberculosis; during a grippe epidemic 
an increased mortality from tuberculosis is noticed; (4) abscess or 
gangrene of the lung. A grippe epidemic may double the number of 
lobar pneumonia cases; when it complicates grippe, it is less completely 
lobar and granular. 

Primary pleurisy occurs in 27 per cent, of the fatal cases of influenza; 
its symptoms are frequently severe and protracted. 



INFLUENZA 105 

4. Circulation. — The heart-muscle is directly injured, especially 
affecting the lesser circulation. Weakness or syncope may occur dur- 
ing convalescence, especially from preexisting arteriosclerotic changes. 
The pulse is labile, often arrhythmic or dicrotic; it may be rapid and out 
of proportion to the fever; cyanosis, dyspnea and bronchiolitis are 
frequent in such cases. A slow pulse occurs in 50 per cent, of the severer 
types. Acute endocarditis sometimes follows abscess of the lung; in 
three cases the influenza bacillus was found. Acute phlebitis is seen 
mostly in severe cases with cardiac weakness, most frequently in the 
upper extremities. Arteritis is rare, occurs mostly in the popliteal 
vessels, and may end in gangrene. Leukocytosis occurs in a third of the 
cases Hemorrhages into the skin and mucous membranes indicate 
severe intoxication. 

5. Alimentary Tract. — Digestive symptoms are not important. 
The coated tongue is rarely typhoidal. Vomiting (34 per cent.) is some- 
times persistent (grippe hyperesthesia of the stomach). Constipation 
is more frequent than diarrhea. There are the usual febrile degenerative 
changes in the liver. Icterus is rare (2 per cent.). The spleen is enlarged 
in 15 per cent, of cases. 

6. Genitourinary Tract. — Albuminuria may result from toxemia 
(10 per cent.). Altered red blood cells in the urine are rather frequent. 
Acute glomerulonephritis occurs in 1 per cent, of cases. The diazo 
reaction and indicanuria are noted frequently. 

7. Skin, Muscles, Joints. — Urticaria, herpes (5 per cent.), miliaria, 
erythematous, scarlatiniform or morbilliform eruptions or purpura may 
be noted (16 per cent.). Polysynovitis, pyarthrosis, bone involvement 
and myositis are not common. Eye involvement (7 per cent.), con- 
junctivitis, keratitis, herpes and otitis media (35 per cent.), usually 
purulent and often hemorrhagic, are due to the pyogenic cocci, pneu- 
mococci and the influenza bacillus. 

Diagnosis. — During an epidemic the diagnosis is simple. Respiratory 
catarrh, headache, pains in the joints and back, nervous depression 
and tardy convalescence are significant. The diagnosis of the toxic, 
nervous and alimentary forms is more difficult and many errors may be 
made. The importance of bacteriological diagnosis has been over-rated, 
but positive results are decisive. 

Differentiation. — A clinical picture, identical with the grippe, may be 
due to pneumococcemia, without hepatization. A peculiar streptococcus 
causing influenzal symptoms, is reported by Miiller, Seligmann and 
Richardson in septic sore throat. 

Typhoid fever may be considered when severe influenza begins with 
step-like rise of the fever and tympany, enteritis, intestinal hemorrhage, 
swelling of the spleen and roseolse ; at autopsy, swelling and even ulcera- 
tion of the stomach mucosa and Peyer's patches occur. However, 
the existence of an epidemic and early catarrhal symptoms indicate 
influenza. 

Simple coryza and bronchitis are distinguished by the sudden rise 
of fever in influenza, its nervous manifestations, bacteriology, pains 
in the head, splenic tumor and exanthems. Lord found the bacillus of 



106 BACTERIAL DISEASES 

Pfeiffer in 30 per cent, of bronchitis cases in Boston, in which there 
was no suspicion of influenza. 

Measles. — The early respiratory catarrh and the measles-like eruptions 
in influenza may cause confusion, but the measles fever-curve, rising 
after the prodromes, with the exanthem and Koplik's spots, determine 
the diagnosis on the third or fourth day. 

Miliary tuberculosis is suggested only in severe respiratory types. 
Meningitis, apoplexy, acute psychoses and acute poisoning are rarely 
simulated by influenza. 

Prognosis. — (1) The morbidity is enormous (50 to 75 per cent, of the 
population, pandemic of 1889-90). (2) The mortality is 0.6 to 1 per 
cent. Influenza increases the number of deaths from pneumonia and 
tuberculosis, especially in the weak and aged. In some cases the course 
is chronic, the bacillus being found in the sputum for months, especially 
in the remarkably susceptible tuberculous subject. 

Treatment. — There is scarcely any prophylaxis except avoiding crowds. 
Isolation should be practised in asylums, hospitals and prisons. Gargles 
and nasal douches possibly prevent infection and are indicated in grippe 
patients. There is no specific treatment. Influenza must be treated as a 
serious disease, and complications avoided by rest in bed and a restricted 
diet. 

1. Pain. — At the onset, Dover's powder and acetphenetidin, aa grains 
x, are given for pain (phenacetin is superior to acetanilide and is less 
depressing). These measures failing, the salicylates (or acetylsalicylic 
acid, aspirin) are used as in rheumatism. Cold baths are poorly tolerated. 

2. Catarrhal Symptoms. — For conjunctivitis, boric acid solution is 
excellent; for coryza (q. v.) douches with Dobell's solution, tincture 
of belladonna and of aconite in two- and one-drop doses, respectively, 
every half-hour for six doses, and the alkaloid cocaine, gr. j to albolene 
§j, should be used locally; for pharyngitis, silver nitrate (20 per cent.); 
for tonsillitis, nitrate of silver is introduced into the follicles which are 
first opened; for bronchitis (q. v.), heroine or morphine is indicated; 
for enteritis, bismuth and paregoric, aa 3j, are given after each bowel 
movement. 

3. Nervous symptoms are somewhat relieved by warm baths. Neu- 
ralgia indicates acetphenetidin, camphor, iron and arsenic. Headache 
is treated as in typhoid. Flexner and Wollstein prepared a serum against 
experimental influenzal meningitis. 

4. Heart. — Strychnine may be indicated. 

5. Convalescence concerns chronic tuberculosis and bronchitis. 



PERTUSSIS (WHOOPING-COUGH). 

Definition. — A specific infection, characterized by a cyclic course and 
a severe convulsive cough, which ends in a whoop. Cullen's definition 
was ''Morbus contagiosus, tussis convulsiva strangulans cum inspiratione 
sonora iterata, saepe vomitus." 

History. — Pertussis was described by Ballonius (1578). 



PERTUSSIS 107 

Etiology. — (a) Age: It usually occurs in children and is most frequent 
at the fourth year. It is extremely infrequent after the twentieth year. 
(b) Sex: Sixty-six per cent, of cases occur in girls, (c) Most cases occur 
in March and April. 

In 1906 Bordet and Gengou obtained in pure culture a small, short 
bacillus, with rounded ends. It stains feebly and shows polar granules 
with carbol methylene blue. It occurs in the sputum unmixed with other 
organisms at the onset, in the catarrhal stage and for a few days after the 
whoop appears. As the disease progresses, other organisms, especially 
the influenza bacillus, overgrow it. It has been cultivated from the 
blood and lungs. The blood in convalescent cases rather feebly ag- 
glutinates the organism. Specific antibodies have been demonstrated 
in the serum. Mallory and Horner find the bacillus characteristically 
between the cilia of the trachea and bronchi. It interferes mechanically 
with the movements of the cilia, preventing the normal removal of 
secretion. One attack confers almost absolute immunity. Incubation 
lasts from two to eight days. 

Symptoms. — 1. The stadium catarrhale is characterized by headache, 
photophobia, conjunctivitis, coryza, angina and a cough which becomes 
dryer and harder toward the end of this stage. In a few cases there is 
moderate fever. This stage averages one week, or less during an epidemic. 

2. The stadium spasmodicum dates from the first "whoop." The fever 
ceases, aside from complications. The seizures are paroxysmal, con- 
vulsive and accompanied by dyspnea and vomiting. The child is well 
except for the paroxysm, which has for an aura, tickling in the larynx, 
thoracic constriction, vertigo or a creeping sensation, when the child 
braces himself and terrified, runs for support. Then the explosion comes 
in the form of three to ten or more short expiratory coughs following in 
rapid succession until the breath is lost, when the "whoop" is heard 
as a deep, singing or whistling inspiration. Then thin tenacious mucus 
is expectorated and vomiting constitutes the crisis of the paroxysm. 
In severe cases there may be apnea and cyanosis. One to two minutes 
elapse between expiration and inspiration, and inspiratory and ex- 
piratory spasms or generalized convulsions may develop. The eyes are 
injected, the nose runs, the jugular veins are large and the skin is clammy. 
Involuntary evacuations occur; the pulse is small; ecchymoses sometimes 
occur in the conjunctiva?, sclera?, neck or face. After the attack, con- 
sciousness returns, respiration is fast, and there is fatigue, stupor, sweating 
and pain in the abdominal or other muscles from the strain of coughing. 
The attacks occur especially toward morning. The attacks average 
twenty daily. In the free interval there may be euphoria or great de- 
pression, gastric disturbance, inanition or diarrhea. A marked leuko- 
cytosis is observed early in the disease; lymphocytosis occurs in 85 
per cent, of cases. 

3. The stadium decrementi follows, but this stage is longer in pro- 
portion as the case is mild. From its complications (v. i.) it is the 
most dangerous stage. 

Course. — The incubation lasts one week; the catarrhal stage one to 
two, the spasmodic, three to six, and the decline, three weeks. 



108 BACTERIAL DISEASES 

Complications. — 1. Increase or Extension of the Usual Symptoms. 
— Catarrhal inflammation is common in the initial stage — stomatitis, 
laryngitis, diarrhea (10 per cent.) and otitis media (10 per cent.). Bron- 
chitis (bronchiolitis) is not common in the spasmodic stage. It may 
occur with fever, a pulse of 120 to 150, respirations of 30 to 50, many 
rales, cyanosis and atelectasis. Bronchopneumonia is the most frequent 
and severe complication, occurring particularly in rhachitic children 
between the third and fifth years, most often in the convulsive stage. 
The onset is gradual with fever of 100° to 102°, pulse of 130 to 160, 
respirations of 30 to 80, with cyanosis and dyspnea. The mortality 
may reach 25 per cent, and an almost absolutely bad prognosis must be 
given in the very young. Sometimes the pneumonia greatly lessens or 
entirely abolishes the spasms. Lobar pneumonia, exudative pleurisy, 
endocarditis, pericarditis, meningitis and nephritis are very infrequent. 
Spasm of the glottis in nervous or scrofulous children is largely nocturnal 
in incidence, and may cause death from asphyxia even in the lightest 
cases. Convulsions of the carpopedal type, especially in nervous chil- 
dren, are most frequent at the height of the apnea. The eyes are rolled 
upward and outward, the pupils are dilated and coma follows. 

2. Mechanical Complications. — Hemorrhages may occur into the 
skin, conjunctivae, nose, ears and throat. Valentine summarized 83 
instances of paralysis from cerebral hemorrhage. Extravasation of blood 
into the retina, lungs, stomach and intestine is rare. There may be 
edema of the eye-lids, rupture of the tympanum or frenulum of the tongue, 
the ulceration of which is almost constant. Vomiting occurs regularly, 
as a mechanical crisis to the paroxysm. Other mechanical complications 
are cardiac dilatation, pulmonary emphysema (less often interstitial than 
alveolar), bronchiectasis, pneumothorax, involuntary evacuations, pro- 
lapse of the rectum or uterus, aneurysm, muscular rupture, hernias 
and rib fracture. 

3. Toxemia. — Marked toxemia is rare. Parenchymatous degenerations 
are found in the fatal cases. Nephritis is not common. 

Sequels. — The hysterical coughing which sometimes follows pertussis 
may very closely resemble it. Tuberculosis may involve the lungs or 
lymph glands, especially after pertussis with measles, both of which 
infections predispose to tuberculosis. Preexisting tuberculosis renders 
the prognosis of whooping-cough very unfavorable. The heart-muscle 
may suffer permanent weakness. 

Diagnosis. — Diagnosis is made by (1) the definite stages of the disease; 
(2) the presence of an epidemic; (3) the characteristic convulsive seizures; 
(4) the sublingual ulceration, swollen eyelids, facial edema, petechise 
and tender areas in the larynx; (5) pressing the tongue back with a 
spoon often elicits a characteristic attack of coughing. The stridor 
may be absent in nurslings and adults. The diagnosis may be difficult 
between paroxysms in the early or late stages. Intercurrent diseases, 
like pneumonia or measles, may render pertussis atypical. 

Differentiation. — In croup there are fever, aphonia, metallic inspiration, 
lividity and constancy of the symptoms. False croup (laryngismus strid- 
ulus) beginning with acute catarrhal laryngotracheitis, occurs at night 



PERTUSSIS 109 

in healthy children. Spasmodic cough from diseased bronchial glands 
very closely resembles pertussis. Barthez and Sannee give the following 
differentiation : 

Whooping-cough vs. Enlarged Glands. 

1. Contagious, epidemic. 1. Isolated, not contagious. 

2. Three periods, second paroxysmal. 2. No distinct periods. 

3. Paroxysmal cough with whoop, vomit- 3. Paroxysms, without the whoop, expec- 

ing and viscid expectoration. toration or vomiting. 

4. Respiratory sounds normal. 4. Signs of enlarged glands sometimes 

present. 

5. Respiration normal in interval; apyrexia 5. Asthma in some cases, febrile movements, 

if simple. sweats, wasting, etc. 

6. Voice natural. 6. Sometimes a change in voice. 

7. Acute. 7. Chronic. 

Spasmus glottidis in nervous children at dentition, in rhachitis and 
tetany, is a sudden spasmodic closure of the glottis without prodromes, 
but with dyspnea, cyanosis and convulsions. Asthma periodicum (Millar's 
asthma) relates to thymic disease. Hysterical "after-pertussis" presents 
no catarrhal symptoms, fever, vomiting, sublingual ulceration, edema 
of the face, petechias or a tender point in the larynx, and other stigmata 
of hysteria (q. v.) are present. 

Prognosis. — In the United States 10,000 deaths occur each year from 
pertussis, and its death-rate almost equals that of scarlatina (per 100,000, 
diphtheria 21.4, measles 12.3, scarlatina 11.6, and pertussis 11.4). The 
mortality averages 3 per cent., but in certain epidemics reaches 15 per 
cent. The longer the time of development of the convulsive stage, the 
better is the prognosis, and the clearer are the intervals between par- 
oxysms. The outlook is more unfavorable in the poor, nurslings and 
children under five years, especially in colored children. The mortality 
of cases in the first year is about 27 per cent.; in the second year, 14; 
from the second to the fifth year, 3; from the fifth to fifteenth year, 
1.8 (Hagenbach); 90 per cent, of pertussis deaths occur betw T een one 
and two years of age. According to Trousseau, more than forty attacks 
in one day indicate a grave prognosis and over 60 attacks indicate 
a fatal outcome; the writer has seen recovery with over 100 paroxyms 
daily. Coincident measles, pneumonia or early bronchitis, weak heart, 
continued emesis, glottis spasm, eclampsia, skin emphysema, hemorrhages, 
asphyxia and tuberadosis cloud the prognosis. 

Treatment. — 1. Prophylaxis. — Isolation is indicated, particularly in 
tuberculous children. It is never advisable to expose a child to an 
epidemic. The greatest danger of infection exists during the catarrhal 
stage. The sputum, clothes, etc., should be cared for on antiseptic 
principles. It was thought that vaccination mitigated or aborted per- 
tussis, but in eleven personal un vaccinated cases, vaccinia was ineffectual. 

2. Medication. — There is no specific, as proved by the multitude 
of vaunted remedies. All drugs should be employed cautiously. Quinine 
is the foremost remedy (1| times as many grains per diem as the child 
is years old; to children under two years, | grain for each month). 
Children seldom object to its taste. 



110 BACTERIAL DISEASES 

1$ — Extr. belladonnse . . gr. iss 

Quininse sulph gr. viij 

Sacchari albi gr. xxx 

M. et divide in pulv. no. x. 

S. — One powder, three times daily (Widerhofer's formula). 

Camphor may be indicated as a stimulant in asthenia and bronchitis, 
f grain at a dose. Coal tars should not be exhibited. Bromine moderates 
the course of the disease; bromoform should be kept bottled in the dark — 
dose one to five minims. 

The catarrh may be treated with expectorants, alkaline drinks, a steam- 
ing kettle under a tent constructed over the bed, benzoic and tannic 
acids (aa gr. ij, t. i. d.). 

For the paroxysm there is no specific. Belladonna is given, one-sixth 
grain of the extract, to a child of six to eight months, until flushing is 
observed; symptomatically it is also useful for the clammy, cool skin 
and collapse; though children tolerate belladonna well, great care must 
be exercised in very young children. The same caution applies to ipecac, 
chloral and opium. 

Chloroform inhalations are dangerous. Codeine is less effective than 
morphine. Chloroform is advantageous in dry coughs (twice as many drops 
as the child is years old, in one dram of warm water). Adrenalin, Tflj-iij, 
may relieve spasmodic cough. 

1$ — Morphinse hydrochloridi gr. \ 

Sodii bromidi . . . 3 ss 

Chlorali hydrati gr. xvj 

Aqua? chloroformi . ad. gjss 

Misce, fiat mistura. 

S. — One to three teaspoonfuls for a dose, according to age. 

R— Sodii benzoatis gr. lxxij 

Sodii bicarbonatis gr. xlviij 

Aquae chloroformi 3.1 

Aquae anisi ad. §iij 

Misce, fiat mistura. 

S. — One to four teaspoonfuls, according to age, every few hours. 

Digitalis is used for right-heart dilatation. Intubation for the spasm 
of the glottis may induce ulceration from the long-continued pressure. 
Bronchopneumonia (q. v.). 

3. Hygiene and Diet. — A warm climate modifies the course and is 
prophylactic against tuberculosis. The attacks are often lessened by 
removal to the country. Irritants, as beef-tea, stimulants, dry bread, 
cookies and overfeeding, provoke coughing and vomiting. Food should 
be given at frequent intervals in concentrated form — gruels, milk with 
lime-water, zwieback in milk, eggs, meat-juice, etc. Older patients 
tolerate more solid food. Rectal feeding is sometimes advantageous. 

4. Vaccines and Serotherapy. — In reports, bacterins are claimed 
to shorten the course of the disease twelve to twenty-one days, but 
vaccines and serotherapy are still on probation. 



CHOLERA ASIATIC A 111 



CHOLERA ASIATICA. 



Definition. — An infection caused by the comma bacillus and char- 
acterized by vomiting, severe purging, cardiac failure and suppression 
of urine. 

History. — The name has been used since the time of Hippocrates, 
Galen and Celsus, but apparently not for Asiatic cholera. Asiatic 
cholera existed before Christ. Its first European invasion was in 1817, 
from which time our knowledge dates. Cholera visited America in 1832- 
1835, 1836, 1848, 1849, 1854, 1865, 1867 and 1873. Isolated cases have 
occurred since. 

Bacteriology. — Koch, studying cholera in Egypt and India in 1883- 
1884, discovered the comma bacillus in the feces during life and in the 
bowel at autopsy. It is 1 to 1.5/* long and half as wide; smaller than- the 
tubercle bacillus, but more plump and curved and is motile and flagellated. 
Gaffky (1887) first obtained pure growths. In cultures its form varies, 
being sometimes S-shaped, and thread- or spirillum-like. Pure cultures 
are grown from the stools. After several days it may be found in the 
bowel wall, though rarely in the stomach, vomitus, blood or viscera. 
It disappears from the movements after six to eleven days. 

In its dissemination, cholera resembles typhoid, i. e., infection is in- 
direct. Koch maintained that cholera was conveyed by water con- 
tamination. He found the cholera vibrios in a water-tank in Calcutta 
from which infection was clearly traced. Attendance on cholera patients 
is not dangerous if the hands are kept clean. The germ is very susceptible 
to boiling, antiseptics and drying. There is little risk of aerial dissemina- 
tion except by flies. The acid of the stomach protects the individual, 
and animals are infected experimentally only when the gastric acidity 
is neutralized and peristalsis is arrested by opium. Pettenkofer objected 
to Koch's teaching and even swallowed pure cultures, luckily escaping 
infection. Nevertheless, the terrible Hamburg epidemic (1892-1894) 
amounted, as Koch said, to a demonstration of almost laboratory exact- 
ness. The disease developed "explosively." On August 16 there was 
1 case; by August 27 there were 1000 deaths, and September 3, there 
were 10,000 cases and 4300 deaths. The total mortality was over 8300. 
The Hamburg drinking water came unfiltered from the Elbe River, 
which was then at a low level. The germ was found in this supply. 
Altona and Wandsbeck, parts of Hamburg, had a supply of good water 
and escaped. The germ is difficult to find in water because it is so easily 
overgrown by saprophytes. 

Infection by ice, milk, lettuce, flies, the washing of infected linen or 
in the laboratory is less common. In India, hundreds of thousands 
of pilgrims drink the "holy water" of the Ganges, in which they also 
bathe and defecate. Similar infections occur in the pilgrimages to Mecca. 
In former years, caravans carried infection from India through Persia 
and Afghanistan to Russia, which was the route of dissemination in 1892. 
Ships from the Orient are extremely dangerous. Carriers: In Manila 
8 per cent, of 374 healthy individuals were vibrio carriers. In the 
Italian epidemic of 1911, their officials detected 41 carriers about to 



112 BACTERIAL DISEASES 

embark for this country, and at New York the quarantine of 62 sick 
with the disease and also carriers averted an epidemic and its attendant 
panic. 

Decreased physiological resistance, alcoholism, purgation, dyspepsia, 
overexertion, poor hygienic conditions and debilitating diseases are 
predisposing factors. Counting the mortality in a cholera-stricken com- 
munity for a few years, the total death-rate is not increased, which 
indicates that weakly persons succumb to cholera and that later epi- 
demics of other diseases have fewer victims. 

Epidemics end with a lessening mortality; their ending and lessened 
mortality are explained by the decreasing virulence of the germ. Warm 
weather increases and frost usually checks epidemics; nevertheless, 
Russia's severest epidemic occurred in the winter. 

Symptoms. — After an incubation of two or three days, the disease 
develops; several stages are described, which also correspond to clinical 
types of varying virulence. 

1. Prodromal Diarrhea. — The thin stools contain the comma 
bacillus, are voided without pain and sometimes produce only moderate 
malaise. The trouble may cease here, when we speak of cholera diarrhea, 
or it may pass into the choleraic stage. 

2. Choleraic Stage. — The stools, at first yellow and voided fre- 
quently, become colorless because the bile pigment is diluted and de- 
creased, and become thin — the ominous "rice-water'' stools. The stools 
may number twenty or thirty, aggregating a pint to five quarts daily. 
They have a fetid, not a fecal odor, and contain flocculi of comma bacilli, 
leukocytes, epithelial cells, detritus and a few red cells. There is often 
gurgling, although little gas is voided. The fluid thus lost to the circula- 
tion, causes some of the following symptoms: The abdomen is flat, 
usually neither tender nor painful, and fluid may be percussed in the 
bowels. Vomiting is frequent, painless, although exhausting, thin and 
profuse, even to three quarts daily; sometimes Koch's bacillus is found. 
The skin shows the lack of fluid; it becomes shrunken, wrinkled and when 
pinched, its folds disappear but slowly. The nose becomes small and 
pointed, and the malar bones jut out prominently; the extremities, 
nose and ears become cold and cyanotic, and grayish-blue rings develop 
beneath the sunken eyes (fades cholerica). If pleurisy or dropsy is 
present, it is rapidly absorbed. The saliva and urine decrease or disappear. 
The loss of fluid occasions distressing thirst and muscle cramps, especially 
in the calves and other muscles, which are found dry at autopsy. The 
immense transudation into the bowel concentrates the blood, whose red 
cells may total six to eight millions and the serum has a specific gravity 
of 1.040, even 1.070 (1.028 being the normal). The heart tones become 
weak and the pulse rises to 100, because the body cannot lose 10 per cent, 
of its fluid without injury. The heart has not enough blood upon which 
to contract and the blood is viscid; the heart also degenerates from 
absorption of soluble toxins from the bacilli. The difficulty in oxygenation 
increases the respirations to thirty or forty, and occasions precordial and 
epigastric anxiety. The vox cholerica is due to the dry larynx and weak 
muscles, The reflexes are decreased or abolished, the pupils tardy; 



CHOLERA ASIATIC A 113 

the sensorium is normal, although exhaustion and apathy are usual. 
The urine contains albumin and hyaline casts. While the extremities 
are colder by .5° to 10° or more, the patient feels hot; and the rectal tem- 
perature may be 102° or higher. The loss of weight is great (even 1 
per cent, hourly) . In some cases the patient dies before diarrhea develops 
{cholera sicca). Recovery is possible, even with these ominous symptoms; 
the diarrhea and algidity may lessen, the heart may improve and ery- 
thematous, roseolous and urticarial rashes may develop; indican, pre- 
viously absent from the urine, may reappear; the urea and ethereal 
sulphates are increased. The later symptoms probably result from 
acidosis or absorption of toxins from the intestine (the so-called cholera 
typhoid) . 

3. Stage of Collapse. — This stage is characterized by asphyxia 
(literally, without pulse), algidity or collapse. The heart tones are inaud- 
ible, the pulse imperceptible, the arteries empty. In the days of vene- 
section the blood would not drain from the incised veins, and at autopsy 
little or no blood escapes from the vessels. The skin is lead-colored, 
cyanotic, even purple. There is dyspnea, the expired air is cool, the 
voice gone, the mouth dry, the conjunctivae opaque, and the lids are 
parted, yet the mind is clear. The evacuations cease. Pericardial or 
pleural rubs may be heard, due to the great viscidity found in all the 
serosse at necropsy. Very few patients with cholera-typhoid recover; 
most die within a few hours, or a day. After death the muscles contract, 
to the great terror of observers; the face is distorted,, the fingers flexed 
and the legs drawn up. At autopsy the small intestines are injected, 
filled with rice-water contents, their epithelium and villi are desqua- 
mated. Comma bacilli are found in the stools and intestinal wall. 
The muscles are dry and the kidneys show a pale cortex with great 
cortical degeneration, especially in the convoluted tubules, from 
toxemia. 

Complications. — Due to the pyogenic cocci, diphtheroid changes may 
be found in the bowel, uterus, vagina and throat. Small hemorrhages 
from mucous or serous surfaces may occur. Pneumonia (20 per cent, 
of fatal cases), pleurisy or lung infarct; skin, parotid or other suppura- 
tions; icterus, bronchitis, venous thrombosis or postfebrile psychoses, 
are uncommon. Griesinger's "cholera-typhoid" is the most frequent 
sequel (25 per cent, of cases); acidosis, nervous complications and 
uremia are far less common causes than toxemia operating on the ex- 
hausted and anemic brain. 

Diagnosis. — The first cases occasion the most difficulty, especially if 
they are light. Robust individuals may not react to the germs found 
in their stools; simple diarrhea may result in other cases, and a mild 
depression only may mark cholerine. On the other hand, aged or weakly 
persons may succumb before its characteristic stages develop. In sus- 
picious cases, laboratory measures are necessary for diagnosis. The 
pseudocholera vibrios in the Elbe, Seine or Danube Canal (Vienna) are 
differentiated with difficulty. 

Cholera nostras produces a similar, though less severe picture. In 
some few cases the Finckler-Prior bacillus is found, but in the majority 



114 BACTERIAL DISEASES 

other microbes are present, such as the colon bacillus, and less often the 
streptococcus, staphylococcus and a bacillus like the Bacillus subtilis; 
vibrios, proteus and pyocyaneus forms; the dysentery bacillus; Gartner's 
Bacillus enteritidis; in meat, the paratyphoid and anaerobic forms; 
and in mollusks, Zieber's Bacillus piscicidus agilis. Cholera nostras 
bears the same relation to cholera Asiatica as varicella does to variola 
or German measles to measles. 

Arsenical poisoning, peritonitis, and intussusception, without bacter- 
iological confirmation may closely resemble cholera. 

Prognosis. — Cholera ranks next after the plague in death-rate, and 
averages 60 per cent., and sometimes 80 per cent.; 100,000 to 700,000 
die yearly in India. About 45 per cent, of deaths occur in the first twenty- 
four hours and 17 per cent, in forty-eight hours, whence the prognosis 
is more favorable after the second day; when the stage of collapse is 
reached 85 per cent. die. 

Treatment. — 1. Prophylaxis. — Isolation of early cases, disinfection 
of the stools, soiled linen, etc., and special attention to light cases and 
any suspicious diarrhea are most important. In convalescence the stools 
may remain infective for seven weeks. Despite the sudden outbreaks 
in Germany in 1892-1894, sanitary measures kept the total of deaths 
at 10,000, while in Russia 800,000 died in the same period. Individual 
prophylaxis concerns the maintenance of physiological resistance; moder- 
ation in eating; boiling of drinking water and milk; care in regard to 
ice; avoidance of green fruits and vegetables, and contamination of food 
by flies. In quarantine, the stools of all aboard suspected vessels should 
be examined, to detect carriers. In one series the prophylactic serum 
of Ferran and Haffkine reduced the morbidity two-thirds and the mor- 
tality one-half. 

2. Diarrhea. — Absolute rest in bed, an initial cleansing of the bowels 
with calomel and castor oil; thin gruels; red wine, aromatics, tea and 
full doses of bismuth, and morphine, hypodermically, should be given. 
Intestinal antiseptics are inert. The diarrhea, except the early move- 
ments, is not easily stopped, because absorption is arrested. Cantani 
advised that 1 or 2 quarts of 1 per cent, tannic acid solution be 
given slowly by rectum in the hope that it would reach the small 
intestine. 

3. Vomiting. — Vomiting is intractable. Fluids should not be with- 
held. The stomach may be washed with normal salt solution. Hot 
wine, champagne, and hypodermics of morphine are indicated. 

4. Heart. — Failing heart action and renal secretion are sometimes 
helped by a warm bath. Hypodermoclysis and intravenous transfusions 
were studied during the Hamburg epidemic and their employment often 
greatly benefited the heart and the general condition. 

5. Muscular cramps are helped by warm baths, friction, local heat, 
saline infusions and morphine hypodermically. In convalescence, great 
care is necessary lest the diarrhea return. Other symptoms and sequels 
are treated expectantly. 



THE PLAGUE 115 



THE PLAGUE. 



Definition. — The pest, or bubonic plague, is a specific acute infection 
caused by the Bacillus pestis and characterized by a pronounced typhoid 
state, fever, buboes and carbuncles, very frequently by pesticemia, and 
by extremely high mortality. 

History. — The first clear account dates from the times of Trajan, 
in the second century, and of Justinian, in the year 542. In the four- 
teenth century the "black death" swept over Europe with a mortality 
of 25,000,000 (one-quarter of the world's population). It reappeared 
in the sixteenth and seventeenth centuries, but in the eighteenth century 
it withdrew southeast and disappeared from Europe until the small 
Russian epidemic in 1878-1879. Egypt was the early focus for African 
epidemics, and European epidemics started from Syria, the leading 
Asiatic focus for thirteen epidemics (1773-1843). The present Oriental 
focus is Thibet, whence India and China have been invaded thirty 
times between 1823 and 1897. Uganda is considered a permanent 
plague home by Koch; plague is endemic in Asia near Mecca, in Mesopo- 
tamia and in Siberia. In 1899-1900, New York, San Francisco, Cape 
Town, South America and Australia were visited; in 1906 England, 
and in 1912 Cuba and Porto Rico; 4500 died in Manchuria in 1910-11. 
Plague appeared in New Orleans in 1914. 

Etiology. — The Bacillus pestis was found by Yersin in 1894, and 
independently by Kitasato. Its ends are rounded and stain deeply; 
its sides are somewhat convex; it measures 1J to If by f to f ix and is 
encapsulated. It is polymorphous, and appears as rods or diplo-bacilli. 
Atypical forms are ovoid, annular, chain-, thread-, or branch-like; 
involution forms are the pyriform, biscuit, comma-shaped, or sperma- 
tozoid. It contains no spores or flagella. It is found in all organs, in the 
sputum, the urine and feces, and in the bubo and carbuncles. Its 
cultures are typical and superficial, and have bulging, wall-like edges. 
It stains with ordinary stains, but not by Gram's method. 

Atrium. — It may enter (1) by the skin, through invisible wounds, 
scratches or the intact integument. Postmortem and laboratory inocula- 
tion is possible, as in the unfortunate case of Miiller, of Vienna, while 
writing his well-known monograph. Flies, fleas, bed-bugs, etc., may 
inoculate the disease. (2) The mucosa?, conjunctiva?, nose, tonsils, anus 
and external genitalia, may be primarily infected, especially the nose 
and throat in children. (3) The bacillus may cause primary plague 
pneumonia. 

Contagion may be direct or indirect, (a) Direct: Dissemination of 
plague pneumonia by the sputum is most dangerous (v. Flugge's experi- 
ments in tuberculosis). The pest spreads rapidly only when it is of the 
pneumonic type. The bacilli escape from ruptured carbuncles or buboes. 
The urine, the feces and the milk of nursing women are also dangerous. 
Direct contagion may result from autopsies or operations. (b) Indirect: 
This may result from fomites, or bites of animals or insects containing 
the germ. Epidemics among rats precede human epidemics. In Canton 



116 BACTERIAL DISEASES 

35,000 dead rats were found in one district. The disease also exists 
among apes, cats, mice, ground-squirrels, which latter made California 
a permanent pest focus, and marmots (Manchurian epidemic) . Infection 
by rat-fleas is clearly proved. Flies may convey infection from the 
urine or feces of infected rats. The bacillus produces virulent toxins. 

Symptoms. — There are two factors in the clinical picture: (a) The 
local changes, as the primary localization (bubo or pneumonia), and 
(6) the successive septicemia (pesticemia) and toxemia. The average 
incubation is five days. Usually the onset is very acute, with marked 
headache, intense vertigo, severe rigor, sudden fever, vomiting and, 
in children convulsions. There is early glandular pain, profound pros- 
tration, and an early typhoid state. The fever reaches 104° on the second 
day, is continuous or remittent, in convalescing cases falls by lysis 
(fifth to seventh day), or may remain high until death. Crisis is seen 
in light cases only. The skin is hot and dry or covered with sweat as 
death approaches. Skin hemorrhages, due to embolism by the Bacillus 
pestis are frequent before death. Herpes never develops. 

1. Local Lesion. — This is the bubo. The lymph glands are more 
important than in any other infection. The clinical forms of the plague 
are (a) the bubonic type (77.7 per cent.); (6) the septicemic type (14 per 
cent.); (c) the pulmonary type (4.3 per cent.); (d) the carbuncle type 
(2.5 per cent.); (e) mixed infection (1 per cent.); and (f) the ambulatory 
type (pestis minor, 0.5 per cent.), which is considered by Scheube as not 
plague but "climatic bubo." In all except the pulmonary type, the bubo 
is found very early (95 per cent.) ; it occurs in the external lymph glands 
in the region of the atrium; it is large, very painful and tender, and is 
attended by great periadenitis, edema, hemorrhage and vesiculation of 
the skin. Its size and rapid growth are due in part to lymph-medullary 
swelling, but chiefly to hemorrhage, which may spread along the nerves 
or vessels, into which it may break, disseminating the bacilli. The glands 
may fuse into a brawny mass, as large as an egg or a man's fist; they 
and the surrounding tissues contain enormous numbers of bacilli. The 
location is inguinal (70 per cent.), axillary (20 per cent.) and cervical 
(10 per cent.). The inguinal and axillary adenitis is more common in 
males; cervical adenitis results in children from infection of nose and 
throat by dirty fingers; the popliteal and epitrochlear glands, curiously, 
are involved in but 1 or 2 per cent. Strangely, too, the lymph vessels 
are usually unaffected. From the primary bubo the contiguous glands 
are involved, e. g., after the infection of the inguinal glands, the iliac, 
aortic, mediastinal, subpectoral, infra- and supraclavicular or cervical 
glands may be involved, i. e., infection occurs in the direction of the 
lymph current. On the fourth to the sixth day necrosis occurs, and on 
the eighth or ninth day suppuration develops, resulting more often 
from the Bacillus pestis alone (66 per cent.) than mixed infection (33 
per cent.). The primary bubo is often inconspicuous and its size has no 
bearing on the intensity of the disease, yet subjects with marked peri- 
adenitis rarely recover. The bacilli in the blood have a remarkable 
affinity for lymphatic structures ; these hematogenous buboes are smaller, 
less tender, painful, edematous and hemorrhagic, than the primary 



THE PLAGUE 117 

bubo. The mesenteric glands, the pharyngeal follicles, stomach, intestine 
and lung contain bacilli in large numbers. Carbuncles result chiefly 
from pesticemia and occur in 10 to 15 per cent, of cases, often near the 
primary bubo; the crowning serous vesicle ruptures, discharges bacilli 
and leaves an ulcer, whose floor is bluish-red from hemorrhage or yellow 
from swarms of bacilli. A dark crust then forms. There is great per- 
ipheral infiltration and the whole limb may become edematous. These 
lesions indicate that the pesticemia is an integral part of the disease. 
The blood shows polymorphonuclear leukocytosis. The spleen is enlarged 
threefold. Its cut surface is finely granular and slightly glistening. 
It is infiltrated with white cells and bacilli, found in innumerable foci 
of minute necrosis. It is usually palpable on the first or second day. 

2. Nervous System. — There are few anatomical changes except 
meningeal hemorrhages and brain edema. Clinically the toxemic "ty- 
phoid" symptoms are prominent — early headache, marked prostration 
and vertigo, causing a drunken, cerebellar gait. The delirium is most 
often dull, dreamy and docile. Twitching, rigidity of the neck and 
increased pulse and respiration, polyphagia or polydipsia, may suggest 
meningitis. Conjunctival hyperemia, sometimes with ecchymoses, is so 
frequent that Yamagiwa made it a cardinal symptom. 

3. Circulation. — Circulatory and nervous changes measure the 
intensity of infection and forecast the prognosis. There are few cardiac 
poisons as intense as the plague toxin which operates on the medulla 
and its vagus nucleus. Early the pulse is full and dicrotic, with a rate 
of 80 to 90. Later, it increases to 120 to 150; the heart tones become 
muffled; tachypnea, dyspnea and all the signs of acute cardiac insuf- 
ficiency develop. At autopsy the heart is lax, the right ventricle dilated, 
the myocardium cloudy, and the serous investments ecchymotic. 

4. Respiratory Tract. — The plague pneumonia is of two varieties: 
(a) The primary, in which the lung is the atrium (or analogue of the 
primary bubo) — the "black death" of the middle ages. It became 
well known in the Indo-Chinese epidemic of 1896-1897, when Childe 
found the Bacillus pestis in the lung. The bacillus, if inhaled, causes 
confluent lobar pneumonia and salient lymphatic involvement. The 
bacilli exist in hordes in the lung and sputum, and may cause hematog- 
enous buboes and carbuncles. The diagnosis is positive only from the 
sputum, cyanosis, dyspnea, hemoptysis, pleuritic pains, signs of con- 
solidation, adynamia, splenic tumor and collapse. Death occurs in 97 
per cent, of cases. (b) Secondary pneumonia is "(i) embolic, as multiple 
small foci and difficult to diagnosticate without bacilli in the sputum, 
(ii) Aspiration pneumonia in the lower lobes follows bubonic disease 
of the tonsil, pharynx or bronchi and is almost invariably fatal 

5. Digestive Tract. — A moist, then dry tongue, hemorrhage from 
the mouth, and involvement of the tonsils or pharynx are common. 
There may be ecchymoses and erosions in the stomach and intestines; 
bubonic changes in the lymph structures were found in 20 per cent, of 
Wilm's cases, and mesenteric adenitis in 60 per cent. Vomiting is fre- 
quent, meteorism and diarrhea occasional. The liver is swollen from 
degeneration or stasis. 



118 BACTERIAL DISEASES 

6. Genitourinary Traut. — The urine is decreased; and moderate 
albuminuria is very common. Nephritis is frequent. Anatomically, 
degeneration, minute areas of focal necrosis and glomerular hemorrhage 
from capillary embolism of the bacilli are common. Bacilluria occurs 
in about 30 per cent, of the cases. The bacilli have been found in the 
aborted fetus. 

Diagnosis. — The cardinal signs are fever, buboes, pesticemia and 
positive blood cultures, inoculation and agglutination (not well marked 
until the second week of infection, and best developed in convalescence; 
negative results do not exclude plague). 

Prognosis. — A patient, stricken in the morning, may die before night. 
If the patient outlives a week, the chances of recovery are good. Ominous 
symptoms are marked nervous and cardiac toxemia, digestive disorders, 
hemorrhages, cervical buboes, tonsillar involvement and pneumonia. 
The death-rate is often 80 and sometimes 95 per cent. In Toulon (1721), 
77 per cent, of the population had the plague and 62 per cent, died — 
higher percentages than in any other epidemic disease. Nearly 1,000,000 
die yearly in India. 

Treatment. — 1. Prophylaxis. — The plague patient should be isolated 
and carefully covered with netting. Infected houses should be isolated, 
unroofed to admit the sun and fumigated to kill insects and rats. Vigorous 
attacks should be made on rats and ground-squirrels. Ships should 
be held in quarantine until the rats in their holds are killed, the bilge- 
water disinfected, and all clothing fumigated. The sputum may be infec- 
tive for three months and the urine for six weeks. The strictest pre- 
cautions are imperative in those coming into close contact with the 
disease'; besides ordinary antisepsis, goggles and masks should be worn. 
Inoculation with dead cultures and with serum from immunized animals 
and from convalescent patients is a measure assured of success. 

2. Symptomatic Treatment. — Buboes and carbuncles are most 
efficaciously treated with weak sublimate dressings. Surgical extir- 
pation disseminates infection, and injection of carbolic acid into the 
buboes does not stay the septicemia. Digitalis, alcohol and hydrotherapy 
are employed as in other toxemias. Bichloride of mercury is well toler- 
ated and was suggested by the observation that syphilitics under mer- 
curial treatment withstood infection. 

DYSENTERY. 

Definition. — An acute contagious disease, caused chiefly by the Ameba 
dysenterise and Shiga's Bacillus dysenterise; attended anatomically by 
bowel inflammation and characterized clinically by colic, tenesmus and 
mucobloody passages. 

History. — The name dates from Hippocrates (480 B.C.), and the affec- 
tion is clearly mentioned in the oldest medical script, the Papyrus Ebers 
(1550 B.C.), and in the Veda. It has been the scourge of armies from 
the times of the Greco-Persian wars. In our Civil war there were 287,522 
cases among the Northern troops. Among the English soldiers in India 
30 per cent, of the deaths were due to dysentery. It prevailed in the 



DYSENTERY 119 

recent South African and Spanish- American wars, but was practically 
absent among the Japanese forces (1904-1905). Essentially a disease 
of the tropics and subtropics, it is frequently observed in temperate 
zones, especially in prisons and in asylums. Lack of hygiene, overcrowd- 
ing, eating of spoiled food or fruits and impure water are predisposing causes. 

Shiga's Bacillary Form, of Dysentery.— The Bacillus dysenteries was 
described by Shiga (1897), who found it in the intestinal wall; the 
bacillus and its toxins, when inoculated, produce intestinal hemorrhage. 
There is a specific agglutination, increasing in intensity under observa- 
tion and most marked in convalescents; the serum of the immunized 
cases is of prophylactic and therapeutic value. Actual inoculations of 
man produce dysentery, as in Strong's inoculation of a criminal under 
sentence of death, as well as in accidental laboratory infections. The 
bacillus resembles the colon and typhoid bacilli in form, though less 
motile than the latter, and flagellated; it is a facultative anaerobe, con- 
tains no spores, stains readily but not by Gram's method, and grows on 
all media. 1 It is suggested that the Shiga type be called dysentery and 
the Flexner-Harris type paradysentery, but the general term bacillary 
dysentery probably will prevail. The bacilli are less abundant in the 
early diarrheal stools than in the later mucobloody stools; when the 
dejecta become purulent (last stage) the bacillus disappears. It is found 
in the mesenteric glands, but rarely in the blood, spleen or liver. Infec- 
tion is probably carried by contaminated drinking water, milk and flies. 
Healthy bacilli-carriers and convalescents may convey infection. Flexner, 
Barker, Strong, Musgrave and Craig found this type in the Philippines; 
Kruse found it in Germany, Flexner, Goodliffe and others in America 
(1901). Duval, Bassett, Wollstein and other clinicians discovered it in 
infantile types. Epidemics have existed for centuries in Japan. 

Symptoms. — After an incubation of two to eight days, there is a sudden 
onset with fever, reaching 100° to 102° (even 104°), colic and diarrhea. 
The simple diarrheal stools soon show mucus, and then bloody mucus or 
pure blood, voided with severe rectal tenesmus. The passages are small, 
numbering twenty to sixty or even one hundred a day, and contain 
Shiga's bacillus. The urine is scanty. In mild cases the symptoms 
abate in two to three weeks, and the stools become purulent and contain 
few bacilli. 

The symptoms arise from local inflammation and from systemic toxemic 
reaction to solution of the bacilli themselves in the tissues; especially 
when lesions occur in the lower small intestine, the absorptive power 
of which is great, a typhoidal condition results, with coated tongue, 
nervous toxemia, weak pulse, and frequently death in the first week. 
Shiga names this form enterodysentery, as distinguished from the 

1 In gelatin it grows with deep, pin-point cultures, is brownish-yellow without lique- 
faction, and has well-marked borders; it develops best in glucose agar (grayish growth 
along the puncture, without fermentation), or in litmus milk (some slight acidification, 
followed by alkalinization and a brownish color). There are three strains of the bacillus: 
(1) The Shiga type, which attacks glucose but not other sugars; (2) Flexner-Harris type, 
which attacks glucose, mannite and dextrine but not lactose, and forms more acid; (3) 
Hiss-Russell type, which attacks glucose and mannite but not lactose or dextrine. The 
blood of a dysentery subject will agglutinate all types, but particularly the second. 



120 BACTERIAL DISEASES 

ordinary type, colodysentery. If the stools become gangrenous the 
outlook is hopeless. Ecchymoses on the chest, epigastrium and inner 
surface of the limbs are quite frequent. Emaciation is marked in acute 
and chronic forms. 

The symptoms are explained by the anatomical findings: The bacilli 
lodge largely in the small folds and large flexures of the colon and sigmoid. 
The intensely hyperemic mucosa shows various grades of inflammation — 
catarrhal, hemorrhagic, diphtheritic, necrotic or ulcerative. The rugse 
and the entire mucosa are edematous, thickened and show coagulation 
necrosis, fibrinous exudation and cellular infiltration; the submucosa 
is infiltrated; the muscularis is sometimes infiltrated and the serosa is 
ecchymotic and freshly fibrinous. In marked cases the necrotic areas 
become ulcers, in or between the follicles; they have a flat base, occupy 
chiefly the folds, usually reach only the muscularis mucosae, and in severe 
cases impart a sieve-like aspect. The -swelling may obliterate the lumen 
of the intestine. Cocci and colon bacilli infest the upper but never the 
lower layers, where we find the Bacillus dysenterise in and around the 
glands. In the virulent cases the gut becomes gangrenous. Stenosis 
may follow cicatrization of the ulcers. 

Diagnosis. — Local rectal disease (syphilis, cancer or papilloma) may 
possibly confuse. In contradistinction to amebic dysentery, it is generally 
acute; toxemic symptoms and hemorrhages are common, from involve- 
ment of the small intestine; the ulcers are flat, on the folds of the intes- 
tine and never undermined; liver abscess never occurs. Amebic dysen- 
tery is characteristically subacute or chronic; the small intestine less 
frequently suffers; liver abscess is common (20 to 33 per cent.), and 
necrosis begins in the submucosa and produces ulcers with undermined 
edges. Agglutination, similar to the Widal reaction in typhoid, occurs 
in dilutions of 1 to 20 (even 1 to 100 or 1000). It gradually increases as 
the disease progresses, as Forster noted in typhoid fever — a good prog- 
nostic. It is seen in the second week and most clearly in convalescence, 
and therefore late for diagnostic purposes. 

Prognosis. — The prognosis is more favorable in involvement of the 
rectum and sigmoid flexure than when the upper colon or cecum is affected. 
The outlook is grave in patients under five or over fifty years of age. 
Intoxication is a bad prognostic. The effect of serotherapy is' another 
factor (v. i.). The mortality is high, particularly in Japan, ranging from 
20 to 25 per cent. No immunity is conferred. A second attack was 
observed in 2.7 per cent., and a third in 0.3 per cent, in Ogata's collection 
of 25,279 cases. 

Amebic Dysentery. — Lambl (1859) and Losch (1876) discovered an 
ameba in the bowel movements. Kartulis, in Egypt, found the ameba 
in over 500 cases and in the secondary liver abscess; (a) it was constant 
in certain forms of dysentery, in the ulcers, feces and liver abscesses; (6) 
it was inoculable in cats; (c) negative results were obtained with the 
ameba found in normal feces. The home of amebic dysentery is the 
tropics, especially in Egypt, India, Formosa, China, Arabia and Italy. 
Sporadic cases occur in the temperate zone, especially in German}' and 
America, where it is the most frequent form. The author has seen sixteen 



DYSENTERY 



121 



cases, clearly acquired in Chicago. In the Philippines it constituted 67 
to 80 per cent, of Strong's series. The ameba is found in the pus, glairy 
mucus or blood-tinged mucus of the evacuations; introducing a rectal 
tube, the fecal matter in its eyelets shows the ameba. It is round in the 
quiescent stage or irregular from protrusion of pseudopodia, when the 
slide is slightly warmed; for diagnosis it must be motile. It is uni- 
cellular, and measures 10 to 50/x. Schaudinn distinguishes the innocuous 
Entameba coli from the pathogenic Entameba histolytica (Ameba dysen- 
teric), which is larger, has a highly refractile hyaline ectoplasm (more 
clearly differentiated from the endoplasm), contains more vacuoles, 
has a sharper nucleus (5 to 7/x), and more frequent red-cell inclusions. 
Encysted amebse are resistant, dangerous forms, resembling the gametes 
of malaria (Musgrave and Clegg). It stains readily by the Wright- 
Romanowsky method and in tissues best with thionin. Wooley and Mus- 
grave obtained it in pure cultures. The ameba probably enters in the 
food or drink. Unhygienic condi- 
tions favor infection. Amebic dysen- 
tery is probably perpetuated by 
"carriers/" who have had the disease 
or carry the parasites without react- 
ing to them. Intestinal amebiasis 
(Musgrave) occurs largely in males 
in the third or fourth decade. 




Fig. 12. — Amebse (Hallopeau). 



Symptoms. — The symptoms of acute 
amebic dysentery begin abruptly 
with much the same picture as in 
Shiga's type, although the fever is 
lower and rarely lasts over two or 
three days. The movements are pul- 
taceous, fluid and yellow at first and 
later, mucous and bloody. Some- 
times in one movement feces are voided first, followed by mucus and 
blood, or blood-tinged fluid containing amebse, glairy clumps like swollen 
sago or frog spawn, pus cells and detritus. The stools may be chocolate- 
colored, or masses of necrotic tissue are voided. The stools number 5 
to 20 or more daily; their odor is fetid when feces are present; they are 
odorless when only blood or mucus is present; and are stinking when 
gangrene occurs. The repeated and painful movements cause straining, 
sweating and sometimes syncope. Colic and borborygmus are present; 
pain is referred to the navel; tenderness is marked over the sigmoid, 
colon and frequently over the cecum, and tenesmus and a burning anal 
pain mark involvement of the lower bowel, though less than in Shiga's 
type. The rectum may prolapse and vesical strangury appear. The 
abdomen is sometimes distended. Very light cases show only catarrhal 
movements, but blood, pus, membrane or shreds indicate necrosis and 
ulceration; strong men may be ill for months or even die before the 
malady is suspected. Constipation was noted by Musgrave in 50 patients, 
the autopsy showing incipient ulceration or extensive destruction of the 
colon mucosa; abdominal aching, flatulency, loss of weight and sweating 



122 BACTERIAL DISEASES 

characterized these cases. Severe cases may begin with chills, fever of 
103° or 104°, vomiting, herpes and symptoms like those of cholera; 
e. g., 20 to 100 movements daily, leg cramps, scanty urine, failing pulse 
and rapid emaciation. Peracute cases, with chill, high fever, great abdomi- 
nal pain, collapse, and even sudden death, exceptionally result from rapid 
necrosis or gangrene. The average course is one and a half to three 
weeks. Perforative peritonitis (in 19 per cent.), or exhausting hemor- 
rhages sometimes occur. * Neglected cases easily become severe or 
chronic; spontaneous recovery is uncommon. 

Chronic amebic dysentery results from the acute form or is subchronic 
from the beginning. The symptoms are the same but less intense. 
Some patients maintain their weight and suffer only from recurrent 
diarrhea every few weeks, or from irregular moderate intestinal derange- 
ment. In the average case the tongue is lacquered and red, the abdomen 
is somewhat distended and tender and the lower colon and sigmoid are 
palpable as a thick cord. The outcome is (1) recovery after two to four 
months; severe infections generally leave intestinal cicatrices or chronic 
catarrh; after a year's illness recovery is seldom complete; (2) recurrent 
attacks for months or years, constipation alternating with diarrhea; (3) 
complications, such as liver abscess (q. v.) in 20 to 33 per cent. Strong 
reports 10 cases of profuse fatal enterorrhagia coincident with liver 
abscess. Perforative peritonitis, brain or splenic abscess, arthritis, 
myelitis, neuritis and less frequently, endocarditis or chronic nephritis 
are other complications; (4) gradually increasing anemia, marked or 
extreme emaciation and death from exhaustion. 

Pathology. — The early changes in the mucosa are catarrh, inflammatory 
injection, swelling and hemorrhage, mostly in the large intestine. The 
essential change is in the submucosa (John Hunter, Councilman and 
Lafleur). The amebse enter by the tubular glands or sometimes the 
bloodvessels, and reach the submucosa where they cause fibrinous exuda- 
tion and cellular accumulations which are not leukocytes, but connective- 
tissue cells. These foci undergo coagulation necrosis and the mucosa 
which at first covers the small submucous cavities, afterward sloughs, and 
exposes the primary grayish-yellow necrosis. When the necrotic tissue 
sloughs out, the dysenteric ulcers are more apparent. They lie in the 
whole of the large intestine (50 per cent, of cases) ; in the colon descendens 
and sigmoid (25 per cent.); in the cecum, with ascending or descending 
colon, or in the rectum (25 per cent.); in the rectum alone (20 per cent.); 
in the cecum alone (5 per cent.); in the appendix (7 per cent.); ileum 
(3.5 per cent.) and the entire bowel (80 per cent.). The deep ulceration 
exceeds the superficial ulceration, and early ulcers may, by fistulous 
tracts, tunnel the apparently healthy mucous membrane; their edges 
are undermined. The ulcers may be round or serpiginous and are usually 
discrete. They may penetrate to the muscularis or perforate the serosa, 
causing diffuse or localized peritonitis. The lymphatic structures of the 
bowel are less affected than in Shiga's type. Secondary changes include 
streptococcic diphtheroid deposits, diffuse sloughing of entire blocks 
of the intestinal wall and gangrene. In chronic cases the muscularis 
frequently thickens and narrows the lumen. Healing ulcers produce 



DYSENTERY 123 

pigmented stellate scars which sometimes cause stenosis. Amebse may 
enter the mesenteric bloodvessels, by which they reach the portal circula- 
tion (pylephlebitis; liver abscess). The liver shows toxemic focal necroses, 
and, in a large percentage, abscesses; the solitary, large abscess generally 
develops in the right lobe near the diaphragm or colon. The multiple 
small abscesses are also superficial. In both types there is central necrosis, 
the contents are yellow, green or chocolate-colored, contain fat droplets, 
liver detritus and the amebse on the abscess walls. In older cases there 
is a firm connective r tissue capsule, but round-cell infiltration is as infre- 
quent as in the intestine. Amebse may be found in the sputum when the 
abscess ruptures into the lung. The mortality averages 6 per cent.; 7 
per cent, of deaths in Cairo are dysenteric. 

Indeterminate Dysenteries. — Of these forms, some are primary and 
others secondary infections (colon bacillus, proteus, pyocyaneus, pneumo-, 
strepto- and staphylococcus). Varieties: (a) Catarrhal dysentery, in 
which the mucosa is injected, cloudy and infiltrated; the solitary follicles 
are swollen and become round, deep and small ulcers — the "acute fol- 
licular colitis" seen especially in children. The symptoms are mild pain 
and mucobloody evacuations. (6) The croupous or diphtheroid dysen- 
tery represents a severer stage or degree. The epithelium necroses, the 
submucosa is infiltrated, and there are membranous deposits on the ruga? 
over slight superficial ulcerations, or there may be deeper, wider ulcers 
with great thickening of all the intestinal layers. This may occur (i) 
as a primary infection, with dysenteric symptoms, marked typhoidal 
symptoms, fever and chill, and frequently with a fatal outcome; or (ii) 
as a secondary incident in pneumonia particularly, typhoid, scarlatina, 
diphtheria, syphilis, cardiac affections, cachectic conditions, mercurial 
or other poisonings, uremia, etc.; there may be symptoms of clinical 
latency, (c) Gangrenous dysentery results in enormous swelling, soften- 
ing, and sloughing of dark, gangrenous shreds, and sometimes in tubular 
sloughs of the larger part of the intestinal circumference. Perforation 
sometimes occurs. In the Cochin-China endemic form, enlarged glands, 
splenic tumor and intumescence of the liver are found. Coprostasis, 
foreign bodies and parasites are promoting factors, e. g., the cercomonas, 
Trichocephalus dispar, Anguillula stercoralis or Distoma hematobium, 
causing dysentery, bloody urine and strangury, hypertrophy of the 
mucosa and ulceration. 

Treatment of all Forms. — 1. Specific Treatment. — Shiga's bactericidal 
and antitoxic serum reduces the mortality from 35 to 9 per cent., and 
shortens the course; in mild cases 5iiss are injected once; in medium 
cases 3 iiss twice, and in severe cases 5 v daily for three days. The best 
results attend early injection. As Shiga states, specific treatment is 
more potent in reducing the mortality of the disease than in its prophyl- 
axis. Shiga's serum does not help the Flexner-Harris type, nor conversely. 
Vaccines are uncertain, but apparently have checked institutional out- 
breaks. 

2. Prophylaxis. — Drinking water should be boiled, and fruits and 
vegetables should be cooked. In the tropics, sudden variations of tem- 
perature are to be avoided. "Carriers" require consideration. 



124 BACTERIAL DISEASES 

3. Diet. — Acute and chronic cases must be kept in bed. Boiled milk, 
raw or slightly cooked eggs, or the whites of eggs beaten with water are 
given to relieve colic and tenesmus. Lactose may benefit (Kendall). 
Broths and cold drinks excite peristalsis. Some lemonade is permissible. 
In convalescent, acute or in chronic cases, solids should be given late, 
commencing with well-cooked, tender meat and starches, and avoiding 
vegetables and fruit until convalescence is absolutely established. 

4. Eliminative Treatment. — Sodium sulphate is given in early 
cases to cleanse the bowel and to minimize the danger of ascent of the 
virus from the lower intestine (5j every two hours until the bowel is 
emptied). Aromatic sulphuric acid, Tfl.xx p. c, is sometimes given after 
the saline treatment. Castor oil or calomel, in frequent and small doses, 
is of little use except in the early stages. 

5. Antisepsis. — Beta-naphtol and phenylis salicylas, aa gr. x, q. i. d., 
probably do not reach the larger intestine. 

6. Ipecac was introduced from Brazil, by Piso, in 1648, and is con- 
sidered almost specific in India and Brazil. It reduced the mortality from 
11 to 5 per cent, in Frayer's series; food is withheld for five hours, and 
then a hypodermic of morphine, or opium by mouth, is administered 
to quiet the stomach and lessen nausea; 15 grains of powdered ipecac 
are administered 'every hour for two or three doses. If the first dose is 
vomited, the opium and ipecac are given again. Given in salol- or kera- 
tin-coated pills, ipecac passes the stomach and does not induce vomiting, 
whence morphine or opium can be omitted. Vedder's experiments and 
Roger's clinical results have revived the use of ipecac in the form of 
emetin hydrochloride, given once or twice daily, by mouth or hypodermic- 
ally (gr. | in 30 drops of water; f gr. equals 5j of ipecac). 

7. Pain. — Opium quiets the patient, enforces rest and decreases 
tenesmus and peristalsis. It is given most efficaciously by rectum in a 
suppository, or by enema, mixing Tr. opii deodorat. Tfl,xx with an ounce 
of starch water. 

8. Local Measures. — Bismuth by mouth is local in its action; doses 
of 3j~ij are necessary, and even two ounces daily are given. It may 
cake in the ulcers; bismuth poisoning (from liberated nitrous oxide or 
arsenical contamination) is avoided by using the subcarbonate. Lavage 
is difficult because of the tenesmus, and is not without danger in copious 
irrigations. The rectal tube must be introduced carefully as the rectum 
is very sensitive, first using cocaine, opium or iodoform (5-grain) 
suppository. 

1$ — Ac. tannici ' . gr. xv 

Extr. opii gr. iv 

Extr. belladonna? gr. j 

Olei theobromatis q. s. 

M. et ft. suppos. no. iv. 

Bellei employs as an antiseptic and anesthetic douche, carbolic acid 
TTlxx, tannin 5 j, marshmallow root 5 ij to a quart of warm water. Thymol 
is Musgrave's main reliance. Among the other solutions of value are 
quinine, of which Strong advises two quarts of a 1 to 3000 solution, the 
bag being three to four feet higher than the bed and the flow being slow. 



MALTA FEVER 125 

A weak peroxide solution for the amebic variety is recommended by 
Harris; all enemata should be warm. Strong silver solutions (1 to 500 
or less) cause great pain, and weak dilutions are inert; silver, however, 
is most suitable for chronic cases. 

9. Turpentine Emulsion may be used for tympanites, and Leiter's 
coil with opium may be used for hemorrhage. 

10. Colostomy. — In chronic cases colostomy has been advocated, 
and recently, wide-open cecostomy (A. B. Herrick). 

MALTA FEVER. 

Definition. — A specific infection, caused by the Micrococcus melitensis, 
somewhat resembling typhoid, but characterized by a longer course, 
by recurrent fever, severe sweats, splenic tumor, constipation, orchitis, 
and rheumatoid or neuralgic pains. 

History. — It was first described as a separate disease by Marston 
(1858). Marston, Bruce and Hughes, English army surgeons, are the 
largest contributors to our knowledge of Malta fever. Its distribution 
is well covered by its names — Mediterranean, Rock or Gibraltar fever, 
Malta fever, Neapolitan or Levant fever. It is also seen on the Danube, 
Red Sea, Bosphorus; in China, India, the Philippines; in the Canaries, 
Azores and Antilles; in Venezuela (Caracas fever), Brazil and South 
Africa. About a dozen cases have come to this country; H. H. Smith 
reports one from Boston and Gentry and Ferenbaugh 7 cases in Texas. 

Etiology. — The Micrococcus melitensis (Bruce, 1887) is round or oval, 
measures 0.3^, often occurs in chains, is non-motile and stains with 
methylene blue or gentian violet, but not by Gram's method. Cultures 
on slightly acid beef-water, peptone and agar, grow characteristically as 
small pearl-like spots; these after a few weeks become yellowish-brown. 
The bacillus is found in the blood, milk, feces and urine (even two years 
after recovery), and in the liver and spleen. Inoculated apes show a 
typical clinical course and postmortem findings. The disease prevails 
chiefly between the sixth and thirtieth years, in the hot, dry weather 
from May to mid-October, and in old unhygienic buildings. The atrium 
is the lungs (dust), or alimentary tract (food or water). In Strong's 
laboratory infection, the conjunctiva was the point of entrance. It is 
not directly contagious. Mosquitoes and goats convey infection; the 
organism is found in the blood of goats in 50 per cent, and in their milk 
in 20 per cent. In the Texas cases infection came from goats, 34 per 
cent, of which gave a positive agglutination test (v. i.); in 1905 the 
Government imported Malta goats, in which the micrococcus was 
found. 

Symptoms. — Septicemic symptoms appear after an incubation of six 
to ten days. Some symptoms so resemble those of typhoid and malaria 
that the three diseases were formerly confounded. The fever rises grad- 
ually to 104° or 105°. The face is red, there are chilly sensations, frontal 
headache, depression, and pains in the back and legs. The tongue is 
coated, at first moist, and then dry and fissured. The tonsils are fre- 
quently swollen, and the pharynx is red or ulcerated. Anorexia, nausea, 



126 BACTERIAL DISEASES 

epigastric pain and tenderness and constipation, are the rule; vomiting, 
icterus, meteorism and diarrhea, with dark, malodorous, mucous and 
even bloody stools are sometimes seen. Bruce denies that there are any 
anatomical findings in the intestines. There is considerable bronchitis 
and the sputum is often streaked with blood. Dyspnea is quite frequent. 
The pulse-rate, at first between 80 and 90, becomes faster later. Severe, 
repeated sweats occur, usually after midnight, accompanied by sudamina 
(febris sudoralis). An acute splenic tumor and hepatic intumescence 
are due to degeneration and infiltration by round cells. 

After one to three weeks, the continuous fever remits, and convales- 
cence is apparently established; but the symptoms again return, fre- 
quently several times. The fever curve shows waves accompanying each 
relapse (literally "undulant fever"). The patient becomes emaciated 
and pallid. There is no leukocytosis and micrococci are found in the 
blood in 60 per cent, of cases. 

Complications. — Pseudorheumatism (in 50 per cent, of cases) is accom- 
panied by redness, swelling and pain in the joints and sometimes in the 
bursse, periosteum and fibrous tissues. Neuralgias are common. Orchitis 
and epididymitis are usually painless, unilateral and ephemeral. Occa- 
sionally polyneuritis or psychoses are sequels. 

Erythematous or hemorrhagic skin eruptions occur in the relapses, 
sometimes accompanied by hemorrhages from the nose, tongue, gums 
or lungs; desquamation and falling of the hair or a reddish or violet 
circumscribed edema of the feet and ankles are common. In convales- 
cence, tuberculosis not infrequently develops. 

Course and Prognosis. — The majority of cases relapse after three weeks. 
The average duration of the disease is 120 days; Bruce records a case 
which lasted over two years; Melland found that 50 per cent, of cases 
in the Canary Islands lasted from two to three weeks, and in only 10 
per cent, did the protracted undulating type occur. Hughes described 
three types: (a) The undulant, the most common type; (b) the malig- 
nant, which ends in death in one to three weeks from weak heart or 
hyperpyrexia (110° or 111°); and (c) the intermittent, which lasts for 
months. The death-rate in the last century was over 3 per cent., but it 
is now under 1 per cent. One attack usually confers immunity. 

Diagnosis. — The differentiation from typhoid is often difficult. In 
Malta fever the roseolse, diazo reaction, Widal and the bacillemia are 
absent. The course is longer, the sweats more severe and the joints 
inflamed; orchitis and neuralgias develop. A positive diagnosis can be 
made by the use of Wright's serum reaction (1897), after the fifth day; 
agglutination is obtained with living or dead cultures; the dilution of 
the blood is 1 to 50, and the time limit, one hour. The severe bronchitis, 
fever and sweats may simulate tuberculosis and the older writers spoke 
of Malta fever as "Mediterranean phthisis." The bronchi are intensely 
hyperemic and the sputum is frequently blood-tinged. Malaria, ulcera- 
tive endocarditis, liver abscess, etc., are differentiated by the agglutina- 
tion test. 

Treatment. — Among English troops quartered at Malta, 2229 cases 
developed (1898-1904), with 77 deaths; in the fleet there was an equal 



ANTHRAX 127 

number. Avoidance of goat milk reduced the morbidity to 7 cases 
(1907). There is no specific treatment. Quinine and arsenic are 
ineffectual. Headache and backache are relieved by acetanilide and 
morphine; insomnia by bromides, chloral and hyoscine; diarrhea by 
tr. ferri chlor.; pseudorheumatism by heat, wool investment, tr. iodi, 
locally, and by salicylates, internally; orchitis, by local heat and suspen- 
sory elevation. The general therapy is the same as in typhoid. Dalton 
advocates a solid diet. In convalescence a change of climate is necessary. 

ANTHRAX. 

Anthrax is one of the zoonoses (diseases acquired from animals), which 
also include glanders, foot-and-mouth disease, vaccinia and hydrophobia. 
Anthrax is also called splenic fever, pustula maligna and carbunculus 
contagiosus. 

Definition. — An acute infection caused by the Bacillus anthracis, and 
usually communicated to man from the herbivora. 

History. — Over a century ago Morand and Fournier distinguished 
between the simple carbuncle and anthrax. The bacilli were seen by 
Pollander (1855) and Branell (1858), but Davaine (1864-1873) noted 
that the organisms were bacteria. It remained for Koch with his epoch- 
making technique to find the spores and absolutely differentiate the disease. 

Bacteriology. — The anthrax bacillus is the largest pathogenic microbe 
(3 to 10 by 1 to 1.5;u). In growths it occurs singly or in chains. The 
ends are slightly rounded, and the chains resemble the phalanges of the 
finger, the organisms lying end to end. They are non-motile, transparent, 
and stain by Gram's method. At high temperatures they grow in long, 
thread-like, winding, segmented filaments. Spores are absent in the 
cadaver and in the living tissues ; in the living tissues the bacilli multiply 
by -fission. In attenuated cultures, one spore develops for each bacillus; 
these become bacilli which are extremely resistant to drying and heat. 

The bacillus is an obligate aerobe. Stab cultures of agar are character- 
istic; a white, milky yet transparent and band-like growth develops 
horizontally in blood serum, and grows downward at an acute angle, 
so that in three days it resembles a quill with a feathered upper end. 
Growths on gelatin have a thick, wooly covering; the gelatin liquefies after 
a few days, and a white, granular sediment falls to the bottom of the tube. 

Anthrax is endemic and epidemic in Europe and Asia. There are 
persistent foci in Saxony, parts of Bavaria and in Frankfort; in the 
provinces of Burgundy and Auvergne; Hungary; Russia, principally 
in Siberia (the "Siberian plague") ; in China, India and in South America. 
Anthrax is rare in America, though small epidemics have appeared in 
Delaware and Pennsylvania. From Russia, infection may be dissem- 
inated by horse's hair and from Asia by mohair (Angora goats). Among 
animals, the herbivora are most often affected, especially sheep and 
cattle, and in Russia, horses. Omnivora are more susceptible than 
carnivora. Mice, guinea-pigs, rabbits, dogs and fowl rarely acquire 
the disease. Transmission of the spores by means of water, earth-worms, 
snails, flies and fleas is possible. 



128 BACTERIAL DISEASES 

Of Koranyi's cases, 65 per cent, were attributed to sheep and 35 per 
cent, to cattle; Bourgois considers that the greatest percentage comes 
from cattle, the next largest from sheep, and least from horses. 

I. External Anthrax. — External anthrax is by far the more common type. 
The atrium is an abrasion of the skin, possibly through intact hair-fol- 
licles. Koch observed that sheep were infected by fly-bites on the exposed 
skin of the neck. Shepherds, coachmen and those who attend diseased 
animals; butchers, tanners, wool-sorters and persons who handle diseased 
hides or meat; and saddlers, rag-pickers and gardeners are most likely 
to acquire the disease. Jacobi records infection from a hypodermic needle, 
first used on a patient with anthrax. The spores are more virulent than 
the bacilli. 

Site of the Pustula Maligna. — In Koch's series 51 per cent, developed 
on the head and face, 38 per cent, on the upper extremities, 2 per cent, 
on the lower, 5 per cent, on the neck, and 4 per cent, on the trunk, that 
is, exposed parts are the usual seat of primary infection. The lesion is 
usually single, but several pustules may develop, possibly from inocula- 
tion by the finger-nails in scratching. 

Symptoms. — Incubation lasts two or three days. The initial small 
red prominence resembles an insect-bite. It itches and in twelve hours 
develops a small vesicle, which becomes purulent if ruptured and dries 
with scab formation, and a dark, central, leathery slough, caused by strep- 
tococcic infection, and is surrounded by dense round-cell, and often hemor- 
rhagic infiltration. This in turn is surrounded by edema of the connec- 
tive tissue, in the deeper lymph vessels of which the Bacillus anthracis 
abounds. If the pustule extends, a circle or even concentric circles of 
new vesicles appear, which fuse and increase the infiltration. The eyes 
may be closed or the lips may be so swollen that the jaws cannot be 
opened. Demarcation now occurs, followed by sloughing, granulation 
tissue and cicatrization; or general infection develops, and the adjacent 
lymph vessels and glands become infected, soft and hemorrhagic — 
usually on the fourth to sixth day. Anthrax toxemia and bacillemia are 
marked by headache, backache, pain in the limbs, chilliness, leukocy- 
tosis, continuous or remittent fever, soft pulse, rapid breathing, vomiting 
of mucus or blood, colic, diarrhea and collapse. Hemorrhages or even 
gangrene may develop around the carbuncle. Bacilli have been found 
in the cerebrospinal fluid by lumbar puncture. The mind is usually 
clear, although delirium, convulsions or coma may develop, and death 
may occur on the seventh to ninth day with an antemortem fall of tem- 
perature. In fatal cases there is only slight rigor mortis but rapid decom- 
position, dark fluid blood, swelling of the lymphadenoid tissues (glands, 
intestine and sometimes the spleen). In the liver, kidneys, spleen, heart, 
lungs, brain and meninges, hemorrhages and swelling may be found; 
bacilli are seen less in the large vessels than in the capillaries. Bourgois 
describes another cutaneous form, most often on the body, in which 
there is great edema (charbon blanc, anthrax edema), but no pustule or 
carbuncle. 

Diagnosis. — Simple carbuncle resembles anthrax, in that it is also hard, 
has a prominent central necrosis, is surrounded by edema and sometimes 



ANTHRAX 129 

is vesiculated; it usually causes great pain, and has numerous openings 
which discharge ordinary pus. The anthrax carbuncle may be differen- 
tiated by the bacilli, depression of the necrotic centre, the corona of 
vesicles, more rapid evolution, greater edema, remarkable freedom 
from pain, and lack of odor. Glanders may be distinguished by involve- 
ment of the mucosa?, painful nodes without eschars, and ulcerations 
which discharge the Bacillus mallei. Cultures from the pustule or blood 
disclose the anthrax bacilli. 

Prognosis. — The prognosis is more favorable in children, in cases with 
local symptoms only, and those with simple carbuncle without edema. 
Even patients with bacillemia may recover. In Koch's collection, 68 
per cent, recovered. Nasarow's figures show 26 per cent, mortality when 
anthrax occurs in the head and face, 23 per cent, when it occurs in the 
trunk, 19 per cent, in the neck, 14 per cent, in the upper, and 5 per cent, 
in the lower extremity. 

Treatment. — Prophylaxis. — Infected animals should be cremated 
entirely. Industrial hair (especially when blood-stained), wool and hides 
should be thoroughly disinfected. Toussaint (1880) and later, Pasteur, 
Chauveau and Colbert used attenuated cultures to immunize animals. 
In France (1882-1893), 1,788,677 sheep were thus inoculated, with a 
resulting mortality of 0.9 per cent.; and 200,962 cattle were inoculated, 
with a 0.3 per cent, mortality. 

Active Treatment. — Wounds in those exposed to infection should 
be promptly washed with strong sublimate solution. Cauterization 
with the live cautery, carbolic or nitric acid or caustic potash; surgical 
excision through sound tissue; and injections of iodine or corrosive 
sublimate have been recommended, but equally good results are obtained 
by elevation, the use of mercurial paste, and expectant treatment, which 
at least avoids dissemination of the parasite through sound tissues. In 
1073 cases treated with Mendez's serum, the mortality was but 4 per 
cent. Salvarsan is recommended. 

II. Internal Anthrax. — Internal anthrax is less frequent. 

1. Alimentary Form. — In mycosis intestinalis, first described by Wahl 
and Recklinghausen, bacilli may enter through cuts in the mouth and 
throat, but usually directly invade the intestines and stomach, which 
are most frequently infected by spores in milk or water. The gastric 
juice kills the bacilli but not the spores, yet peasants often eat the pickled 
meat of diseased animals without being infected. In Wurzen, Saxony, 
there were 206 cases of intestinal anthrax in 1877. 

Symptoms. — The onset is usually abrupt, with fever and vomiting of 
mucus or blood, followed by pain in the bowels, serous and afterward 
bloody movements, meteorism, dyspnea, weak pulse, and by collapse, 
as seen in anthrax generalization in the cutaneous form. Secondary 
carbuncles, or more often hemorrhages into the skin of the neck and the 
abdomen, may develop. The course is severe; death results in five or 
six days, although recovery is possible. 

Diagnosis.- — Bacilli in the stools and blood determine the diagnosis. 
Changes like the cutaneous carbuncle consist of localized induration 
with central sloughing, opposite the mesenteric attachment and accom- 
9 



130 BACTERIAL DISEASES 

parried by surrounding hemorrhage and edema in the mucosa, and 
swelling of the solitary follicles, Peyer's patches, mesenteric glands and 
omentum and retroperitoneal tissue. The bacillus is found in these 
lymphadenoid structures in large numbers and sometimes in the chyle 
vessels and portal bloodvessels. The greatest changes most frequently 
occur in the upper small intestine, sometimes in the stomach or ileum, 
seldom in the colon and most rarely in the rectum. Thirty or forty foci 
may be seen in the small gut, but the lesions in the stomach or rectum 
are fewer and more discrete. Secondary embolism of the intestinal 
arteries from anthrax of the skin seldom cause hemorrhagic stools. Sero- 
hemorrhagic fluid may be found in the peritoneal cavity. Treatment 
by ipecac, calomel and bichloride of mercury is without effect. 

2. Respiratory Form. — The respiratory form was described by Bell 
(1879), in England, as the " wool-sorters' disease;" and by Eppinger 
(1894) in Austria, as the "rag-sorters' disease." Infection may, on rare 
occasions, occur in the nose, larynx, tonsils or bronchi. The bacilli are 
capable of entering the uninjured bronchioles and alveoli. Wool-sorters' 
disease results especially from infection by hides imported from Russia 
and Brazil, and, in 1897, anthrax developed in this country from hides 
of Chinese origin. 

Symptoms. — The affection begins suddenly with chill, high fever, 
tachypnea, dyspnea and bronchitic and irregular pneumonic findings; 
the viscid or hemorrhagic sputum in some instances contains the pathog- 
nomonic bacilli. The later symptoms are cyanosis caused by diffuse 
mediastinal infiltration; serous pleurisy, weak heart, vomiting, terminal 
collapse and antemortem fall of temperature. Icterus, hematuria and 
anthrax endocarditis have been observed. The sensorium is clear to the 
end in most fatal cases; convulsions and coma are due to meningeal 
hemorrhage. The patient may die on the second or third day. The 
mortality in rag-sorters' disease is 50 to 87 per cent., and rather lower 
in wool-sorters' disease. The bacilli enter the alveoli, wherein they pro- 
duce alveolar desquamation and cellulofibrinous exudation — the analogue 
of the carbuncle — and much serohemorrhagic exudate, comparable to 
the skin edema. Where there is much cellular exudate, recovery may 
result from demarcation; where there is much serous infiltration the 
bacilli are abundant and the lymph vessels infect the mediastinum, 
peribronchial glands and pleurae, which may hold quarts of anthrax- 
infected serohemorrhagic exudate. 

Treatment.— The therapy is wholly supportive. 

3. Anthrax Septicemia. — Anthrax bacillemia (septicemia) is a rare, fatal 
form, in which no atrium can be found. 

GLANDERS. 

Definition. — An acute or chronic contagion, mainly acquired from 
horses, caused by the Bacillus mallei, and characterized by nodules and 
ulcers, chiefly in the nose and skin. 

Etiology. — Glanders and farcy were known to Aristotle and Hippo- 
crates. The Bacillus mallei was discovered by Loeffler and Schuetz 



GLANDERS 131 

(1882), and independently by Bouchard, Capitau and Charrin, which 
identified glanders and farcy as one disease. Weichselbaum (1885) 
first found the bacillus in human infection. It closely resembles the 
tubercle bacillus morphologically, but is shorter and thicker and measures 
2 to 5 by 0.4 to 1.5/*; it is straight or slightly bent; its ends are some- 
what rounded; it is usually single, and not motile. It stains with the 
alkaline anilines, easily in cultures but with more difficulty in sections, 
and the bacillus tinges unevenly, with lighter areas, resembling spores. 
It is a facultative aerobe and its most characteristic growth is on potato, 
on which a thin light yellow film develops in two days, soon becomes 
amber-colored and in eight days assumes a weakly red tinge with some- 
what greenish-blue borders. The atrium is usually the skin, through 
which the bacillus enters by some small, perhaps microscopic lesion; or 
by horse-bites; infection may take place through the intact mucosa of 
the nose and air-passages, the conjunctiva, or very rarely, the digestive 
tract. Man is usually infected by chronically diseased horses; man-to- 
man infection is far less frequent. The bacillus is found in the nasal 
nodes (glanders); in the skin nodes (farcy); in the lymph vessels and 
glands (in which its virulence is greatest); in the excretions and blood 
current, where it occurs more frequently in man than in animals. 

The bacillus soon dies in pus, but may endure for three or four weeks 
in the viscera of cadavers; it is rapidly killed by sunlight. Babes (1890) 
and Kalming (1891) isolated a toxin, and Kalming, during his researches, 
succumbed to acute glanders. Hellmann (1891) isolated mallein and 
Babes (1892) morvine, both of which are successfully injected for diag- 
nosis and immunization. The horse, ass and mule are the most susceptible 
animals and from them other animals may be inoculated. In some 
localities half the horses have latent glanders (Babes). Infection is 
carried by the nasal or cutaneous discharge, whence glanders and farcy 
are chiefly observed in stable-boys, coachmen, farmers and veterinary 
surgeons. In 1909, Robin collected 156 human infections. 

Symptoms, Pathology and Course. — These are considered under two 
topics: (A) Farcy, the cutaneous type and (B) glanders, the nasal 
type. In most cases the types are not wholly distinct. 

(A) Farcy. — 1. Acute Form. — The incubation is three to five days, 
attended by depression, nausea, headache and pains. The infected 
skin shows infiltration, which may heal only to break out anew. Lym- 
phangitis and lymphadenitis are less marked than in the horse. Subcu- 
taneous and cutaneous nodes or areas of diffuse infiltration develop. 
These lymphangitic farcy-buds or areas are infective granulomata, com- 
posed of epithelioid, lymphoid and white cells, and contain the bacilli, 
which are free, rarely intracellular and most abundant in the centre 
of the nodes. Early sections are succulent and show central necrosis, 
which is followed by suppuration and ulceration. The ulcers are painful, 
deep and crater-like, with sharply cut, everted borders and speckled 
bases; they have a thin, puriform, hemorrhagic or ichorous discharge 
and they often fuse. Thrombophlebitis, diffuse phlegmons or gangrene 
may develop. The initial fever may resemble the ladder-like ascent of 
typhoid, yet chills, polyarthritis and large muscular abscesses are fre- 



132 BACTERIAL DISEASES 

quent. In some cases a successively macular, papular and pustular 
skin eruption resembles that of smallpox except that it is rarely umbili- 
cated; it may be scant and scattered, very diffuse or even confluent; 
and it may affect the mouth, throat and conjunctiva. The patient 
is often delirious, the pulse becomes rapid and small and fresh skin 
nodes develop, with ulceration or perhaps gangrene. The urine shows 
albumin, casts, or the diazo reaction, the frequent movements are offen- 
sive, and death occurs in two weeks from exhaustion or lung inflammation. 

2. Chronic farcy shows the same changes, but they are gradual in 
onset, slow in progression and unaccompanied by essential inflammatory 
reaction or lymphatic invasion. For the first month or two there are 
pains in the limbs and joints, and then indolent swellings appear in the 
extremities and in the periarticular tissues, which ulcerate. The ulcers 
may cicatrize, but break out again after months, resembling lupus, 
which heals on one side and advances on another. Muscular abscesses 
may appear, most often in the pectoralis, biceps, brachialis and gas- 
trocnemius. The course lasts for months or years (2-11). Recovery 
occurs in 50 per cent, of the cases, or death results from exhaustion and 
acute dissemination. In horses the greatly swollen lymph vessels and 
glands appear as sausage-shaped masses, whence the term "farcy" was 
used by Vegetius. In horses the skin eruptions and orchitis are more 
frequent than in man. 

(B) Glanders. — 1. The acute nasal form begins in the nose after an 
incubation of three days. Miliary nodules develop, which are elevated, 
yellowish-white in the centre, the size of a pea, surrounded by a pale 
red zone and ulcerate. New nodes form on the edges of the ulcers, which 
break down, fuse with them, and discharge a thin, puriform, dirty, 
sanguinolent fluid. Diphtheroid deposits or crusts form. Ulceration 
may erode the bone or cartilage and perforate the septum. The nose 
is swollen and eroded externally. The process reaches the mouth by 
lymphangitis or thrombophlebitis. The palate may perforate; the 
tongue, gums or tonsils are invaded; the angular lymphatic, parotid 
and submaxillary glands are swollen, and the larynx, and finally the 
lungs are infected. The leukocytes are increased. Beregin found micro- 
scopic nodes in the liver, kidney, spleen and brain; in the lungs they 
resemble miliary tubercles, or pneumonia malleosa may develop, accom- 
panied by hemorrhage, abscess formation, gangrene, a distressing cough 
and raspberry, mucopurulent sputum. Secondary suppuration in the 
bones, muscles, joints or skin complete the pyemic picture. The course 
is that of acute farcy, though more rapid, and death occurs in two weeks. 

2. Chronic Nasal Form. — This is similar to acute glanders except 
in its chronicity. It is less frequent, and when nasal involvement is 
slight it may resemble pulmonary tuberculosis, chronic coryza, pyemia 
or osteomyelitis. The malady may "slumber," to be aroused later by 
trauma or symbiosis with the staphylococcus. Death occurs from exhaus- 
tion or generalization by lymphangitis or thrombophlebitis. In Robin's 
series G per cent, recovered. 

Diagnosis of Glanders and Farcy. — Typhoid, pyemia, variola, syphilis, 
lupus, tuberculosis and anthrax may cause confusion, but the history 



TETANUS 133 

and bacteriology determine the diagnosis. In thick smears, the chromatic 
bodies in the bacilli may simulate staphylococci (Zeit). The cultural 
findings are proved by intraperitoneal inoculation of a male guinea-pig, 
in which orchitis develops rapidly (Strauss's reaction, 1886). Injections 
of mallein differentiate in 90 per cent, of cases, producing fever of three 
degrees or more. The bacilli are agglutinated by the serum of normal 
horses in a dilution of 1 to 200, and of those subject to glanders in a 
dilution of 1 to 1000. 

Treatment. — The prophylaxis of glanders is like that of anthrax — 
isolation of diseased, and cremation of dead animals, and strong antisep- 
tics in wounds of persons exposed to infection. Skin ulcers are curetted 
and bandaged antiseptically, 'and if they are obstinate, touched with 
the live cautery. Infection of the nose demands carbolic douches, zinc 
chloride paste or iodoform. Arsenic, mercurial inunctions, quinine and 
alcohol are recommended. Injections of mallein and large doses of 
potassium iodide are recommended. Among others, Cramp records a 
recovery under vaccines. 

TETANUS. 

Definition.-^Tetanus, or lock-jaw, is an acute infection caused by the 
tetanus bacillus and characterized by greatly increased reflexes, muscular 
rigidity and tonic spasms. Tetanus is literally stretching. It is described 
in Hippocrates's aphorisms. 

Etiology. — In 1884, Carle, Rosenbach and Rattone produced the dis- 
ease by inoculations of pus, and in the same year, Nicholaier discovered 
the tetanus bacillus, of which Kitasato (1889) first obtained pure cultures 
from wounds and from earth. The bacillus measures 3 to 5 by i to \ix 
and is enlarged at one end, in which there is a spore, thus having a pin- 
head or drum-stick shape. It becomes thread-like in cultures. It stains 
readily by Gram's method, and is delicately flagellated and motile. 
It is anaerobic and cultures emit an onion-like smell. It grows well in 
sugar solutions. The bacillus is very enduring and the spores may live 
nineteen years. It exists in the primary wound and. in the brain and cord 
in 44 per cent, of severe infections, so that tetanus no longer ranks as a 
simple toxemia. The bacillus has been found in the blood and sputum. 
Tetanus is traumatic; in the so-called idiopathic, rheumatic form, the 
atrium is either microscopic or pharyngeal. The bacillus produces toxins 
which are 100 to 400 times as toxic as strychnine. They are tetano- 
spasmin and -lysin. Tetanus symptoms result from the tetanus toxins 
alone, but both infection and virulence are enhanced by association 
with various putrefactive microorganisms, and innocuous solutions of 
tetanus poison become lethal if combined with sterilized cultures of these 
putrefactive bacteria. The bacillus does not produce inflammation, 
though mixed infections are usual. Mice, guinea-pigs and rabbits are 
inoculable. In nature the bacillus is found in the alimentary tract of 
herbivora, whence it occurs in manure, garden earth, street or house 
dust, hay, putrefying fluids and splinters. The disease is ten to twenty 
times as frequent in the tropics as in temperate zones, because the bacillus 
thrives in heat. It may lurk in certain districts, as in Prague, the eastern 



134 BACTERIAL DISEASES 

end of Long Island, or the West Indies where negroes are more often 
and more seriously affected than whites. 

Mode of Infection. — Incised wounds are obviously less dangerous than 
punctures, gunshot or contused wounds or hematomata. Tetanus 
occurred less frequently in our Civil War than in the Spanish-American 
conflict, in which many cases developed among the Spaniards. It may 
result from circumcision, hypodermic injections, tooth-extraction and 
vaccination (95 cases), and Peterson (1910) collected 150 cases of post- 
operative tetanus, of which 70 dated since 1890; and in all, catgut was 
used. Parturition, lack of attention to the navels of the newborn, the 
use of imperfectly sterilized catgut, leech-bites or pin-pricks may cause 
its development. Chauffard (1903) collected 18 cases of infection from 
injections of gelatin for acute hemorrhage, Dieulafoy 11 cases after 
injections for aneurysm, Seibert 18 cases after antitoxin given for diph- 
theria, and preventive inoculations against the plague caused 19 deaths. 
The germ is very frequently found in gelatin, which should therefore 
be sterilized three times in very small amounts, each time for thirty 
to forty-five minutes at 212°. There is danger from the use of toy pistols 
and blank cartridges for Fourth-of-July celebrations; 415 deaths from 
tetanus are listed in the United States for 1903 as against 10 in 1912 
(Jour. Amer. Med. Assn.); French clinicians describe a visceral tetanus 
originating from the intestines in which latter tetanus spores have been 
found. 

Incubation. — This lasts from six to twelve hours in severe experi- 
mental inoculations, from two to nine days in less intense inocula- 
tions, and in man, in 33 per cent, of cases the symptoms appear in one, 
and in 66 per cent, in two, weeks. 

Symptoms. — These appear suddenly. Ehrlich's side-chain theory gives 
a satisfactory explanation, the anterior horn cells of the cord and 
medulla combining with the toxins and causing the spasms. The first 
signs are rigidity of the jaw ("lockjaw," trismus) and stiffness of the 
neck. In most animals the muscles become rigid near the seat of 
inoculation first, and sometimes, in injuries received in war, the muscles 
of a limb may be first involved; the toxin travels along the nerve trunks. 
The horse, like man, develops trismus first. The poison incites the 
anterior cells of the cord and medulla to tonic contraction. 

The fades tetanica results from zygomatic spasm, which produces 
the risus sardonicus — a smiling expression to the upper and a sad ex- 
pression to the lower part of the face; the forehead is lined, the eyebrows 
raised and approximated, the eyeballs fixed, the masseters prominent, 
the teeth set and the nares dilated. The spinal extensors are tonically 
contracted, arching the head backward and the trunk forward (opistho- 
tonos); the abdominal muscles are retracted stiffly; in rare cases the 
contracture is lateral (pleurothotonos), or forward (emprosthotonos), or 
the body is straight and rigid (orthotonos) . The limbs are extended, the 
legs more so than the arms, and the feet and hands least. The spasms 
are chiefly tonic, but momentary clonic exacerbations may result from 
peripheral stimulation of the sensory nerves or those of special sense, 
by the least touch, jar, draught, light or sound. The reflexes are enor- 



TETANUS 135 

mously increased, particularly those of the skin. The spasms occasion 
violent muscular pain, oppression over the lower chest and epigastrium, 
speechlessness, insomnia and, from participation of the medulla, profuse 
sweats and increased and irregular heart action. The temperature may 
be high, normal or subnormal. After death a temperature of 114° has 
been observed. The sensorium is usually clear! Evacuation of the 
bladder and rectum is difficult, and erection or ejaculation may occur. 
The urine is decreased and sometimes contains albumin, sugar, acetone 
or indican, but no increase of urea and creatin. In some cases the lymph 
glands adjacent to the seat of infection are enlarged. In very rare 
cases the toxins cause death without muscular spasm; i. e., they combine 
with other than nervous tissues. Axhausen collected 10 instances of 
localized tetanus, in which the disease did not extend from parts first 
involved. 

Diagnosis. — The diagnosis is based on the nature of the wound, the 
Bacillus tetani, trismus (necessary for diagnosis), the facies and opisthot- 
onos. Serum from cases of tetanus obtained by blistering, is fatal 
to white mice in twelve to twenty-four hours. In strychnine poisoning 
the history, tests for the drug in the stomach washings and urine, the 
more abrupt onset of the spasm and reflex excitability, the more diffuse 
and violent clonic intermittence of the convulsions, their greater involve- 
ment of the hands and feet, and the later appearance of trismus and its 
interparoxysmal relaxation, are entirely distinctive. Hysteria, hydro- 
phobia and tetany (q. v.) are wholly different from tetanus. In menin- 
gitis the sensorium is affected. Trismus may be due to dental caries, 
parotitis, or temporomaxillary arthritis with a tender area in front 
of the tragus. Escherich's pseudotetanus is characterized by tonic 
contractures of the jaw, back and limbs after an acute - infection and 
convalescence after a few weeks. 

Prognosis. — The following factors are important: 

1. Incubation. — The later after inoculation tetanus develops, the 
lower is the mortality; it is 91 per cent, if it appears in the first week, 
81 per cent, in the second, and 53 per cent, if later. 

2. Site of Infection. — Infection in the arms results in a 70 per 
cent, mortality; in the legs, 90 per cent. (Norris); in cephalic tetanus 
(tetanus facialis described by Charles Bell in 1830), the mortality is 
almost 100 per cent.; Brown (1912) found 94 records of cephalic tetanus, 
and in all but 1 case, the trauma was cephalic; in 84 per cent, the first 
symptom was trismus, followed later by various paralyses; in 16 per 
cent, paralysis antedated the trismus; paralysis may be facial or involve 
the pontine and medullary nuclei, which sometimes causes dysphagia 
(hydrophobic type) or paralysis of the eye muscles. The author observed 
these symptoms in a boy who had been kicked over the ear by a horse. 
Lloyd found 7 cases of facial diplegia. Tetanus or trismus neonatorum, 
especially described by Beumer (1887), is due to an infection of the 
navel in the second week of life. It prevents nursing and is fatal by 
the fourth day in 83 per cent, of cases. In the West Indies 50 per cent, 
of the children died of tetanus at one time, in the Western Hebrides, 
67 per cent., and in Iceland, 100 per cent. Anders and Morgan collected 



136 BACTERIAL DISEASES 

1307 cases (1850 to 1905). Tetanus puerperalis, particularly described 
by Heyse (1893), usually follows difficult labor, abortions or ministration 
by mid-wives, and is generally fatal. In three years there were 232 
cases in Bombay (Gowers). 

3. Course. — Hippocrates observed that patients who survive the 
fourth day may recover; 68 per cent, die in the first four days; 88 per 
cent, of acute and 75 per cent, of chronic cases die. 

4. Trauma. — The death-rate in traumatic cases is over 80 per cent.; 
in the so-called idiopathic cases it is 50 per cent, or lower. 

5. Sex. — More women recover than men. 

6. Symptoms. — Slight trismus is favorable; high fever, involvement 
of the pons or medulla, respiratory spasm, dysphagia and ocular paralysis 
are unfavorable. 

Treatment. — 1. Prophylaxis concerns surgical antisepsis in punctured 
wounds, hematomata, trauma due to blank cartridges or toy pistols, 
in labor and care of the navel in the newborn. Immense credit is due the 
Journal of the American Medical Association in its campaign for a rational 
Fourth of July. Since the bacillus is anerobic, punctured wounds 
should be widely incised, treated with iodine, phenol or peroxide, and 
packed. In extensive injuries, extirpation of the regional lymphatics, 
or amputation may be indicated. 

2. Antitoxin Therapy. — Behring and Kitasato (1890) discovered 
an antitoxin and were able to immunize animals by cultures heated 
or treated with Lugol's solution, which changes the toxins to toxoids 
(Ehrlich). The antitoxin is found in animals immune to tetanus, as 
crocodiles and chickens, and in the blood, milk and bile but not in the 
tissues. Tetanus antitoxin is not bactericidal, i. e., it does not act 
on the bacilli. It neutralizes the tetanus toxin in the blood before it 
has become fixed in nervous tissue. From the above it is obvious that 
(a) serum prophylaxis may be successful in Fourth-of-July wounds; 
in the Prague obstetrical clinic it abolished tetanus after every other 
measure failed. (6) If used early it may neutralize circulating toxins 
which have not yet become attached to nervous receptors, (c) -When 
the toxins have combined with the motor cells, it may abstract some of 
the virus fixed in the cells; 15,000 to 25,000 units for adults and 10,000 
units for children (or 1500 and 1000, respectively, for prophylaxis) 
are injected daily near the site of inoculation. As absorption requires 
three days, intravenous administration has been advised (as well as 
subdural injection, which some consider dangerous). The antitoxin is 
eliminated in eight days. Anaphylaxis has resulted (v. page 88). 
Antitoxin reduces the mortality of established tetanus 20 per cent. 
(Permin). 

3. Clonic convulsions may be minimized by absolute quiet, seclusion 
and darkening the room. Morphine hypodermically relieves pain 
and cutaneous reflex irritability, one-quarter grain every four to six 
hours for a day or two, but the pupils and respiration-rate must be 
carefully watched. An occasional corrective hypodermic of atropine 
should be given. Chloral hydrate depresses the motor elements of the 
cord; twenty grains may be given every two hours for three doses, but 



GONORRHEAL INFECTION 137 

even this amount may cause dangerous cardiac symptoms in alcoholics 
or arteriosclerotics. Digitalis may be given with chloral hydrate to 
steady the heart, and morphine and potassium bromide to enhance its 
depressomotor action and lessen the cutaneous irritability. The bromides 
are given, 5iss every three hours for six doses, after which the interval 
should be lengthened. Inhalations of chloroform and amyl nitrite, 
or lumbar puncture may inhibit the onset of severe attacks. 

4. Nutrition. — The nasal catheter or feeding by rectum overcomes 
the difficulties offered by trismus or dysphagia. 

5. Other Measures. — (a) Baccelli secures better results with hypo- 
dermics of 2 per cent, phenol solution than with serotherapy (150 to 
300 drops daily); in 190 cases, the mortality was only 17 per cent. 
(b) Wassermann advises subdural injection of an emulsion of sheep 
brains, (c) Meltzer and Auer use, after lumbar puncture, intraspinal 
injections of a 25 per cent, solution of magnesium sulphate — 1 c.c. for 
each 25 pounds of the patient's weight; Kocher prefers a 10 or 15 per 
cent, solution; the magnesium paralyzes the motor nerves, and relieves 
the symptoms, giving the patient rest and ease; six out of seven of 
Kocher's patients recovered and in Fox's 24 cases the mortality was 
46 per cent. The dangers are excessive bronchial secretion (relieved by 
atropine) and paralysis of the respiratory centre. In one case the writer 
observed retention of urine, maniacal delirium and quadriplegia. It 
must not be injected unless spinal fluid first runs out through the 
aspirating needle. 

GONORRHEAL INFECTION. 

Lightly spoken of as "the badge of virility," gonorrhea is often 
neglected. In its so-called latent form it 'may be conveyed to the wife, 
on whom it entails suffering, sterility and invalidism. 

I. Regional Invasion. — Gonorrhea may invade the prostate, seminal 
vesicles or testes, the vagina, uterus, tubes or peritoneum, the rectum, 
bladder and kidneys and, in children, it causes institutional epidemics 
of vulvovaginitis. 

II. Gonococcal Septicopyemia. — Thrombophlebitic or lymphangitic 
generalization has been discussed under Septic Infections. The fever 
is toxemic or septicemic, intermittent and often marked by great varia- 
tions. The gonococcus has been found in the blood (Thayer and Blumer, 
1895); myocardium; pleura (15 cases collected by Lemoine and Gallis, 
1905); and in the joints (v. i.), kidneys, spleen, muscular abscesses and 
lymph glands; in meningomyelitic foci (30 cases, Barrie); in myositis 
(7 cases collected by Harris and Haskell, 1904); in arteritis and phlebitis 
(25 cases collected by Heller, 1904) ; in felons, osteomyelitis and perios- 
titis; perichondritis (of the ears); horny skin eruptions or keratosis (21 
instances, F. E. Simpson, 1912); 49 cases of ulcerative gonorrheal 
endocarditis were collected by Kulbs in 1907, of which only 12 were 
above criticism. Septicopyemic lesions may be due to Neisser's diplo- 
coccus alone or to mixed infections. 

Gonorrheal arthritis is a form of mild septicemia — occasionally part 
of a septicopyemia. It was described by Selle and Sweidiaur in 1781, 



138 BACTERIAL DISEASES 

but first clearly by Brande, 1854; the gonococcus was first found by Pet- 
rone (1883) and cultivated by Hoch (1893). It develops in 2 or 3 per 
cent, of gonorrheal infections and is the most common disease of the 
joints. Eighty per cent, show an acute urethritis; in the balance the 
urethritis has subsided or become chronic. It has followed experimental 
gonorrhea, cuts during operating and primary gonorrheal conjunctivitis 
(18 cases reported by Lucas). About 90 per cent, occur in males, and 
50 per cent, between twenty and fifty years of age. Too active treat- 
ment and sexual indulgence during the florid stage of gonorrhea are 
predisposing causes. 

Symptoms. — Fever rarely exceeds 102°. The joints alone may be 
involved, or there may be more septicemic evidences, as endocarditis. 
Gonorrheal " rheumatism" is more than synovitis; the accessory bursse, 
contiguous tendon sheaths and extracapsular structures are often in- 
volved — gonorrheal arthritis. It is often held that it affects one joint 
(monarticular) or at least few joints (oligarticular) ; though fewer joints 
are involved than in genuine rheumatism, in Gerhardt's series two to 
nine joints were involved in 87 per cent., and one joint only in 13 per 
cent. Gonorrheal arthritis frequently involves joints which usually 
escape in acute articular rheumatism, e. g., the sacro-iliac synchondrosis, 
sternoclavicular, temporomaxillary and intervertebral joints. The 
knee is affected in 70 per cent., the ankle in 27, fingers and toes in 19, 
hip in 13, wrist in 12, shoulder in 10 and the elbow in 9 per cent., of 
the cases. Within the joint a greenish serofibrin exudes, and without 
the joint there is edema and infiltration. Suppuration may occur 
sometimes with or without coincident pyogenic infection, especially in 
the joints and tendons of the hand. Gonococci are found with variable 
frequency, the highest reported percentage being 75. Injection of a 
sterilized emulsion of gonococci may cause subcutaneous local reaction 
and induration, slight fever and local swelling in the joints (Bruck 
and Irons) — a form of cutaneous allergy. A positive complement- 
fixation test is indicative of gonorrhea. 

Konig's pathological classification includes (1) simple hydrops of the 
joint, (2) catarrhal or serofibrinous hydrops, (3) py arthrosis and (4) 
gonorrheal phlegmon, affecting the soft parts. A clinical classification 
may be made as follows: (1) Arthritic form, pain with exudation; (2) 
acute or subacute polyarthritis, by itself or with septicemia; (3) the 
periarthritic form (polytendosynovitis and polybursitis, often with 
periostitis) ; (4) acute monarticular form, with local reaction, sometimes 
with suppuration; (5) the chronic monarticular hydrarthrosis especially 
of the knee, a far less frequent form; and (6) simple arthralgia (the 
painful heel, talalgia or Jaquet's blenorrhagic foot). 

Course. — The course is chronic and sometimes relapsing; iritis is 
fairly frequent; atrophy in the contiguous muscles may occur, or anky- 
losis; which is oftener plastic than osseous. In exceptional instances, 
sciatica, permanent arthritic changes resembling arthritis deformans 
(q. v.), exhaustion psychoses or multiple neuritis develop. 

Treatment. — Recovery is a matter of time and nature, rather than 
of therapy. The salicylates are inert and the iodides unsatisfactory. 



TUBERCULOSIS 139 

In the acute stage, immobilization by plaster casts or splints, and in 
the chronic stage, blisters, Pacquelin cautery, massage, passive move- 
ments and extension, to overcome residual exudation and contractures, 
are useful. Some cases are helped by Rontgen rays and superheated 
air (see Arthritis Deformans). Passive congestion frequently benefits. 
In intractable cases incision and drainage are indicated. Vaccine 
therapy is promising in chronic and subchronic complications; it is 
generally futile in vulvovaginitis of children, chronic deep urethritis 
and blenorrhagic endocarditis; in polyarthritis opinions differ; 25-100 
million are used. 

TUBERCULOSIS. 

Definition. — A specific infection, characterized (a) etiologically by 
the Bacillus tuberculosis, (b) pathologically by nodes or tubercles, or 
diffuse tuberculous infiltration, and (c) clinically by symptomatology 
varying with the tissues or organs invaded. 

History. — The term phthisis (wasting) was first used by Hippocrates. 
The history of tuberculosis includes several epochs: 

Epoch I. — The anatomical tubercle was recognized by Sylvius (1614- 
1672), Morton (1689) whom some consider the real pioneer, Mangetus 
(1700) and Bayle (1810), who described the miliary tubercle. Laennec, 
in 1819, spoke for the unity of phthisis. Virchow held that caseation 
was only a retrogressive change and not necessarily tuberculosis. In 
1857 Buhl described miliary tuberculosis. Cruveilhier, Rillet and 
Barthez identified scrofula and tuberculosis. 

Epoch II. — Villemin (1865) positively established the inoculability 
of tuberculosis by experiments on animals. From the time of Hippo- 
crates and Aristotle, tuberculosis was feared as a contagion, and the 
older pathologists, as Morgagni, dreaded to section phthisical subjects. 
The histology of the tubercle was developed by Wagner, Schuppel and 
Virchow; Langhans fully described the giant cells previously seen 
by Virchow and Rokitansky; tubercles were found in lupus (Friedlander, 
1875), lymph glands (Schuppel, 1871) and fungus joints (Koster, 1876). 
The firm and ancient belief in its contagiousness led to the successful 
search for the cause. 

Epoch III began with Koch's announcement, in 1882, of the tubercle 
bacillus. His report, as health officer in an obscure German town, was 
so complete that scarcely a single point has been added to his initial 
communication. The bacillus was found in all tuberculous lesions, such 
as chronic phthisis, miliary tuberculosis, intestinal ulcers, "scrofulous" 
lesions, bone and joint disease, lupus and in the sputum, in cattle, etc.; 
it occurred in no other disease; it was cultivated by him and inoculated 
into animals with reproduction of tuberculosis, thereby fulfilling what 
has become known as " Koch's law." 

Bacillus Tuberculosis. — 1. Morphology. — It is a thin, slightly curved, 
narrow rod, measuring 1J to 4//, long; it contains no spores, the light 
unstained areas in its body being vacuoles or degeneration; it is im- 
motile; in young cultures it is shorter than in the sputum; in old cultures 
and in lung cavities it is longer and is frequently thread-like. Pleomor- 



140 BACTERIAL DISEASES 

phism is often noted, as bulging sides or ends, thread-like, or branching 
forms and forms like actinomyces. (See Plate V). 

2. Staining Reaction. — It stains slowly and gives up the stain 
reluctantly. Ziehl's solution is the best (fuchsin 1, absolute alcohol 
10 and 5 per cent, carbolic solution 100). The sputum is spread out in a 
dish over a black background and the yellow-green areas selected are 
thinly distributed on the slide which is held in the hand, and dried at 
some distance from the flame; it is then stained by the carbol-fuchsin, 
being passed repeatedly but lightly through the flame (without boiling) 
to deepen the stain; it is then washed, treated with 33 per cent, nitric 
acid, washed well in water and then alcohol, and dried. Uhlenhuth's 
method, as modified by Loefner detects bacilli in 15 to 35 per cent, 
when not found by other methods. 1 The bacillus resists destaining 
because of its wax-like envelope, an almost pathognomonic feature. For 
clinical purposes only (a) the bacilli found in bronchiectasis and gangrene 
of the lung (q. v.), (b) the smegma bacillus and (c) the leprosy bacillus 
need be considered; the leprosy germs are intracellular, cover the 
nucleus of the containing cell, and are stained in six or seven minutes 
with alcoholic fuchsin, while tubercle bacilli are extracellular and stain 
slowly; the smegma bacillus causes many errors in genito-urinary 
examinations; it grows rapidly in twenty-four hours, does not show 
the beaded appearance seen in the Bacillus tuberculosis, and stained 
and counter-stained in the usual way, becomes tinged with methylene 
blue. Much found that some tubercle bacilli stain by Gram and not 
by carbol-fuchsin; he proved by culture and inoculation that they were 
Koch's bacilli and that they could be converted into the less virulent 
acid-fast form. 

3. Cultures. — The bacillus develops best at body heat in one or two 
weeks; blood serum is the best medium, but growths are also successful 
on bouillon, glycerine-agar and potato; they are dry, thin, grayish and 
scale-like. The germ is a facultative aerobe and multiplies by transverse 
fission. It does not lead a saprophytic life in nature, outside the bodies 
of animals and of man. 

4. Chemistry, Metabolism, Resistance, Virulence, Etc. — It con- 
tains two to sixteen times as much fat as other bacteria. A waxy sub- 
stance envelops the bacillus; it also develops tuberculin whose chief com- 
ponents are peptone, albumose and alkaloidal substances; it is soluble in 
glycerin. It is not proved that it develops a definite toxin. Its resisting 
powers are as a rule limited. Drying is endured by the bacillus for six or 
even ten months. In decomposing media its average life is one to one 
and a half weeks. Heat (106°) kills it in a few minutes. It may survive 
14° below zero for weeks. Sunlight kills the bacillus in minutes to hours. 

1 5 to 20 c.c. of sputum are placed in a flask with an equal quantity of 50 per cent, 
antiformin and the mixture is boiled. Solution of the sputum occurs at once. To 10 c.c. 
of the cooled solution (which is sterile and from which cultures or inoculations can be 
made) 1.5 c.c. of a mixture of 10 volumes of chloroform and 90 volumes of alcohol are 
added and the whole thoroughly shaken. The specimen is centrifugalized about fifteen 
minutes. Chloroform is found at the bottom of the tube, and on its upper surface the 
sediment collects. The supernatant fluid is poured off, and with a pipette the sediment is 
transferred to a glass slide. 



PLATE V 





Tubercle Bacilli and Elastic Fibers. 



) 



TUBERCULOSIS 141 

Koch assumed an equal virulence, while the Arloing school finds that 
it has an attenuated virulence in glandular and osseous lesions, and 
Theobald Smith holds that bovine cultures are more virulent for rabbits 
than is human sputum. Large numbers are found in fresh tubercles; 
few are found in chronic articular, osseous or glandular foci, and 
inoculations may be necessary to demonstrate the nature of long- 
standing lesions. Arloing and Courmont found that serum from inoculated 
rabbits or goats, agglutinized tubercle bacilli in a dilution of 1 to 5 or 
20, in two to twenty-four hours; agglutination was noted in 95 per cent, 
of the cases of lung tuberculosis and in 50 per cent, of the cases of surgical 
tuberculosis. 

Associated or Mixed Injection. — Symbiosis has been noted with the 
streptococcus, staphylococcus and pneumococcus, to a lesser degree 
with the Bacillus pyocyaneus, influenza, etc. (v. i.) 

Prevalence in Man. — Tuberculosis is the greatest foe of man and 
five million die yearly from this plague; it causes 14 per cent, of all 
deaths, and 33 per cent, of deaths between fifteen and forty-five years of 
age; it causes more deaths than war, famine, plague, cholera, yellow fever 
and smallpox combined; in Germany, in 1894, the deaths from diphtheria, 
croup, measles, scarlatina, pertussis and typhoid, together, were 7000 
less than those from tuberculosis. 

Quiescent (latent), obsolete or healed tuberculosis was found by Heitler 
in many postmortems upon those dying of other diseases (4.8 per cent, 
among 16,562 autopsies). Latent tuberculosis occurs in 25 to 33 per 
cent, of the population (Baumgarten, Birch-Hirschfeld), and 50 per cent. 
(Cruveilhier and Dejerine), 91 per cent. (Burkhardt) and in 97 per cent, 
of all necropsies (O. Naegeli). 

Prevalence in Animals. — (a) Cattle. — In Germany it is found in from 
4 to 20 per cent. In New York the tuberculin test was positive in 17 
per cent. Theobald Smith,, and later Koch, contended that bovine 
and human tuberculosis were separate infections; most writers incline 
to this view. In cattle tuberculosis is less often attended by softening 
of the tubercle, and the serous membranes are more often involved; 
the lungs and pleurae are involved in 40 per cent., the lungs alone in 20 
per cent., and the pleurae and peritoneum in 15 per cent. (b) Swine 
are affected more often in Europe than in this country; in Saxony tuber- 
culosis occurs in 1 per cent, and in Copenhagen and Dantzig, in 11 per 
cent.; because their infection commonly results from eating tuberculous 
offal, the type is alimentary (90 per cent.), (c) Other mammals: Dogs, 
cats, horses and sheep are rarely diseased. Monkeys in captivity die 
frequently (43 per cent.) from tuberculosis, referable to foul cages. 
(d) In reptiles, it is rarely seen except in captivity, (e) In birds, tuber- 
culous lesions are more frequent in the liver, spleen, intestine, mesenteric 
glands, bones and joints, than in the lungs, though parrots suffer from 
skin and lung localizations. Avian, bovine, reptilian and human tuber- 
culosis are closely related types. Tubercles are not uncommon in animals 
from nematodes, protozoa and bacteria and in man, from the streptothrix 
and aspergillus (pseudotuberculosis) . 



142 BACTERIAL DISEASES 

Atrium. — The details will be considered under the different clinical 
localizations of the disease. 

1. By the Respiratory Tract. — The bacillus enters the respiratory 
tract by inhalation. In the vast majority of cases the sputum of diseased 
persons is causative both of the disease and its great frequency of local- 
ization in the respiratory organs. It has been estimated that a phthisical 
person voids three millions of tubercle bacilli daily. Cornet holds that 
the greatest danger lies in the drying of the sputum in the room, on the 
handkerchief, the lips, beard, hair, fingers and clothing or in the street 
and other open places. Fltigge contends that dried sputum is rapidly 
sterilized by sunlight and is less dangerous than the moist expectoration, 
and demonstrated that in coughing, which seemingly voids no secretion, 
in singing, sneezing or talking, small and almost invisible drops of moisture 
containing the bacilli are voided; he cultivated bacilli from glass plates 
covered with solid culture media and held near the patient; he believes 
that minute particles remain in suspension in the air and thus infect 
other individuals. The ubiquity of the tubercle bacillus is exaggerated, 
though of great importance in poorly ventilated, dark dwelling-rooms, 
hospitals, cloisters, hotels or prisons, frequented by victims of tuber- 
culosis. Cornet found the bacilli in the dust of such rooms in large 
numbers, and demonstrated that animals confined in rooms with dried 
tuberculous sputum readily acquired tuberculosis. Straus collected the 
germ from the nose in 31 per cent, of the attendants in tuberculous 
wards. The closer the contact with tuberculous subjects, the greater is the 
danger of infection. In crowded prisons in Austria the prison mortality 
is 40 to 60 per cent., against the general mortality of 11 to 15 per cent. 
In nursing sisterhoods, the death-rate exceeded 75 per cent., as observed 
by the writer in one small, closely cloistered community. In Phila- 
delphia, Flick's studies showed that 33 per cent, of infected houses 
contributed more than 1 case. In our dispensary service, 7 rapidly 
fatal cases were observed in one family (Harpole). Oral breathing, 
caused by adenoids and inhalation of coal-dust or stone-dust, are 
favoring factors. 

Dusting, sweeping or shaking the bedclothes disseminates the virus; 
there is less danger of infection when the windows and doors are open 
and when dusting is done with moist cloths rather than with feather- 
dusters. In hospital wards there are more germs in the air during the 
cleaning hour than during the other twenty-three hours. However, if 
bacilli are in the dust, they are not necessarily in the inhaled air; if 
inhaled, they may be caught in the upper air-passages whose secre- 
tions antagonize their development, and are often waved back by 
the ciliated epithelium of the lower air-passages; when bacilli are 
inhaled into the respiratory tract (a) no lesions may result, (b) the 
lungs may become diseased, or (c) the germs may pass the mucosa of the 
mouth or bronchi and cause cervical or peribronchial tuberculous adenitis. 
Cornet holds that the statement that "every man lives in the environ- 
ment of tuberculosis" is exaggeration. Married persons, because of 
their intimate association, may contract the disease from each other, 
as was noted by Ettmuller and Morton in the seventeenth century. 



TUBERCULOSIS 143 

2. By the Digestive Tract. — Bacilli may pass the mucosa, espe- 
cially in children, and produce the first lesions in the mesenteric glands. 
Park and Krumwiede hold that in young children 6 to 10 per cent, of 
tuberculous deaths are due to the bovine type of bacillus, and that 
juvenile tuberculous adenitis and abdominal tuberculosis are more often 
due to bovine than the human bacillus. In pulmonary tuberculosis 
in adults, Park and Krumwiede did not once find the bovine bacilli in 
the sputum in 1042 cases; Kossel found in 709 sputa, 705 bacilli humani, 
2 certain and 1 doubtful bacilli bovini and 1 with both types; in other 
words, the bacillus humanus is found almost exclusively in pulmonary 
tuberculosis of which twelve times as many people die as from all other 
localizations combined. In cows, a tuberculous mastitis was formerly 
thought necessary to milk infection, but milk may be infective from cows 
with tuberculosis which does not invade the udders. Pigs, fed on tuber- 
culous milk, develop intestinal or pulmonary tuberculosis. Butter may 
contain tubercle bacilli. Meat is less dangerous, as it is usually well cooked, 
but tubercles in raw offal frequently infect swine. Harbitz's figures 
show that the entry of tuberculous infection is (i) respiratory in 41 per 
cent., (ii) digestive in 22 per cent., (hi) respiratory or digestive in 21 per 
cent., and (iv) in the lymph nodes, elsewhere or doubtful in 16 per cent. 
Gohn holds that 95 per cent, of infections in children are pulmonary or 
aerogenic, not lymphadenogenic, in origin. 

3. Direct Inoculation. — Inoculation through the skin, genito- 
urinary tract, trauma or operations is far less significant. 

Predisposing Factors. — These are important, but tuberculosis is best 
considered and treated as an injection, communicated and acquired by 
direct personal contact. 

1. Heredity. — (a) Hereditary Predisposition to Tuberculosis. — A 
tuberculous family history is obtained in infected individuals in 25 per 
cent. Kuthri found essentially the same percentage of family tuber- 
culosis in non-tuberculous as in tuberculous cases. Tuberculous parents 
may infect their children (50 per cent.), as they may infect others, but 
97 per cent, escape the disease when removed from their parents. Accord- 
ing to Rieffel, 3 per cent, of children acquire tuberculosis when both 
parents are sound and 22 per cent, when both parents are tuberculous. 
Hereditary predisposition is no obstacle to prevention and treatment. 
Cornick argues that heredity promotes resistance. 

(6) Congenital Tuberculosis. — Baumgarten thought that children 
actually inherit the bacillus, which remains latent for years, and then 
develop an active tuberculosis. Congenital tuberculosis can be acquired 
only through the spermatozoon, ovum or placenta. The spermatozoon 
and ovum can not carry bacteria. Placental tuberculosis has been ob- 
served according to Warthin and Cowie in only 5 human cases, and in 
slightly over 100 cases in animals (Friedman, 1905). Virchow never 
saw a case. Usually there is a placental focus before the fetal blood is 
infected, but the bacillus may pass directly to the fetus. Schmorl and 
Geipel found tuberculosis in 50 per cent, of placentae of tuberculous 
mothers. 

The arguments against hereditary tuberculosis are (1) that children 



144 BACTERIAL DISEASES 

born with the disease die very early; (2) that tuberculosis in the first 
months of life is extremely rare; (3) in congenital infection, the liver is 
chiefly diseased because of its vascular relations to the placenta; in 
tuberculosis of children, the lungs and glands are more often diseased, 
i. e., respiratory infection is extra-uterine. (4) Removed from their 
tuberculous parents, children thrive well. 

2. Environment. — Environment is but another name for exposure 
or contact-infection. Dampness and poor drainage reduce the physio- 
logical resistance. Trudeau showed that inoculated animals, kept in 
dark, damp cellars, die, while others, allowed to run at large, outlive 
the infection. Density of population raises the proportion of tuberculous 
cases. In recent years the large cities have shown an apparent decrease 
of tuberculosis, e. g., Chicago, Glascow, New York and London. In 
Massachusetts the total is less by half than fifty years ago. The decrease 
is attributed to more intelligent hygiene. It is possible that this decrease 
is explained by the fact that pneumonia carries off the less resistant of 
the population; in Munich the death-rate from tuberculosis was 12 per 
cent, when typhoid was epidemic; when typhoid was practically abolished 
the tuberculosis-rate increased to 16 per cent., i. e., 4 per cent, of those 
with tuberculosis had previously died from typhoid. 

3. Occupation. — Work in close, damp rooms, in dust, in crowded 
quarters, particularly when associated with poor food, alcoholism, worry 
and overexertion, lowers resistance and promotes tuberculosis when 
exposure to infected individuals exists. Clerks, stenographers or waiters 
are more easily infected than are those working in the fresh air. Miners 
do not suffer more frequently, as dampness prevents the drying of in- 
fected sputum. 

4. Age. — Cornet's figures show the following death-rate per 10,000 
of population: First year 2 to 3, the child being in close contact with 
the mother. These figures grow smaller, until the lowest figure is reached, 
namely, \ from the fifth to tenth years; fifteenth to twentieth years, 
17 to 19; twentieth to thirtieth years, 32 to 36; thirtieth to fortieth 
years, 44; fortieth to fiftieth years, 55; fiftieth to sixtieth years, 76; 
sixtieth to seventieth years, 100; seventieth to eightieth years, 70; 
over eightieth year, 20. In the first decade of life, glandular, meningeal, 
osseous and cutaneous tuberculosis are more frequent. 

5. Sex. — Before twenty years of age girls are more prone to tuber- 
culosis, because their life is more sedentary. After twenty years males 
more often contract the disease, because of their greater exposure to 
infection. Repeated pregnancies and protracted lactations lower re- 
sistance to infection. 

6. Climate. — Warm, dry climates, high altitudes and lack of sudden 
variations in temperature are inimical to tuberculosis. The French 
Alps and other localities were long free of tuberculosis until crowded by 
infected subjects. The chief advantages of many resorts seem to be 
their sparse population and inaccessibility. 

7. Race. — In this country the Irish and negroes are most frequently 
diseased. The Indians have justly come to dread the ''coughing white 
man," and they die in large numbers from consumption. These instances 



TUBERCULOSIS 145 

are explained by exchanging a country for a city life. Infection among 
Jews is peculiarly infrequent. 

8. Individual Pkedisposition. — The oldest medical writers described 
the winged scapulae, paralytic thorax and depressed sternum; but 
poor development is often an expression of already existing tuberculosis; 
phthisis also occurs in splendidly developed chests, exposure to infection 
being the most important factor. Tuberculosis confers no immunity 
to relapses or to new localizations; a lung lesion may heal while a co- 
incident intestinal lesion progresses. 

9. Trauma. — Bacilli in the blood may be localized in a bone or joint 
by trauma; a blow on the head or spine may initiate meningitis in a 
tuberculous subject; pleurisy or pulmonary tuberculosis may be initiated 
by injury to the chest, arousing latent lesions in the peribronchial glands. 

10. Other Factors. — These are diabetes, in which 25 to 50 per cent, 
die of tuberculosis of the lung; psychoses, especially of the depressive 
type; anemia, which, however, is more often the result than the cause 
of tuberculosis ; heavy colds, measles and pertussis, and less often scarlatina, 
influenza or diphtheria, may predispose to infection, or more probably 
often awaken slumbering glandular tuberculosis by the irritative action 
of products absorbed from the bronchi or lungs. Enterocolitis in children 
or typhoid in adults may in a similar way awaken or initiate abdominal 
tuberculosis. Contracted kidney, cirrhotic liver, sclerosed arteries, stenosis 
of the pulmonary artery, aneurysm and a hypoplastic aorta are pre- 
disposing factors. Rokitansky noted that valvular disease of the left 
heart prevents or checks infection, because it congests the lungs; Bier's 
congestion treatment of surgical tuberculosis is based on this point; 
Birch-Hirschfeld, in 4359 autopsies, found chronic pulmonary tuber- 
culosis in 21 per cent., and in 107 autopsies of valvular heart disease 
it was present in but 2.8 per cent. Potain, in 54 cases of mitral stenosis, 
found pulmonary tuberculosis in 16.6 per cent, (see Valvular Disease 
of the Heart). Syphilis, cancer, pleurisy (q. v.) and hemoptysis (q. v.) 
are occasional predisposing factors. 

General Histopathology of the Tubercle. — The only pathognomonic 
feature of the tubercle is Koch's bacillus, as similar infective granulomata 
are seen in strongylus in sheep, in actinomycosis, syphilis, etc. Baum- 
garten described the changes following inoculation of the anterior chamber 
of the eye : (a) On the first day the bacilli increase and spread along the 
lymph spaces, (b) By the sixth day, the fixed connective-tissue cells 
proliferate under the stimulus of the bacillus; these epithelioid or endo- 
thelioid cells are large, rounded or polygonal, with distended nuclei, 
sometimes contain tubercle bacilli and show karyokinetic figures; the 
bacilli multiply and the endothelial cells of the vessels proliferate. In 
this stage it is called the epithelioid tubercle, (c) On the tenth day 
leukocytes emigrate, an inflammatory reaction to the toxins secreted 
by the bacillus; most of the white cells are polymorphonuclear, many 
of which degenerate; later there are mononuclears which do not suffer 
retrogressive changes; the mononuclears crowd the epithelioid cells and 
dominate the histological picture, especially with complicating trauma 
(lymphoid tubercle), (d) The reticulum of the tubercle consists of the 
10 



146 BACTERIAL DISEASES 

stretched fibers of the infected tissue. Tubercles contain no bloodvessels. 
(e) The epithelioid cells increase in size and are often multinucleated. 
From them or the extravasated leukocytes, by growth or fusion, giant 
cells develop; they contain many large, oval nuclei and tubercle bacilli; 
the bacilli may number 50 to a cell in very active processes or even may 
be the chief histological finding in very chronic forms, such as lupus, 
scrofulous glands or fungoid joint disease; they are few or absent in 
miliary tuberculosis; there seems to be an antagonism between the nuclei 
and bacilli, for if the nuclei lie on the margin of the cell, the bacilli are 
centrally grouped, and if the nuclei lie at one pole of the cell, the bacilli 
concentrate at the other pole. The cellular inclusion of the bacilli is 
possibly a phagocytosis. The completed miliary tubercle is non-vascular, 
cellular, millet-seed (miliary) in size, gray in color and translucent or 
opaque from later caseation (v. i.); it is the invariable pathological 
unit of all tuberculous lesions and, more or less, is a continuous process. 
In the diffused inflammatory tubercle, the diffuse areas result from the 
fusion of myriads of miliary tubercles. 

The tubercle then undergoes one of two degenerations, caseation or 
induration: (1) Caseation results from degeneration of the tubercle, 
beginning at its centre, from ischemia (vascular obliteration) and 
coagulation necrosis (the bacillus and its toxins). Inoculations with 
dead bacilli may cause tubercles and even caseation. The area of 
coagulation necrosis then gradually becomes more yellow and granular, 
and finally results in an amorphous, homogeneous, cheesy debris. Casea- 
tion is a dangerous, destructive degeneration. (2) Induration or encap- 
sulation results from growth of connective tissue around the conglom- 
eration of tubercles; it limits the tubercle, is the measure of the resisting 
power of the surrounding tissue, of the process of bacteriolysis, and is 
a conservative change. It occurs most frequently in the peritoneum, 
but also in the lungs and other tissues. Inflammation, varying with the 
tissue involved, may complicate the histological findings. Suppuration 
may result from mixed infection with streptococci, though Koch held 
that pus may be formed by the tubercle bacillus itself; the ordinary 
tuberculous "cold abscess" is not actual pus, but merely thick, amor- 
phous, granular debris. 

Extension. — (1) Tubercles develop at the point of infection ' and in 
the nearest lymph glands, which permanently or temporarily arrest the 
process. (2) Infection may occur through the uninjured mucosa or 
skin, but the process rarely passes beyond the tributary lymph glands. 
(3) The later advance of the process can be traced clearly at autopsy, 
along the lymph vessels. 

I. Tuberculosis Miliaris Acuta. — Definition. — An acute general, some- 
times almost universal, embolic dissemination of the tubercle bacillus 
in great numbers by the blood or lymph stream, resulting pathologically 
in the . wide-spread formation of miliary tubercles in various tissues, and 
clinically in fatal toxemia, pulmonary, meningitic or other symptoms. 

Etiology. — 1. Development. — Acute miliary tuberculosis always de- 
velops from a tuberculous focus, which is found in 97 to 100 per cent, by 
careful dissection; it may be small or even miscroscopic; von Buhl, 



TUBERCULOSIS 147 

who first fully described the affection (1856), recognized that miliary 
dissemination occurred by absorption from old tuberculous foci, as 
pyemia results from local suppuration. It is curious that miliary tuber- 
culosis occurs from foci so small as to be easily overlooked, and that large 
tuberculous lesions seldom result in miliary dissemination. 

2. Lesion. — A description of all primary foci would enumerate every 
possible localization of tuberculosis. Pulmonary tuberculosis causes 
over 50 per cent, of cases of acute miliary tuberculosis. Glandular 
lesions rank next, and articular, osseous, genito-urinary and serous- 
membrane tuberculosis cause most of the balance. The more the tubercle 
is indurated, the less is the danger of dissemination. Acute generaliza- 
tion only follows the introduction into the circulation of large numbers 
of bacilli, for they do not multiply in the blood. A few bacilli reaching 
the circulation cause a solitary tubercle. Repeated ruptures of moderate 
numbers of bacilli cause the so-called chronic miliary tuberculosis (v. i.). 

3. Access of Bacilli into Blood Stream. — Sir Astley Cooper, 
in 1798, found tubercles in the thoracic duct. In 1877, Weigert demon- 
strated that tubercles invade the vessel walls, which Rokitansky had de- 
clared immune. Tuberculosis reaching a vessel usually causes its gradual 
obliteration and thus localizes the process, but in some cases bacilli reach 
the lumen of the vessel and are distributed in the direction of its current. 
The most frequent process is periangitis, by which a tubercle adheres 
to and empties into a vein. Less common is endangitis, by which bacilli 
lodge in the intima, and, grouping there, further disseminate the infec- 
tion. The most common method is periadenitis of a tuberculous bronchial 
gland, its adhesion to a pulmonary vein and final rupture into it. Tuber- 
culous lesions may rupture into the azygos, cavse, pulmonary artery, 
aorta, thoracic duct or jugular or other veins. 

4. Organs Involved. — (a) Rupture into a pulmonary vein floods 
the arterial circulation with bacilli, whence miliary deposits occur in 
the brain, choroid, liver, spleen, kidneys, myocardium, bones, serous 
and mucous membranes and in the bloodvessels themselves, (b) Rupture 
into a portal venous radicle affects chiefly the liver, (c) Into the pul- 
monary artery, the lungs and (d) into a peripheral artery, the tissue 
supplied by it. 

5. Predisposing Factors. — Miliary dissemination is most frequent 
in children, especially between one and four years of age, because the 
circulation is faster, metabolism is quicker, thrombosis of the vessels 
is less frequent, tissue reaction is less marked and the lymph vessels 
and spaces are wider. Depleting factors, pregnancy, the puerperium, 
trauma, bone operations, measles, pertussis and mixed infections are 
somewhat predisposing causes. 

Symptoms. — The clinical picture varies greatly, depending on the 
quality (virulence) and quantity of bacilli; the toxins thrown into cir- 
culation from the primary focus; and the localization of the tubercles 
formed. Toxemic precede local symptoms. 

Types. — Waller (1845) distinguished the following forms: 
1. Typhoid Type. — The febrile onset may be gradual or sudden, 
with or without chills. The patient often exhibits only great toxemia 



148 BACTERIAL DISEASES 

with little local reaction from the tubercle, therefore with few local findings; 
this type may be due to a large caseous focus flooding the blood stream 
with toxins. The status typhosus, delirium, headache, continuous or 
weakly remittent fever, enlarged spleen, diazo reaction and bronchitis 
suggest typhoid but the fever is more variable and the pulse runs higher ; 
less frequently roseolse, meteorism, diarrhea and intestinal hemorrhage 
may cause even a closer resemblance to typhoid (see page 46). Unless 
the meninges or lungs are involved the diagnostic confusion may be in- 
superable. Epistaxis is less common; hyperesthesia and herpes are 
more common but all symptoms may be deceptive except the typhoid 
bacillemia and Widal reaction in typhoid, as opposed to the choroidal 
tubercles, etc., in miliary tuberculosis. Acute miliary bacillemia is more 
common in children than in adults, and runs a course of ten to twenty 
days, or somewhat longer. The writer saw typhoid and miliary tuber- 
culosis in the same subject. 

2. Respiratory Type. — In this type the toxemia is subordinated 
to the local miliary eruption. Tachypnea, dyspnea and cyanosis, without 
proportionate physical findings are almost unmistakable ; the respiratory 
urgency and rapid pulse, without cardiac disease and with a tympanitic 
pulmonary resonance declare the diagnosis. The following forms are 
less characteristic: Pneumonia may be closely simulated by the fever, 
chills, pain, cough, rusty sputum, increased breathing, dyspnea, cyanosis, 
or even by tubular breathing (in children). Capillary bronchitis (broncho- 
pneumonia) requires differentiation after recent measles, or after pertussis 
with patches of atelectasis. Diagnosis should be made from senile 
bronchitis and emphysema in the aged, in whom the miliary type is 
frequently afebrile. Tubercle bacilli in the sputum or urine may occur 
accidentally. The course averages three or four weeks. 

3. Meningeal Type. — Tuberculous meningitis appears as the only 
apparent trouble, whereas it is but a part of a miliary dissemination. 
Meningitis occurs in 80 per cent, of cases of miliary tuberculosis. The 
increased respiration, deep breathing and increased irregular pulse are 
suggestive and the choroid findings, lumbar puncture and Kernig's sign 
are corroborative. In children who are prone to this type of miliary 
tuberculosis, toxemia may closely simulate actual meningitis, as in 
Henoch's cases, where only brain edema was found. 

4. Other Types. — The mention of these infrequent types shows the 
liability of diagnostic error; the latent type, marked only by catarrhal 
symptoms, and often called grippal; the ambulant type, with death 
after a few days of indisposition; nephritic; apoplectiform, delirium 
tremens, suffocative or asthmatic type; and the fulminant type, where 
the patient dies in a few hours. Sepsis, miliary carcinosis, uremia or 
the cyanosis of nitrobenzol poisoning may be suggested. 

Individual Symptoms. — 1. Temperature. — Continuous fever may be 
observed in very diffused acute forms, but it is lower than in typhoid. 
Remittent or intermittent fever is more common; miliary tuberculosis 
following pulmonary phthisis may change neither the hectic fever of 
the latter nor its euphoria. The typus inversus usually lasts but a few 
days. In 17.5 per cent, of cases the course is afebrile; involvement of the 



TUBERCULOSIS 149 

meninges, hemorrhages, vomiting or diarrhea may depress the fever; 
low temperatures are common in the aged, in ambulant, bronchitic and 
cardiac types. 

2. Circulation. — (a) The pulse is fast in proportion to the fever, 
120 to 140-160; the blood-pressure is low but dicrotism is infrequent; 
a pulse under 100 is very rare (in old people or meningitic localization). 

(b) The heart is somewhat dilated and an apical systolic murmur, with 
accentuation of the second pulmonic sound, is frequent. On rare occasions 
a pericardial rub is due to roughening of the serosa by the miliary eruption. 

(c) Tubercle bacilli were first found at autopsy in the blood by Weichsel- 
baum and Meisels, and clinically by Lustig and Rutimeyer. In the 
death agony from lung tuberculosis, bacilli may enter the blood, (d) 
The leukocytes are usually not increased; Matthes notes increase in the 
polymorphonuclears . 

3. Respiration. — Early symptoms are frequent, (a) There is very 
often a severe continuous cough, always a suspicious symptom. It is 
due to the toxins or to irritation of the vagus twigs by miliary nodes 
in the lung; it causes muscular pain, voids little sputum and ceases later 
if the brain becomes involved. (6) The breathing is increased to 40 to 
60 in adults, and to 80 to 90 in children, (c) Dyspnea and cyanosis 
develop from irritation of the vagus or involvement of the diaphragm. 
The tachypnea, dyspnea and cyanosis are peculiarly significant diagnostic- 
ally in that they have no adequate explanation in the physical findings. 

(d) The sputum is scant, foamy white and mucous; it seldom contains 
dots of blood, and is rarely rusty without complicating pneumonia. 
It may be more abundant in subacute cases, (d) The physical findings 
are not as marked as the urgent respiratory symptoms would indicate. 
A tympanitic note is very frequent, resulting from relaxation of the lung, 
or acute emphysema from coughing. Dulness only results from older 
tuberculous foci in the lung, or from complications. Auscultation reveals 
fine rales, especially suggestive over the upper chest, where stasis is 
uncommon. The a>rays reveal small, bright pin-head spots early in the 
disease. Jiirgensen noted a fine pleural rub, due to pleural tubercles. 
Terminal pulmonary edema is frequent. At autopsy innumerable 
translucent nodes are scattered through the lung, most apparent on 
oblique illumination. 

4. Nervous System. — Nervous symptoms may predominate, and 
are toxemic or organic: (a) The toxemic symptoms are headache, dulness, 
vertigo and tinnitus; these are followed by delirium, muscular adynamia 
and tremor, and eventuate in stupor, broken by fits of delirium, and 
coma. In rare instances coma may develop early in an apoplectiform 
fashion, or the sensorium may be normal, (b) Meningitic symptoms 
may develop, such as headache, retraction of head, spinal tenderness 
and rigidity, paralysis of the cranial nerves, Kernig's sign, convulsions 
and coma. The cerebrospinal fluid is generally under increased pressure 
and contains globulin, lymphocytes and often tubercle bacilli. The 
findings at autopsy are those of tuberculous meningitis (page 150). 

5. Digestive System.— The tongue is coated and there is anorexia 
and constipation. Nausea and vomiting are usually meningitic. Diarrhea 



150 BACTERIAL DISEASES 

is infrequent, but bloody stools may occur with tympany. Ascites is 
infrequent in miliary tuberculosis of the peritoneum (as distinguished 
from tuberculous peritonitis). Litten once heard a friction rub over the 
liver. Miliary tubercles may occur in the stomach and bowels, most 
frequently in children. 

6. Choroidal Tubercles. — These occur in 16 to 75 per cent, of 
cases, after one or several weeks. They occur singly or in large numbers 
in very generalized tuberculosis, usually in both eyes, as whitish-yellow 
protuberances with irregular washed borders. They become large and 
cause so much atrophy of the retinal pigment layer that they can be 
seen through it. Daily examination for them is necessary. (See Plate 
VI, Fig. 6.) 

7. Other Symptoms. — One of Wunderlich's cases was reduced to 
one-quarter of his ordinary weight. The spleen is enlarged in 70 per 
cent., but is usually smaller than in typhoid, except in children, where it 
may assume great dimensions, with swelling of the lymphatic glands. 
The urine is concentrated and dark, may contain albumin and often 
shows the diazo reaction. Hemorrhages into the gums, nose, retina? 
and intestines are infrequent. The skin is pale, cyanotic, damp and 
sudaminous. Herpes may be observed, as well as rose spots, petechia? 
and terminal edema ; miliary tubercles in the skin were found by Tileston, 
especially in children; the pin-head eruption is a red papule, becoming 
vesicular and finally encrusted and appears in crops on the buttocks, 
thighs and genitalia; in 71 per cent, the tubercle bacillus was found. 

Remissions may occur, even for a month or two, the toxemia subsiding 
while the tubercles continue to develop. The fall of the fever resulting 
from brain implication may be deceptive. As a rule the course is acute, 
even stormy or peracute, and death may occur before the tubercles have 
time to form. Severe infection is fatal in two or three weeks, moderate 
infection in one or two months. Chronic miliary tuberculosis is rare. 
Recovery is almost impossible; Waller and others believe that it excep- 
tionally occurs, even with bacilli in the blood. Therapy is unavailing; 
symptoms should be treated expectantly, as in typhoid or meningitis. 

II. Tuberculous Meningitis. — Etiology. — Most cases occur between the 
second and tenth years (75 per cent.), some in adolescence and few late in 
life. Tuberculosis in children is usually generalized, and miliary tubercu- 
losis is in 80 per cent, associated with meningeal disease. Tuberculous 
meningitis is always secondary to pulmonary or glandular tuberculosis, 
less frequently articular, genito-urinary, cerebral and other localizations. 
Measles, whooping-cough, typhoid or pneumonia may seemingly arouse 
latent tuberculous foci. Trauma is of occasional clinical and medico- 
legal importance. In the case of a baggage man thrown upon his occiput 
an acute tuberculous meningitis resulted in death; the autopsy disclosed 
an apical focus, from which the bacilli infected the injured brain. In 
one instance, meningitis and coma followed an anesthetic, given to 
examine a tender spine, and was fatal within a week. 

Pathology. — The diagnosis is made macroscopically in the majority 
of cases. The exudate is gray, yellow or green, gelatinous, purulent or 
serous and covers the base from the chiasm to the medulla (basilar 



PLATE VI 







Retinal Findings in the More Important Diseases. 

Q. Tubercles in choroid.. 7. Syphilitic ehoroidoretimtis. 8. Albuminuric 
retinitis. 9. Hemorrhages in pernicious anemia. (From Sahli.) 



TUBERCULOSIS 151 

meningitis) . Tiny tubercles are found on the nerves and along the Sylvian 
artery where "they look like lice eggs on a hair." Careful search is some- 
times necessary for their detection. They are more clearly seen in the 
translucent arachnoid, and on superficial examination look like minute 
air bubbles. They are seen frequently over the convexity or between the 
two hemispheres. The ventricular fluid is increased and tubercles and 
inflammation of the ependyma are not uncommon; the external and 
internal communications of the ventricles may be obliterated. The 
substance of the brain shows ischemic or encephalitic softening. The 
cerebrospinal fluid is increased and is clear or cloudy, rarely purulent. 
In the cord the exudate may be a quarter of an inch in thickness, and 
is largely disposed over the posterior part of cord because of the patient's 
dorsal decubitus; the membranes sometimes appear granular, as " though 
sown with fine sand." Wartmann found tubercles in the substance of 
the cord in 87 per cent, of his cases. The cranial and spinal nerve sheaths 
are bulging. Microscopically, exudation is found. The nodes are proved 
to be tubercles; bacilli are found in them and in the cerebrospinal fluid. 
The microscope in some cases proves the existence of tuberculous menin- 
gitis not visible to the naked eye. Neuritis of the cranial and spinal 
nerves is constant. The optic, oculomotor and facial nerves are the 
most often affected. The usual histopathology of tubercle is seen with 
tuberculous endarteritis and periarteritis, small encephalitic and myelitic 
foci, swelling of the neuroglia and degeneration, especially of the axis- 
cylinders. 

Symptoms. — Prodromes are more prominent in children than adults; 
fever, emaciation and anemia are due to preexisting lung or glandular 
tuberculosis. Irritability, change in disposition, tendency to cry, in- 
ability in children to play or in adults to work, unrest, insomnia and 
headache may develop in a week to three months. Trauma, measles 
or pertussis may be the inciting cause. The onset, in 86 per cent, develops 
more gradually than in the epidemic form, so that the classical description 
comprises three stages: (a) The stage of irritation, with headache, vomit- 
ing, remittent fever reaching 102°, the cri hydrencephalique of Coindet, 
night terrors, pain and rigidity in the neck and spine, small, irregular 
pupils, delirium, grinding of the teeth, hyperesthesia, rigidity of the 
limbs, the neck sign (page 91) and Kernig's sign (in 22 of Koplik's 
82 cases); (6) the stage of brain pressure, with paralytic and irritative 
conditions in the eye muscles, as ptosis or strabismus; with paralysis 
of other cranial nerves or monoplegia or hemiplegia from involvement 
of the cortex, and frequently aphasia and dulness; with general or 
Jacksonian convulsions ; slow, irregular and variable pulse ; retracted ab- 
domen, constipation, continued vomiting; sighing respiration; and very 
frequently with optic neuritis; and (c) the stage of paralysis, in which 
the vomiting and often the headache cease, absolute coma develops, 
and the rapid pulse vacillates in rate and rhythm. Biot's alternating 
apnea and hyperpnea or Cheyne-Stokes's breathing appears, emaciation 
is extreme, the pupils are wide and immobile, the eyeballs roll upward, 
and a typhoid state with dry tongue or abdominal distention prevails. 
Temporary remissions of days or weeks are occasional, in which the 



152 ■ BACTERIAL DISEASES 

pulse remains irregular, but the patient lapses again into coma, the fever 
rises very high (107°) or falls low (even to 93°), and death occurs in some 
weeks from cardiac or respiratory failure, dysphagia or inanition. This 
division into stages is not wholly satisfactory, because the stages may 
overlap but the progression of symptoms is somewhat as described. 

Tubercles in the choroid are found clinically by Eichhorst in 17.5 per 
cent, of cases. Heinzell did not find them in 41 cases. At postmortem 
examination Litten found them in about 75 per cent. (See Plate VI.) 
Leukocytosis is absent and the spleen is enlarged in 33 per cent. 

Many variations exist. The process may be wholly latent, being 
masked by miliary tuberculosis (or meningeal symptoms may dominate 
when the greatest pathological changes are in the lungs). Coma may be 
sudden, resembling apoplexy, especially in adults; in these cases the 
hemiplegia probably results from changes in the arteries. Only rarely 
is the course very chronic. It may appear to be a psychosis. In adults 
the course is more rapid, the headache and delirium more marked and 
the convexity more frequently involved than in children. In Holt's 
series, three-quarters of sporadic meningitides were tuberculous and 
most arose from contact with infected adults. 

Death is usual, but Bokay collected 37 undoubted recoveries (1914). 
(See Cerebrospinal Fever for differentiation and treatment.) 

III. Tuberculosis of the Lungs (Phthisis, Consumption). — The lungs 
are involved with great frequency, not because they are peculiarly 
susceptible, but because aerogenous infection is the most frequent cause 
of tuberculosis. Hematogenous infection, as in miliary tuberculosis, 
and lymphogenous infection also occur. 

Pathology.— The tubercle bacillus localizes in the bronchi (tuber- 
culous lymphangitis), bronchioles or alveoli (tuberculous pneumonia), 
and causes tubercles as described in the general pathology. There 
is cellular hyperplasia of the alveolar, epithelial and endothelial cells, 
and fibrinous inflammation develops. Isolated tubercles, by fusion 
cause the conglomerate tubercle. 

Extension. — (a) Lymphatic extension is the most common form. In 
young individuals the lymph paths are wider and absorption greater, 
so that intoxication and bacillary migration are more active. Absorption 
is greater after trauma, pneumonia, measles, pertussis, emaciation, e. g., 
as convalescing typhoid, etc. Bacilli may pass the bronchi and reach 
the glands at the hilum, which in turn may infect the blood or break 
into the lung. Extension is usually along the lymph vessels in the 
bronchial walls (lymphangitis tuberculosa). (b) Extension by the 
air passages is common; when a tubercle ruptures into the bronchi, its 
contents may be coughed or waved upward by the ciliated epithelia if 
they are intact; on the other hand, a deep breath may aspirate, or cough- 
ing may impel, infected particles into sound areas, where they develop 
new foci; if the bacilli are living, an active tuberculosis develops; if 
dead, a lobar or lobular pneumonia is more common, (c) Extension by 
the bloodvessels may cause a miliary dissemination in the lungs or in the 
entire body. Preliminary to the clinical description in which special 
pathological features will be described, it may be said that some caseated 



TUBERCULOSIS 153 

areas fuse into large infiltrations; some encapsulate or calcify and thus 
effect a temporary arrest or a permanent recovery; other caseated areas 
soften, forming ulcers and cavities. 

Symptoms. — A clinical description covering all types is impossible, 
as the course may be galloping or extremely chronic; one form is marked 
pathologically by caseation, another by ulceration; one symptom, as 
hemoptysis, may indicate the type and may be the first and chief symp- 
tom; in some persons the symptoms suggest other diseases and the 
physical findings are indeterminate ; in others the findings are remarkably 
dissociated from the usual symptoms. Therefore the symptoms and 
signs usually found will be covered first and the special types will be 
dealt with afterward: 

1. Local Respiratory Symptoms. — These are usually the first noted, 
but may only appear months after the primary focus has begun to spread ; 
they are due to the local tubercle and its toxin. 

(a) Cough. — Cough is one of the first symptoms and is the most constant 
symptom; it is usually present from the incipiency to the close of phthisis. 
It is due to toxins irritating the vagus twigs, which irritation is referred 
to the medulla, from which issue muscular contractions with the glottis 
closed, to evacuate the slight secretion; the sensitive inter arytenoid 
space and tracheal bifurcation initiate this reflex. Less often coughing 
is due to pleurisy, pharyngitis, enlarged bronchial glands or laryngitis. 
It is slight at first, and has no characteristic, other than being dry, 
difficult and paroxysmal. Later it becomes more frequent but less 
difficult as the secretion increases. In some cases it is most severe in the 
morning, the secretion having accumulated over night, while in others 
it is most severe at night, for the lungs become congested by the dorsal 
decubitus; saliva reaching the larynx during the night, may cause a 
sudden explosive cough. It is provoked by dust, smoke, variations in 
temperature, opening windows or getting into the cool bed, by exertion, 
laughing or taking alcohol. It is less conspicuous in the phlegmatic, 
aged and insane. When obstinate it may invoke constant vomiting and 
induce great emaciation. 

(6) Sputum. — The sputum is first caused by the toxins, and later 
by the secretion from the tuberculous focus. At first it is glairy and 
contains myelin, sago-like bodies composed of transformed alveolar 
cells. It later becomes yellow from admixture of pus, yellow, green or 
red from saprophytic organisms, and blood may give it a red, rusty, 
flesh-like or chocolate hue. Other bacteria and saprophytes are frequent 
(v. Bacteriology). It tastes sweet and smells slightly fetid. Its amount 
varies from a few globules to over a pint. It is most abundant in cavities; 
it stagnates before death, because of the patient's muscular weakness; 
children are prone to swallow the sputum. Nummular sputum from 
cavities is flat, " coin-like," greenish-gray, extremely abundant and sinks 
in water, as it is airless; it occurs in other cavities as in bronchiectasis. 
The only characteristic of the sputum is the tubercle bacillus (v. s.); it 
may be seen before the advent of any physical finding, but in other 
cases it must be sought repeatedly, as it appears only when ulceration 
communicating with a bronchus develops. The tubercle bacillus is found 



i54 BACTERIAL DISEASES 

in only one-third of the cases of incipient tuberculosis. Falk and Tedesko 
found that salicylic acid may be detected, after administration by the 
mouth, in any of the serous fluids and inflammatory exudates, but not 
in the saliva or bronchial secretion. If found in the sputum it is believed 
to be evidence of involvement of the lung substance itself. Elastic fibers 
are found in 80 per cent., and originate from the vessels or parenchyma 
of the lung. They are elongated and twisted, and sometimes shreds of 
the vessel wall are seen; those from the lung substance often show its 
alveolar arrangement. Elastic fibers can often be located by flattening 
the sputum between two plates of glass and picking out the yellowish 
areas for microscopic examination. Treatment with caustic potash and 
centrifuging, facilitate their detection when they are scanty. They 
merely denote a destructive process, hence are also found in abscess, 
gangrene, infarction and pneumonia (see Plate V). Detritus, pus cells, 
red cells, alveolar, bronchial and buccal epithelium, myelin droplets 
and pigment, are also found. The so-called lung calculi are sometimes 
voided; they are calcified particles from old areas of caseation, from 
bronchial obstruction, or from peribronchial lymph glands; from the 
glands large calcareous masses may cause fatal obstruction of the trachea, 
or suffocation may be averted only by immediate low tracheotomy. 
The significance of albumin in the sputum, emphasized by Roger and 
Levy-Valensi, is not great. 

(c) Hemoptysis. — Hemoptysis (hsemoptoe, spitting of blood) occurred 
in 37 per cent, of Prior's 1000 cases; others place it at 66, even 90 
per cent.; it is most frequent in adult males and is rare before puberty. 
(a) Early hemoptysis is due to erosion of a small vessel by tubercles in its 
perivascular lymph sheath. The toxins, by causing coagulation in the 
vessels in and near the affected lung area, usually prevent extensive 
early hemorrhage. Hemoptysis is the first symptom in 4 per cent, of 
phthisis cases and in 16 per cent, the only symptom; in most cases, 
however, other symptoms develop; bacilli and elastic fibers may be 
seen at the time of bleeding. Reiche recently corroborated the old 
statement that early hemoptysis is not unfavorable. The bleeding 
develops in quietude in 66 per cent, of cases but may be induced by 
coughing, laughing, exertion or excitement; there may be a premonitory 
rise of blood-pressure. Often without cause, it comes on suddenly with 
a warm, salty taste in the mouth and the evacuation of a dram or more of 
bright frothy blood, clear or mixed with mucus; small particles of darker 
blood are brought up, for a few days, after which it disappears; in 
4125 of the Brompton Hospital cases, 69 per cent, evacuated less than 
half an ounce. Bubbling rales may be heard on the side of the lesion, 
and moulds of the bronchioles may be voided. F. Strieker collated 900 
cases of hemoptysis in the German army; in 480 cases there was no 
apparent cause and of these 87 per cent, were tuberculous; of 43 cases 
brought on by exertion, 74 per cent, were tuberculous; and of 24 cases 
due to trauma, half were tuberculous. The occurrence of early hemor- 
rhage, before other symptoms of phthisis, led Hippocrates, Boerhaave 
and Van Swieten to think that hemoptysis caused phthisis, while Laennec, 
Louis and Traube correctly regarded it as a symptom of already estab- 



TUBERCULOSIS 



155 



lished phthisis; the earlier idea is explained by the fact that blood and 
bacilli may be aspirated into other parts of the lung, in which the process 
develops anew; fever, rapid pulse and dyspnea following hemoptysis 
are ominous (v. i. Acute Forms), (b) Late hemoptysis may be slight or 
profuse. Profuse bleeding is usually due to erosion of aneurysmatic 
bloodvessels running across, or in the walls of cavities (Rasmussen); 
Kidd found ruptured aneurysms in 70 of 82 fatal cases; occasionally 
larger vessels, as the pulmonary artery, are ulcerated. A pint or a quart 
may spurt out of the mouth causing acute anemia, suffocation or rapid 
exsanguination. Blood may accumulate in large cavities, never reaching 
the air passages. Hemoptysis is usually a sign of tuberculosis but also 
occurs from other causes (v. Diseases of the Lungs). 

(d) Dyspnea. — Just as it is absent in pleurisy of. gradual onset, it is 
often absent even when the respiratory area is enormously contracted 
(great infiltration, great cavity formation or induration of two-thirds 
of the respiratory space); in sudden miliary tuberculosis the dyspnea is 
great. In some cases dyspnea may follow pressure of glands on the 



104 


DAY 1 


2 


3 


4 


5 


6 


103 














102 














101 














100 














99 




























98 















Fig. 13. — Hectic fever curve in phthisis. 



vagus, stagnating secretion, extensive vicarious emphysema or massive 
pleural adhesions, yet it is most often due to the rapid heart action. In 
the last stages it may cause orthopnea and result from intercurrent 
pneumonia or pneumothorax. Germain See described a tuberculous 
pseudoasthma. 

(e) Pain. — Pain is observed in 66 to 75 per cent, of cases. Its location 
may be apical, diaphragmatic, anteriorly from the clavicle to the third 
rib or under the scapula. Its character is sticking and intermittent, 
but not intense; the skin is often hyperesthetic. Its cause is chiefly 
acute pleurisy, for lung disease and chronic pleurisy are generally painless; 
other causes are muscular fatigue from coughing, intercostal neuralgia 
and pneumothorax. 

2. General Symptoms. — These result from absorption of the toxins 
secreted in the local lesions. 

(a) Fever. — This is present in the great majority of cases and is almost 
invariable in the early stages. Probably the dominant cause is the 
tuberculous toxin. Fever marks the tubercle formation, fusion of foci, 
advance of the disease, degeneration of the tubercle, and probably 



156 BACTERIAL DISEASES 

secondary infection, though the associated streptococci are usually far 
from virulent. Enzymes and their action upon the body cells (auto- 
lysis) may be causative. The cessation of fever is synchronous with 
temporary or permanent arrest of the disease, as manifested by improved 
health, strength and weight. It is easily increased by exercise, excitement 
or trivial causes. 

Types. — There is no typical curve nor can fever be classified as initial 
or ulcerative fever. The vesperal hectic is the most common curve, 
and indicates slow disintegration and absorption of toxins. Intermittent 
fever may resemble malaria and usually indicates rapid and marked 
tissue-disintegration; remittent fever most often occurs late in the 
clinical course; continuous fever occurs early or in acute consumption, 
but rarely resembles the typhoid curve; in some unfavorable cases the 
fever falls from high to subnormal registers, sometimes with collapse; 
the typus inversus with morning exacerbation and vesperal fall is very 
uncommon. Fever may be absent in patients with old cavities and 
fibrous induration. Chills have no relation to the fever or its intensity. 
As fever is indicative of toxemia, it is often associated with anorexia, 
accelerated pulse and emaciation. 

(b) The Blood. — (i) The red cells rarely number less than three 
million; anemia may antedate all other symptoms, whence the frequent 
confusion with chlorosis. Rarely severe anemia of the aplastic form 
or with hemolytic icterus develops. Again, anemia may be incon- 
spicuous or late. In some cases the red cells are increased, notably 
in individuals prone to hemoptysis, (ii) The hemoglobin averages 
75 per cent.; it may be decreased more than the number of red cells 
(chlorancemie tuberculeuse) . (hi) The leukocytes may be normal; they 
are increased in cavity formation (secondary infection), caseous pneu- 
monia or protracted pyrexia; after injection of tuberculin the eosinophiles 
show a decided increase. Steffen holds that the lymphocytes are increased 
early and the polynuclears later (mixed infection), (iv) Recent reports 
of positive bacillemia are ascribed to acid-fast bacilli in the water employed 
in staining. 

(c) Sweating. — Night sweats, more important than in any other dis- 
ease, occur in 90 per cent, of cases (Louis), and are due to the action 
of toxemia on the sweat-centre. Heavy coverings sometimes induce 
sweating. The term " night sweats" refers to their usual occurrence 
between 2 and 5 a.m. They are more frequent in acute than in chronic 
phthisis, in younger than in older subjects, when cavities are forming 
and the fever is variable. 

id) Pulse. — The rapid pulse is associated with indigestion, muscular 
adynamia and malnutrition (v. page 166). 

3. Physical Signs. — In adults the apex of an upper lobe, more often 
the right than the left, is first affected (Laennec) . The reasons ascribed 
are various, such as a poor apex blood supply, slower lymph current 
and less expansion — which are scarcely proved. More probably cough- 
ing drives infection upward from the bronchi, and the clavicle or first 
rib compresses the bronchi passing to the apex and thus lessens its venti- 
lation. The summit of the apex is not invaded first; Birch-Hirschfeld, 



TUBERCULOSIS 157 

in early cases which died from causes other than tuberculosis, found that 
in 24 per cent, the disease began iu the fourth or fifth order of bronchi 
in the upper lobe and that the posterior were affected earlier than the 
anterior divisions. 

(a) Inspection. — (i) The nutrition may be good, but, later, emaciation 
is marked. The face is pale, the cheeks hectic, the nose pointed, the 
eyes hollowed and glistening, the neck thin and the chest is altered in 
various ways; in some cases it is long and narrow, with wide interspaces, 
sharp costal angles, prominence of Louis's angle, atrophy of the scapular 
muscles and more vertically directed ribs; in others it is flattened 
anteroposteriorly and the ribs are closely apposed; in still others the 
funnel-chest may be seen. Laennec recognized that the " paralytic 
chest" was the result and not the cause of phthisis. Examining the 
patient in a good light, the following may be noted: (ii) Deficient ex- 
pansion above or below the clavicles, especially when examined from 
behind and above; in the lower chest, impaired excursion of the dia- 
phragm. Deficient expansion may be due to pleural adhesions, to atel- 
ectasis of the lung resulting from caseous nodes obstructing the bronchi, 
to a cavity, or to induration, an effort toward encapsulation and recovery. 
(iii) Distention of the chest may be due to vicarious emphysema, effusive 
pleurisy or pneumothorax, (iv) The cardiac impulse may be widened 
by retraction of the left lung away from the heart. 

(b) Palpation. — Palpation shows (i) decreased expansion, elicited by 
standing behind the patient with the thumbs above either clavicle and the 
fingers below it, or by standing in front of the patient and spreading the 
hands over the anterolateral parts of the thorax, (ii) Increased vocal frem- 
itus, obtained when the lung is infiltrated (caseous foci or pneumonia), 
indurated or the seat of cavities, all of which increase conduction of the 
voice-sounds from the bronchi. Superficial show more clearly than deep 
lesions; thick, pleural adhesions or plugging of the bronchi with caseous 
material decrease the fremitus, (iii) The systolic distention of the 
pulmonary artery and the second pulmonic closure are better felt when 
the lung retracts from the heart or when it is infiltrated in its vicinity. 
(Pottenger describes intercostal rigidity over the disease focus.) 

(c) Percussion. — (i) Incipient infiltration gives a short percussion note, 
which later becomes dull; the apex is first involved in 88 per cent, of 
cases. Dulness may be found under the middle of the clavicle, at which 
level Birch-Hirschfeld found the anatomical beginning of tuberculosis. 
The apices are best percussed when standing behind the patient; the 
right apex is normally less resonant than the left. The lung lying behind 
the clavicle can be tested by gently tapping the clavicle with one finger. 
To detect slight early alterations in note, percussion should be gentle, 
symmetrical parts should be compared, the patient should hold his 
breath in full inspiration and the muscles must be relaxed ; each patient 
has his own percussion note, varying with his muscle, fat and bone. The 
apex reaches 1 to 2 inches above the clavicle, and behind to the vertebra 
prominens. A focus as large as a cherry may cause dulness, but usually 
impaired resonance is produced only by consolidation measuring 1J by 
2\ inches in area and within f inch of the surface, and foci of these 



158 BACTERIAL DISEASES 

dimensions lying deeper than 2 inches escape detection. Small, multiple 
or deep foci give a tympanitic note. The dulness may extend from the 
clavicle to the second and third costal cartilages, then to 1.5 inches below 
the apex of the lower lobe (level of the fifth dorsal vertebra) ; this area 
is almost always involved when the upper lobe shows distinct con- 
solidation; extension occurs outward and downward along the interlobar 
fissure; then it extends to the apex of the upper lobe on the other side. 1 
Often the first dulness of consolidation is found behind, in the supra- 
or interscapular region, (ii) Shrinking, fibrous induration and a thick- 
ened pleura give apical or other dulness. Sometimes the lung becomes 
vicariously emphysematous about an old focus which is thus hidden 
clinically and pathologically, (iii) A tympanitic or cracked-pot resonance 
may be obtained over cavities (v. i.). 

(d) Auscultation. — This is the most important aid, next to the micro- 
scopic examination of the sputum, (i) The vesicular murmur, especially 
at the apex, is altered, for detection of which the patient is best examined 
without deep breathing or coughing; the jerky "cog-wheel" breathing, 
described by Jackson (1833), may be due to small tubercles in the bronchi, 
somewhat stenosing their lumina; it also occurs in normal individuals 
from forced, muscular breathing, or pounding of the heart on the lung 
during inspiration. The breathing may be wavy, weak, indeterminate 
or puerile. Rude, rough inspiration is due to peribronchial tubercles 
compressing the bronchioles. The expiration is frequently prolonged, 
rougher and higher pitched, in apical "catarrh;" it is long, sharp and 
bronchial, in older foci; what seems clinically to be catarrh is often 
consolidation pathologically. In comparing the breathing, inspiration 
on one side should be compared with that of the other, and expiration 
similarly noted. The breath-sounds are physiologically higher pitched 
on the right than on the left side, (ii) Bronchial breathing is caused by 
various consolidations (tuberculous, pneumonic, neoplastic or gangrenous) 
and by cavities, tuberculous and otherwise. Bronchial breathing of 
moderate degree is physiological in the interscapular region, but is less 
intense than that of consolidation, (iii) Rales are rather an evidence of 
infiltration (consolidation) than of " catarrh." If they are heard in the 
apex, the presence of tuberculosis should be suspected, though they may 
occasionally occur there physiologically, or after influenza. The vibra- 
tions of the accessory muscles of respiration, when the patient takes a 
long forcible breath, are easily differentiated from rales after a little 
experience. Rales may not be heard unless the patient breathes deeply 
or coughs; auscultation should be made before, and then after, coughing 
noiselessly and inspiring with the least muscular force. In incipient 
consolidation, small, crackling, crepitant rales are heard over the alveoli 
and smaller bronchioles at the end of inspiration; they later become 
larger, ringing and resonant, indicating that the alveoli and bronchioles 
have become airless over a considerable area, or that softening or forma- 
tion of cavities is in progress; scattered, clear, large, crackling rales are 
heard over small cavities in the apex or the smaller bronchi, and indicate 

1 there is a non-tuberculous shrinking of the right upper lobe, in mouth-breathers, due 
to collapse of the apex [Kronig], or to tuberculous glands about the right bronchus (Bing) 



TUBERCULOSIS 159 

a viscid secretion. Clicking rales are generally attributed to softening; 
they may occur near the heart as it beats upon an adjacent infiltration. 
Gurgling and consonating rales suggest cavity or bronchiectasis. In 
emphysematous patients, whose chests exhibit sibilant and bubbling 
rales, diagnosis of developing tuberculosis may be most difficult, (iv) 
Bronchophony (a bronchial quality imparted to the voice-sounds) is 
heard when the patient speaks during auscultation; it indicates infil- 
tration or cavity formation but is absent when the bronchi are plugged. 
Often testing the whispered voice is of value. Egophony is merely a 
higher grade of bronchophony and occurs as Skoda demonstrated, in 
cases of consolidation, in medium-sized cavities and above pleural exu- 
dates, (v) Pleural friction results from fibrinous pleurisy or rough 
turbercles in the pleura, (vi) A systolic bruit over the subclavian artery 
is probably due to pleural adhesions to the artery. 

(e) Rontgen Rays. — Shadows may be due to consolidation, thick- 
walled cavities, calcified foci, gangrene, pleural callus or pleural exudate. 
The excursion of the diaphragm can be followed; shadows, due to the 
muscles, may be readily eliminated by moving the arms. 

Summary. — The above findings may be grouped together, because they 
are found together clinically, one part showing consolidation, another, 
cavity formation or induration, (a) The signs of consolidation are 
decreased expansion, increased vocal fremitus, initial tympany followed 
by dulness, high-pitched expiration, then distinct bronchial breathing, 
crepitant rales and bronchophony, (b) The signs of induration are re- 
traction or lagging behind of the fibrous area on breathing, increased 
vocal fremitus, dulness, usually large rales, bronchial breathing and 
bronchophony, (c) The signs of cavity formation are: (i) Increased 
vocal fremitus, if it is near the surface; (ii) tympanitic note, which 
may increase in intensity when the cavity is percussed with the mouth 
open (Wintrich's change of note), when percussed during inspiration 
(Friedreich's change of note), or with the patient in the sitting posture 
(Gerhardt's change); the note may be metallic; the cracked-pot note, 
Laennec's bruit de pot fele, is obtained in cases of superficial cavities 
measuring 2 J inches with thin walls, which communicate with an open 
bronchus by a small opening; variation in the percussion note from 
accumulation (dulness), or emptying of secretion (tympany), is most 
suggestive of cavity formation; percussion may cause the patient to 
cough and void much sputum; (iii) the breathing, which is loudly 
bronchial, or if the cavity is quite large, metallic, amphoric or metamor- 
phosing (which begins normally and suddenly becomes bronchial or 
vice versa); (iv) bronchophony and egophony; (v) large, resonant rales, 
which are the most frequent and important finding ; metallic rales in the 
apices are most suggestive of cavities; they may acquire an amphoric 
character in very large, thin- walled excavations; (vi) nummular sputum; 
(vii) systolic, sometimes booming or metallic murmurs, due to propagation 
of the heart tones; they may be heard at some distance from the patient. 

Cavities are due to the breaking down of caseous areas and are 
usually connected with the bronchi, into which their emptying is partly 
favorable, in that the infective material is evacuated; and partly un- 



160 BACTERIAL DISEASES 

favorable, because it opens up avenues for infection by aspiration. Once 
formed, they generally remain or increase; they may leave fistulous 
cicatrices (Laennec's cicatrices fistuleuses) ; if they are held by adhesions 
the cavities persist, contracting cicatrization being impossible; there is 
danger of their further extension by secondary infection, or of gangrene. 
The cavity has a well-marked limiting membrane, from which pus, 
nummular sputum, elastic fibers, and grayish, granular detritus composed 
of masses of tubercle bacilli are voided; the cavities are frequently 
multilocular, may heal on one side and extend on another, and sometimes 
occupy an entire lobe or even an entire lung. They may rupture into the 
pleura, pericardium or bloodvessels; the author saw a rupture into the 
mamma, resulting in diffuse subcutaneous emphysema. 

Stages of Pulmonary Tuberculosis. — Tuberculosis usually proceeds for 
six to eighteen months before any symptoms appear. 

1. Phthisis Incipiens. — The general and local symptoms appear as 
above described, with fever, anemia and rapid pulse. The modes of onset 
are various. The most frequent picture is that of a patient with an 
obstinate cold or a " grippe" which does not regress; the sputum may show 
tubercle bacilli and the apex some rales. In others, disordered digestion 
and a rapid pulse awaken suspicion. The voice may be lost, passing 
as a simple laryngitis. There may be only a moderate depreciation 
of health, languor and neurasthenic manifestations; in young girls a 
chlorosis may be hastily diagnosticated. Malaria is a common escape 
in explaining an obscure fever. Tuberculosis may appear in other more 
directly suggestive forms, such as hemoptysis, pleurisy or cervical adenitis. 
The physical findings are often uncertain or absent. 

2. Phthisis Confirmata.- — Distinct physical findings indicate not 
incipient phthisis, but confirmed, established phthisis. 

3. Phthisis Consummata. — This is advanced consumption, with 
marked hectic fever, cavity formation and emaciation. 

Course. — The average case of "chronic ulcerative phthisis," with 
the symptoms and signs already described, stands midway between the 
following very acute and extremely chronic groups: 

1. Acute, Galloping or Florid Consumption. — This type con- 
stitutes 10 per cent, of phthisis and develops from some old focus, as 
tuberculosis of the bronchial glands, or a small cavity which by intra- 
bronchial rupture disseminates the process; possibly the virulence of the 
germ is greater in these cases; diabetes, alcoholism, measles, ivhooping- 
cough or influenza, may be the immediate cause. 

(a) Acute Pneumonic Form. — The acute pneumonic form is acute 
caseous pneumonia. This term indicates the great clinical resemblance 
to, and confusion with, acute lobar pneumonia; but it must be remem- 
bered that genuine lobar pneumonia does not caseate, and that this 
form is not synonymous with tuberculosis complicated by pneumococcic 
pneumonia, which, in this association, runs its usual course. Acute 
caseous pneumonia begins in an individual in seemingly perfect or but 
slightly reduced health. An initial rigor is fairly common, or spitting of 
blood may be the first .symptom. There are often herpes, cough, pain 
in the side, rapid breathing and sudden fever, which frequently imitate 



TUBERCULOSIS 161 

exactly the onset of genuine pneumonia. The resemblance may persist 
but often certain variations arouse suspicion. The fever is remittent or 
intermittent, and more variable than in lobar pneumonia; dyspnea and 
cyanosis are less frequent than a gradually increasing pallor; sweating 
is usually copious. In a few days dulness prevails over a lower lobe but 
much more often over an upper lobe or over an entire lung. The breathing 
at first indistinct, may remain so, but often becomes bronchial. The 
sputum is often typically pneumonic, viscid and rusty, or of an olive or 
grass-green color; elastic fibers are seldom found. Tubercle bacilli are 
sometimes found, but in this case originate not from the fresh pseudo- 
pneumonic patches, but from the causal focus; in few cases can the 
physical signs of the primary cavity in an upper lobe be elicited. The 
physical findings change but little, though the crepitant rales are replaced 
by coarse mucous rales; the anticipated crisis does not occur, and most 
cases are called unresolved pneumonia until the increasing anemia, loss 
of strength or rapid pulse, suggests tuberculous pneumonia. Albuminuria 
is uncommon; the diazo reaction is present. Five-sixths of the cases 
die within six weeks ; in some few cases considerable regression may occur 
and it is barely possible for the course to last three months or more. 
The findings at autopsy are an old focus of tuberculosis, a ruptured cavity 
or gland; from it caseous material, containing bacilli and tuberculous 
toxins, is aspirated into many finer alveoli and bronchioles, where it 
excites a miliary, caseous, lobar pneumonia. The inflammation is due 
wholly to Koch's bacillus or its toxins, and is (i) partly fibrinous and 
desquamative, red and white polynuclear and mononuclear cells being 
poured out; proliferative changes are noted, as the epithelioid and giant 
cells seen in the typical tubercle; caseation ensues, as shown in the 
already fused and fusing yellowish-gray areas; (ii) the most rapid exuda- 
tion is serous, Laennec's "gelatinous or smooth pneumonia," probably 
due to the tubercle toxins and not to mixed infection; this part of the 
inflammation may regress without caseation. Cavities rarely form in 
this type. 

(6) Acute Disseminated Form. — It may occur as a special type, or may 
complicate the ordinary form of phthisis. Following the rupture of a 
small area of softening, usually located only at the postmortem, and 
following dissemination by aspiration, there develop (i) fever, repeated 
hemoptysis, chills, rapid pulse, increasing dyspnea, diffuse crepitant or 
bubbling rales, delirium, or even a status typhosus, (ii) The sputum 
is absent or scanty, and the bacilli are sometimes absent throughout 
the course. Death may occur acutely in three or four weeks without 
physical signs having appeared and without breaking down of the foci; 
or a remission may take place, after which there is (iii) breaking down 
of the indistinct foci which cause slight dulness and distant bronchial 
breathing, simulating lobular pneumonia. At autopsy scattered, yellow, 
partly caseous, peribronchial, nodular foci are seen; in some cases the 
presence of tuberculosis is proven only by microscopic examination, for, 
without caseation, the foci may resemble ordinary bronchopneumonic 
patches; secondary infection with streptococci is said to cause these 
lesions, but they result from the tubercle bacillus alone. 
11 



162 BACTERIAL DISEASES 

(c) Acute Disseminated Ulcerative Form. — This type is often observed 
in children between two and six years of age, in pregnancy, alcoholism, 
diabetes and influenza. The foci, which vary in size from a pea to a 
walnut, are widely disseminated; they fuse, soften early and develop 
cavities without walls, which are only ulcers or necrotic caseous material. 
There are present clinically hectic or continuous fever, - pronounced 
anemia, exhausting sweats, rapid emaciation and viscid, purulent and 
bacilli-laden sputum ; diffuse, fine and large rales and bronchial breathing 
may be heard, but the physical signs are often vague. The galloping 
course ends fatally in one to four months. 

(d) Acute Miliary Form. — Acute miliary tuberculosis (q. v.) develops 
in 3 per cent, of cases of pulmonary phthisis. 

2. Chronic Tuberculosis. — (a) Chronic Ulcerative Form. — The 
ordinary phthisis may run a course which is long latent, except for 
anemia, dyspepsia or other indistinctive symptoms. After the detection 
of an apical catarrh, the cough, fever, sweats and anorexia may subside; 
another relapse may occur after years of quiescence, or exacerbations 
develop, with loss of weight and strength. Recovery may occur, even 
with pronounced physical signs. New tuberculous manifestations may 
be reinfections rather than relapses. 

(b) Phthisis Fibrosa. — The fibrosis excited by the tubercle bacillus 
may begin acutely or insidiously. Auclair thinks the bacillus secretes 
two toxins, one with a necrosing action which leads to caseation, and 
another with an indurating action which leads to fibroid phthisis. 
There may be no cough, sputum, bacilli, fever, emaciation or anemia. 
Ulceration may result only from mixed infection. Sometimes there is 
hemoptysis. If left-sided, the spleen rises higher and the retraction of the 
lung away from the heart makes the cardiac shock more diffuse, and the 
pulsation of the pulmonary trunk more visible. If right-sided, the liver 
rises, the right ventricle is apparently enlarged (from lung retraction) 
and is often actually hypertrophied and dilated from increased tension 
in the pulmonary circuit. The heart may be drawn to the right or left 
by the inevitable pleural adhesions, bronchiectases are not uncommon, 
the sound lung is vicariously emphysematous, and the diseased lung is 
smaller, flatter and depresses the shoulder, impairing expansion and often 
presenting bronchial breathing and large rales. 

(c) Pleuritic Form. — The pleuritic form follows small latent feci 
in the lungs, lymph glands, etc. (See Pleurisy.) Exudates not due 
to rheumatism, inflammation in contiguous organs or tumor always 
suggest tuberculous pleurisy. Pleurisy, in fact, more often precedes 
than succeeds pulmonary tuberculosis and repeated attacks are frequent, 
with moderate, irregular or continuous fever, perhaps with rales in the 
apex of the affected side (not the rales frequently heard just above the 
upper level of the exudate), or with dulness in the contralateral apex. 
Bowditch, following up 90 cases of pleurisy, found that 33 per cent, 
developed phthisis. 

Variations According to Age. — 1 . Children. — Tubercle bacilli pass the 
bronchial mucosa and produce tuberculosis of the bronchial and medi- 
astinal glands; the wide lymph vessels and more active metabolism have 



TUBERCULOSIS 163 

already been noted; the process in the glands attacks secondarily the 
hilum of the lung and the lower lobes (90 per cent.), which explains the 
frequency of miliary tuberculosis from involvement of the thoracic duct 
and bloodvessels. 

(a) Chronic Generalized Tuberculosis. — The younger the child the 
more general is the tuberculosis. Measles, pertussis and influenza are 
prone to arouse a latent tuberculosis in the bronchial glands. The course 
is generally more active than chronic, like that of tumors in children. 
Emaciation, anemia, enlargement of the spleen and liver, and moderate 
intumescence of the peripheral lymph glands are the variant features of 
this type. Hectic fever is seen chiefly in children over three years. The 
sputum is swallowed, but washing the stomach recovers bacilli-laden 
sputum. 

(b) Acute Miliary Tuberculosis (q. v.). 

(c) Localized Lung Tuberculosis. — (i) The acute caseous type resembles 
pathologically bronchopneumonias of other causation; the microscope 
may be necessary to detect its nature. Hemoptysis is rare; Henoch 
observed over a dozen cases under six years of age. (ii) Chronic forms 
are very infrequent under six years. 

In children, physical findings are often absent except rales between 
the third and fifth ribs in front or over the lower lobes. Cavities are 
rare, and if softening develops do not freely communicate with the 
bronchi. In half the cases the wrong diagnosis is made (Henoch). Per- 
cussion is more difficult than in adults, because of the small chest and its 
thinner walls. (A cracked-pot resonance can be obtained in a normal 
young chest by strong percussion.) Children breathe irregularly, and 
puerile respiration is physiological. Induration is rare. 

2. The Aged. — Hemoptysis is rare, physical findings are less frequent 
than in adolescence, because the breathing is weaker, and emphysema 
is more common. Cough and fever are less conspicuous. 

Diagnosis of Pulmonary Tuberculosis. — Early diagnosis is most im- 
portant, (i) A positive family history is of some value, but it does not 
establish the diagnosis in a doubtful case, nor does its absence exclude 
tuberculosis, (ii) The symptoms of onset, toxemic, digestive, etc., are 
important, (iii) The Bacillus tuberculosis distinguishes pulmonary tuber- 
culosis (a) from other catarrhs, such as acute and chronic bronchitis 
or influenza; (b) from other consolidations, e. g., pneumonia, broncho- 
pneumonia, neoplasm or syphilis; (c) from other vomicae, such as abscess, 
gangrene, actinomycosis, echinococcus, syphilis or bronchiectasis; and 
(d) from indurations other than tuberculous. Every sputum should 
be examined. Cultures and inoculations are made in doubtful cases. 
(iv) In doubtful cases repeated physical examinations are imperative; 
auscultation is more valuable than percussion; too great reliance should 
not be placed on negative findings; coincident lesions in a lower lobe and 
in an upper apex are almost surely tuberculous. Many patients are 
needlessly alarmed by precocious diagnoses. 

(v) Tuberculin Tests. — The principle is the same in all; the tuber- 
culous subject develops a hypersensitiveness to the tuberculous poison — 
known as the allergistic reaction, i. e., a specific reaction of the organism 



164 BACTERIAL DISEASES 

to poisons with which it is already acquainted; the tuberculin seeks out 
the point (of disease) in which the receptors are accumulated, (a) The 
ophthalmoreaction of Wolff -Eisner and Calmette (1907) consists of drop- 
ping in the eye one drop of 1 per cent, old tuberculin which is followed 
in 12 to 24 hours by a reactive conjunctival hyperemia. In 6300 tests 
Calmette found a positive reaction in 90 per cent, of tuberculous patients, 
in 57 per cent, of suspected tuberculosis and in 17 per cent, of apparently 
healthy persons; the only complications were keratitis in three instances, 
conjunctivitis in 20 and a reaction lasting over three weeks in 72 instances. 
Ulcers may develop if tuberculin is instilled into diseased eyes. The 
reaction may develop in typhoid, and fails in advanced tuberculosis, 
whence the poor outlook of an absent reaction in manifest phthisis. 
(b) Von Pirquet's test is vaccination of the skin under a drop of 25 per cent, 
old tuberculin (in salt solution); in 24 hours a small papule appears. 
This method is absolutely safe, mostly adapted to children (up to the 
fourth year), but too delicate to be valuable in adults unless it is negative. 
It is positive in 50 per cent, of apparently healthy adults. It is absent 
in children in advanced and cachectic tuberculosis, whence its poor 
prognostic significance, and in many intercurrent, acute infections, as 
measles, scarlatina, typhoid, etc. (due to insufficient antibodies to react 
to the tuberculin or to antianaphylaxis) . The test may react in 24 
hours, resulting in a large papule or dense infiltration; again the reaction 
may be prolonged, chiefly in adults, developing -a papule on the second 
or third day and lasting a long time. In Moro's test equal parts of lanolin 
and old tuberculin are rubbed into the skin, (c) The intracutaneous test 
(Mantoux and Roux). They inject, by a fine very sharp needle, 0.01 
mgm. tuberculin, in a dilution of 1 to 5000, not beneath but into the 
skin itself. A positive reaction consists in the appearance, after a few 
hours, of a small papule, which on the third day attains its maximum. 
It is more sensitive than the cutaneous test, id) Hypodermic injection 
of Koch's tuberculin produces (i) a local exudative reaction, and after 
four to ten hours, a (ii) systemic reaction, characterized by chill, fever 
of even 5 degrees, headache, general pains, malaise, nausea, sometimes 
erythema nodosum, and (iii) an increase of sputum, rales, or even 
a slight area of pulmonary dulness; the first injection of Koch's older 
tuberculin should be small, in adults 0.2, 0.5, 1 or 5 milligrams — in chil- 
dren 0.1 to 1 milligram. It is held that in a positive reaction with less 
than 5 mgm., the focus is active; if with 5 to 10 mgm., it is inactive. The 
reaction is specific and indicates that there is a tuberculous focus in the 
body, but not necessarily in the lungs, unless rales develop at the suspected 
spot after the injection. Contra-indications to its use are, fever, hemop- 
tysis, weak heart, nephritis or a certain diagnosis. In veterinary 
medicine it is more valuable, leading to a correct diagnosis in 90 or 97 
per cent. The author admits a reluctance to use tuberculin; four cases 
of miliary tuberculosis apparently resulted from its employment. 

Sticker recommended the use of potassium iodide in small doses (gr. iij) ; 
it congests the lungs at the seat of the lesion, possibly makes the aus- 
cultation findings clearer, and carries bacilli into the sputum; its use 
is dangerous. 



TUBERCULOSIS 165 

Pseudotuberculosis. — The Rhizomucor parasiticus, the ray fungus, 
streptothrix, blastomycetes, yeasts, the aspergillus and Pfeiffer's pseudo- 
tuberculosis bacillus, which is not acid-fast, may cause pseudotuber- 
culosis. The form caused by the Aspergillus fumigatus is described 
as a primary lung affection, but many writers consider it secondary 
only. The symptoms of streptothricosis are hemoptysis (23 per cent.), 
fatigue, emaciation, anorexia, dry cough and, later, a greenish, purulent 
sputum. The physical findings are bronchitis, less often slight consolida- 
tion or cirrhosis of the lung. Ashton and Wright (1905) collated 26 cases, 
most of which resembled phthisis; over 50 per cent, were unmixed 
infections and 76 per cent. died. Pulmonary thrush is rare, Garin finding 
only 6 recorded cases (1911); the symptoms resemble tuberculosis and 
the Endomyces albicans is found in the sputum and lung. 

Prognosis of Pulmonary Tuberculosis. — Two issues are possible: 

1. Recovery. — Autopsies on hospital cases show 25 to 97 per cent, 
of healed tuberculosis. Many recoveries are only relative, since Kurlow's 
inoculations from seemingly latent caseous foci into guinea-pigs were 
positive in 77 per cent.; such foci may be aroused by intercurrent 
disease, though some writers regard recurrence as fresh infection. Re- 
covery is effected by agglutinins (precipitins) and other specific antibodies 
(opsonins) which aid in phagocytosis. The result is encapsulation, cica- 
trization and calcification. Liebermeister believes recovery is possible in 
50 per cent, of incipient cases. The outlook depends on several factors: 
(a) The hereditary vital endowment of the patient; (b) his environment, 
social situation, habits and intelligence; (c) whether the localization is 
single or multiple; (d) secondary or mixed infection; (e) digestion; 
(/) degree of toxemia (fever and emaciation); (g) youth, diabetes, 
pregnancy and lactation are unfavorable; (h) 80 per cent, with normal 
pulse-rate were alive after four years and 97 per cent, with rapid pulse 
were dead (Schneider); and (i) complications (v. %.). 

2. Death. — The clinical course is variable, even in chronic cases; 
it averages two years (Bayle, Laennec, Andral), over two and a half 
years (Pollock), three years (Cornet) and seven years (Williams and 
Dettweiler, though not including acute or infantile forms) ; the course 
may last 30 to 55 years. Death is usually peaceful and painless, though 
at times it comes with dyspnea, delirium or convulsions. Mechanism 
of death: (a) Heart failure is the common cause, associated with edema, 
asthenia, anemia and marasmus. Other causes are less frequent, as (b) 
profuse hemoptoe; (c) pneumothorax; (d) pulmonary embolism (clots 
or gas); (g) uremia; (J) meningitis; (g) perforative peritonitis; and 
(h) sudden death without adequate pathological findings, in which 
Arnold, Brissaud and Toupet found in the liver large numbers of bacilli, 
which probably caused an acute intoxication (the injection even of dead 
bacilli causes rapid marasmus and death). 

Complications. — Tuberculosis in other organs will be considered below 
under separate headings. 

1. Respiratory. — (a) Tracheitis and bronchitis occur in almost every 
case. (b) Dysphagia usually results only from local involvement of the 
pharynx or larynx; swallowing into the larynx is the result of paralysis 



166 BACTERIAL DISEASES 

of the epiglottic depressors. Hoarseness, dysphonia and aphonia sug- 
gest laryngeal tuberculosis, but may develop from syphilis, toxemia or 
catarrh; from paralysis of the recurrent laryngeal nerve from pressure 
by lymph glands; from inflammation, on the right side by pleural scars, 
and on the left by large pleural effusions; or from thickening at the 
hilum. (c) Pulmonary gangrene may develop in the cavity wall. Lobar 
pneumonia is not infrequently a cause of death, (d) Dry pleurisy is 
an almost constant complication, and is a conservative process, militating 
against pneumothorax. Exudative pleurisy more often develops pre- 
viously to lung phthisis than during its course. In the latter instance 
it is usually serofibrinous, and not extensive. Effusions, by compression, 
sometimes seem to exert a favorable effect on the lung lesion. Litten 
thought that their sudden absorption might occasion miliary tuberculosis. 
Chyliform or adipose effusions may occur (see Chylothorax and Chylous 
Ascites) ; purulent forms result from mixed infection, cavities or pneumo- 
thorax, (e) Pneumothorax is observed in 5 per cent, of cases, and results 
from rupture of superficial rapidly forming cavities without a limiting 
membrane. Perforation occurs most frequently between the second and 
fourth interspaces, and between the mammary and axillary lines. Its 
onset is spontaneous, or results from straining or coughing, whereon 
sudden symptoms develop, as great dyspnea, orthopnea and cyanosis, 
and sudden physical signs, as dislocation of the heart, spleen or liver, 
sudden ectasia, unilateral thoracic immobility, weak vocal fremitus, 
voice sounds and breathing, a tympanitic note, and succussion when 
serum or pus forms. The onset is occasionally gradual or even symptom- 
less. Death may result in a few hours, but life may be prolonged weeks 
or months. Infrequently pneumothorax (q. v.) may exert a beneficial 
effect on the lung trouble. 

2. Circulatory. — (a) The typical rapid pulse first appears only 
after meals or exertion, but later becomes permanent. It is chiefly 
toxemic, but may be due to compression or inflammation of the vagus 
from lymphadenitis, hyperthyroidism, mediastinitis, pleurisy or peri- 
carditis. There is a constant and early lowering of the blood tension, 
and the vasomotor instability causes the bright red cheeks. (6) The 
heart is pale, fatty, flabby and weak, and has been described as atrophied 
since the time of Laennec, but Potain considers that the small heart is 
merely accommodative to the malnutrition and anemia. Cardiac hyper- 
trophy and dilatation are due to renal disease, pericardial or pleural adhe- 
sions, or pulmonary induration; the second pulmonic tone is accentuated 
in one-third of the cases. Adhesive or effusive pericarditis (in 3 per cent.) 
may result by extension from pleurisy or caseated lymph glands, or 
pyogenic infection. Endocarditis tuberculosa is infrequent (1 per cent.) ; 
tubercle bacilli may be deposited in cardiac clots, or endocarditic ex- 
crescences of non-tuberculous origin; this endocarditis is due to miliary 
deposits in the intima, and clinically escapes recognition in most cases. 
Woolley reported 11 cases of tuberculosis of the aorta (1911). (c) A 
functional, systolic murmur is very common. (d) Thrombophlebitis 
occurs in less than 1 per cent, of cases. 






TUBERCULOSIS 167 

3. Nervous and Muscular. — (a) The mental power may be normal; 
oftener there is a slight mental weakness, irritability, self -concentration, 
triviality and lack of endurance. Consumptives are usually optimistic, 
even on the day of their death (spes phthisicorum) ; occasionally melan- 
cholia or mania develops; anemia, toxemia, marasmus and edema of the 
brain may cause terminal aberration, (b) Neuralgia and hyperesthesia 
are not uncommon. Toxemic multiple neuritis develops in 1 per cent.; 
it may cause pain, sensory disturbance or amyotrophy, (c) The toxins 
which reduce the body weight one-half or more, result in marked muscular 
degeneration and atrophy, which cause the flat chest, and possibly the 
cardiac wasting. Wasting is expressed in terms synonymous with tuber- 
culosis^ — consumption, phthisis, tabes. The muscles are dry, pale, fatty; 
they show transverse rents, obscure markings, granular degeneration 
or hyperplasia of the connective tissue, or myositis. Their wasting and 
the nervous toxemia explain the asthenia and incapacitation for work, 
a matter of national economical importance. The muscles are often 
irritable, show fibrillary contractions and when tapped or pinched show 
local lumpy contraction, known as myoidema. 

4. Digestive .—(a) The tongue may be furred, or red and clean. 
Aphthse are frequently distressing. Excessive redness of the gums is 
frequent, (b) Stomach disorder is present in 50 per cent, of cases; it 
may be the initial symptom of toxemia, or appear only late in the process. 
Anorexia varies in degree and occurrence, being most marked when the 
fever is high, and most frequent in those with previous dyspepsia or poor 
appetite; again it may be due to glands compressing the vagus (Peter, 
de Mussy). Cornet instances an advanced patient who complained that 
he could only eat four beefsteaks for dinner. "The patient, with fever, 
who eats and digests well, is tuberculous" (Lesegue). Brieger found 
the chemism normal in 50 per cent, in the incipient stage, in 33 per cent, 
in moderately severe, and in but 16 per cent, in severe advanced cases. 
After eating there may be a sense of fulness or pain. Nausea, gagging 
and vomiting may result from pharyngitis, forced feeding or coughing 
(Morton's "emetic cough"). In advanced cases, nausea and vomiting 
occur from overeating, toxemic gastric catarrh, swallowing of sputum, 
etc.; anatomically, the stomach shows catarrh, fatty degeneration of 
the glands, interstitial hyperplasia and amyloid infiltration, (c) Intes- 
tines: Diarrhea is usually late; it may be caused by toxemia, swallowed 
sputum, intestinal catarrh, toxemic obliteration of the lymph and blood- 
vessels, ulcers or amyloid degeneration of the gut. Tuberculous ulcers 
in the small gut, cecum and ascending colon cause diarrhea in but half 
the cases and probably only when combined with catarrh or amyloid 
degeneration; ulcers in the lower colon and rectum almost constantly 
induce diarrhea, which may therefore occur from causes other than 
ulceration, and ulcers may exist without it. Blood, pus, hematin crystals 
and tubercle bacilli are not always present. Tubercle bacilli may pass 
through with the sputum swallowed, without intestinal tuberculosis. 
Anal fistula occurs in 3 per cent, of cases, (d) The liver is fatty (in 10 
per cent.); Jonescu (1902) collected 33 cases of cirrhosis cardiotuber- 
culosa — induration from stasis, with tuberculous granulations and fatty 



168 BACTERIAL DISEASES 

degeneration, (e) Tuberculous peritonitis (v. i.) occurs in 10 per cent, of 
pulmonary tuberculosis. 

5. Amyloid Degeneration. — Of all amyloid degeneration 80 per cent, 
is due to tuberculosis, and 69 per cent, to ulcerative phthisis. It is 
found in 8.8 per cent, of tuberculous autopsies. The spleen is affected 
in 93 per cent., the kidney in 77, the liver in 62, the intestines in 28 and 
the stomach in 12 per cent, of cases. 

6. Genito-urinary. — Urinary. — The loss of weight causes phos- 
phaturia and increase of chlorides (0.5 to 1 or even 12 gm.). More 
protein is excreted than is ingested. Albuminuria indicates nephritis, 
amyloidosis or local tuberculous disease. Acute and chronic parenchy- 
matous nephritis is not infrequent, due to long-standing toxemia. Amy- 
loid disease of the kidney produces albuminuria in but 50 per cent, 
of the cases; nephritis is also present in 75 per cent., and the chronic 
parenchymatous type in 66 per cent. Flick and Walsh found tubercle 
bacilli in 84 per cent, by inoculating guinea-pigs with the urine; tubercles 
were found in 63 per cent. Ehrlich's diazo reaction is very frequent 
and usually of unfavorable import. 

Sexual. — The sexual desire may be more intense, though its increase 
is exaggerated. The menses often disappear early, and conception is 
less apt to occur. Pregnancy often temporarily betters the condition, 
but a more rapid course is usual after delivery (v. page 190). The 
mammary enlargement described by Bedor, particularly in males, is 
rather a chronic interstitial mastitis than an actual hypertrophy. Bacilli 
have been found in the milk of tuberculous mothers. 

7. Skin. — Pityriasis versicolor occurs very frequently. Piery claims 
that bacilli exist in the sweat. Cyanosis, chloasma, desquamation, 
coarseness of the hair, herpes, lichen and purpura are sometimes 
observed. Clubbing of the fingers ("Hippocratic fingers") and toes 
develops chiefly in chronic cases, is largely due to hypertrophy of the 
soft tissues and is not pathognomonic, for it occurs also in congenital 
cardiac disease, aneurysm, bronchiectasis, emphysema, etc. (See Acro- 
megaly.) Emphysema of the skin is very uncommon; it follows inter- 
stitial emphysema of the lungs (due to rupture of the alveoli), pneumo- 
thorax or cavities. Edema results from anemia, cardiac weakness, 
phlebitis, nephritis or neuritis. 

Treatment of pulmonary tuberculosis is considered later, after descrip- 
tion of other localizations of the tubercle bacillus. 

IV. — Tuberculosis of the Lymph Glands. — Of glandular adenopathies 
68 per cent, are found in the first ten years of life. It occurs fairly 
often in adolescence and sometimes even in the aged. It is found ana- 
tomically in 85 per cent, of tuberculous children, and in 25 per cent, of 
all autopsies on children. Scrofula is glandular tuberculosis, but it 
presents different characteristics from those of pulmonary infection 
(decreased virulence of the bacilli in scrofulous glands, infection with 
the bovine bacillus, or infection with very few bacilli). The skin, mucous 
membranes and lymph vessels are physiologically more permeable in 
the very young, and an increase or persistence of this condition is regarded 
as an embryoism, i. e., a structural tendency toward infection. The 



• TUBERCULOSIS 169 

accessory causes are the same as in pulmonary tuberculosis: (a) An 
hereditary tendency; (b) poor hygiene, dark damp dwellings and inade- 
quate nutrition; (c) infections, as pertussis and measles, to a less extent 
scarlatina, diphtheria, variola and syphilis. 

General Characteristics. — (a) It usually runs a chronic course, (b) 
Recurrence is frequent, (c) Multiple lesions are usual, (d) Glandular 
involvement is frequently associated with affections of the skin (as 
eczema, scrofuloderma or lupus), inflammations of the mucous mem- 
branes (as conjunctivitis, otitis, rhinitis or bronchitis), and disease of the 
bones or joints (as coxitis or Pott's disease). Escherich refers the hyper- 
sensitiveness of the skin and mucosae to the presence of the antibody — 
tuberculous "allergy." This association is frequently known as scrofula. 

General Anatomy. — (a) In infection with very few bacilli regression 
is possible, (b) If the infection is sharper, conglomerate tubercles form, 
with the following issues: death of the bacillus in the central caseation, 
softening and external rupture, sometimes calcification or extension 
locally, generally by the blood current, (c) Hyperplasia without any or 
with very late caseation results from infection with few bacilli. The 
lymphadenoid tissue is compressed by epithelioid spindle-shaped cells; 
the glands may reach the size of an egg, and their cut section may show 
no gross evidence of tubercle, (d) Mixed infection causes rapid caseation, 
necrosis, softening and early rupture; their cut section appears "like 
that of a raw potato but not so moist"; the inflammation often causes a 
periadenitis, whereby the glands fuse, a phlegmon results, and general- 
ization of the process throughout the body ensues. 

1. Cervical Tuberculous Adenitis. — Infection occurs through the 
tonsils, nose, etc.; the bacillus may pass through the mucosa? without 
producing any lesion in them. The cervical glands constitute 96 per cent, 
of Wohlgemuth's series. In cervical lymphadenitis, the glands at the 
angle of the jaw and beneath or anterior to the sternomastoid muscle 
are most often involved; in bilateral involvement the glands of one 
side are usually larger. The glandular swelling is slow in onset, inter- 
mittent in progression and usually unattended by pain or other symptoms. 
In some cases the first symptoms are acute, but the trouble subsides in 
a few weeks. The nodes first are discrete and freely movable; they may 
blend into large nodular masses, and periadenitis may fuse the glands 
and cause their adherence to the skin, which becomes edematous from 
lymph stasis, dough-like and reddened. Softening and fluctuation are 
then frequent, with burrowing of pus and external rupture through 
small fistulse. The fistulse widen, discharge cheesy and milky material 
and form intractable ulcers covered with granulation tissue. Cicatri- 
zation leaves deep, deforming, depressed scars. Extension may occur 
to the deeper or subpectoral or axillary glands. Fever, anemia and other 
toxemic manifestations may develop as in lung tuberculosis, or the 
adenopathy may be the sole clinical fact. 

2. Bronchial Glands. — In autopsies on tuberculous children these 
were affected in 100 per cent, of Northrup's series, and in adults in 60 
per cent. In children tuberculosis of the bronchial glands is primary 
and tuberculosis of the lung secondary. In adults lung involvement is 



170 BACTERIAL DISEASES 

usually primary and bronchial adenitis secondary. Biedert, in 1346 
autopsies on tuberculous children, found the lungs diseased in 80 per cent., 
the bronchial glands in 78, the intestines in 32 and the mesenteric glands 
alone in 40 per cent. 

Symptoms. — In most cases no symptoms develop; in others pul- 
monary lesions overshadow the bronchial involvement; in others 
miliary tuberculosis develops, promoted by rupture of the bronchial 
glands into the pulmonary vessels; in still others mediastinal symptoms 
result; in very few cases are there actual physical findings. 

Pressure Symptoms. — Pressure on the vagus, known to Wrisberg, 
causes the rapid heart, so frequently remarked in tuberculous children; 
paroxysmal dyspnea, or spasmodic cough which sometimes resembles 
whooping-cough (v. page 109) ; lessening of the sensitivity of the bronchi, 
which favors infection; and finally cardiac dilatation. Pressure on the 
recurrent laryngeal nerve is marked by hoarseness, aphonia, dyspnea or 
laryngospasm. The air passages may be compressed, as evidenced by 
dyspnea, holding the head backward and impaired expansion of one or 
both sides of the chest (Grancher's sign). The pupils may be unequal 
from pressure on the sympathetic nerve. Other pressure symptoms are: 
hypertrophy of the heart, or the paradoxical pulse, from pressure on the 
aorta; edema and cyanosis of the face and arms, from compression 
of the superior vena cava; cough, rales or hemoptysis, from stenosis of 
the pulmonary veins; a murmur over the innominate vein on throwing 
the head backward; and dysphagia, from esophageal compression. 

Signs. — Bronchial breathing is occasionally heard between the second 
and fourth dorsal vertebrae, more clearly behind than in front; more 
on the right than on the left side (since more glands are clustered around 
the right bronchus) , and more markedly than the high-pitched breathing 
heard physiologically over this region. Propagation of the whispered 
voice is D'Espine's sign. If the bronchus is compressed there is neither 
bronchial breathing nor increased vocal fremitus. An irregularly out- 
lined dulness is elicited on exceptional occasions either between the 
clavicle and third rib, on either side of the sternum, or behind, on per- 
cussing the third and fifth dorsal vertebrae (de la Camp's sign). Ad- 
jacent interscapular tenderness constitutes the spinalgia of Petrusky. 
A tympanitic note in the upper lobes denotes relaxation of the lung. 
The symptoms and signs are extremely variable, appearing suddenly 
and remitting unaccountably. 

Issues. — (a) Tuberculosis of the lung; (b) miliary tuberculosis; (c) 
tuberculous pleurisy or pericarditis; (d) rupture into the air passages, 
causing sudden suffocation; (e) fatal hemorrhage into the air tubes, 
which is less frequent; (/) rupture into the esophagus, or traction upon 
it causing an esophageal diverticulum. 

Diagnosis. — The direct diagnosis rests upon tuberculous adenopathies 
elsewhere, pressure symptoms, physical signs and avray plates. As 
Henoch puts it, "A diagnosis can rarely be made (from the physical 
signs), but if made, is nearly always correct." 

3. Mesenteric Glands. — The bacilli pass the intact intestinal 
mucosa and settle in the mesenteric glands. Carriere found that but 1 



TUBERCULOSIS 171 

per cent, of cases were primary; of the secondary cases, the primary 
focus was in the peritoneum in 40 per cent., in the lungs in 30, in the 
intestines in 20, in other glands and bones in 5 per cent. each. Hess 
holds that in over 60 per cent, of the primary infantile cases the infec- 
tion is by bovine bacilli; in adults it is by the human type (v. page 143). 
The glands may be palpable as thick, nodular masses through a thin 
abdominal wall, but are often obscured by the abdominal distention 
which contrasts strikingly with the general emaciation (tabes mesaraica) . 
Digestive disturbance is frequent, and there is usually a diarrhea with 
thin, stinking stools. Compression is less frequent in the abdomen 
than in the less yielding thorax, though the veins of the abdomen may 
stand out and edema of the legs may appear. The glands sometimes 
heal by induration and calcification, or, by softening, rupture into the 
intestine or peritoneum. 

4. Geneealized Lymphadenitis may closely resemble Hodgkin's 
disease (Paltauf and Sternberg). This form is common in the negro. 
In two personal instances the clinical and gross pathological findings 
were typically pseudoleukemic, and only the epithelioid hyperplasia and 
the Bacillus tuberculosis stamped them as tuberculous. 

The treatment of tuberculous lymphadenitis is that of tuberculosis 
in general (v. i.). Hyperplastic tonsils and adenoids require removal, 
being the atrium for cervical infections. In 175 cases of cervical adenitis 
treated surgically, 58 per cent, were cured after three years, 8 per cent, 
had recurrence, 11 per cent, developed pulmonary tuberculosis and 23 
per cent. died. In another series of 700 cases treated medically, 28 
per cent, developed tuberculosis in some other organ (Demme). The 
writer relies largely upon full feeding, x-rays, ample sunlight and fresh 
air; if possible, a warm sea-side climate, and operation if finally necessary, 
after puberty. The syrup of the iodide of iron and cod-liver oil are very 
largely used. Inunctions of green soap are recommended, 3ss rubbed 
into the back three times a week. Some 62 iu stances of tuberculous 
mesenteric adenopathy have been operated upon (Floderus). 

V. Tuberculosis of the Serous Membranes. — These membranes may 
be involved separately or simultaneously; multiple serositis or poly- 
orrhomenitis may be acute, subchronic or chronic, serous, fibrinous or 
purulent, solitary or with visceral tuberculosis. 

1. Pleura. — Tuberculous pleurisy has been touched upon as a com- 
plication of phthisis, and is separately considered under Pleurisy 
(q. v.). It may appear as an apparently primary infection, as secondary 
to unmistakable phthisis, or as a terminal infection. Miliary tubercles 
in the pleura may occur without pleurisy. Pleurisy results from direct 
bacillary invasion, or possibly from simple toxic action. In some cases 
the pleura proliferates and forms a massive, adhesive, obliterative mem- 
brane. Sometimes the interstitial tissue of the lung is invaded (pleuro- 
genous cirrhosis). 

2. Pericardium. — Accidental miliary deposits are distinguished from 
tuberculous pericarditis wherein inflammation predominates. It is 
less common than pleural and peritoneal involvement (in 3 per cent, of 
phthisis autopsies). Tubercles may be detected beneath the fibrin 



172 BACTERIAL DISEASES 

deposits or adhesions. It may be symptomatically latent; it may form 
an unessential part of a miliary tuberculosis; or it presents the ordinary 
symptoms of pericardial effusion or concretion (q. v.). Only eight primary 
cases are recorded (Scagliosi, 1904). 

3. Peritoneum.- — Tuberculosis of the peritoneum became a clinical 
entity when Louis, in 1825, declared that chronic peritonitis was tuber- 
culous. It complicates 10 per cent, of phthisis, is found in 2 per cent, 
of autopsies and constitutes one-quarter of all peritonitides. 

Age. — It is almost equally frequent in the second, third, fourth and 
fifth decades (20 per cent, in each) ; 66 per cent, of cases occur between 
ten and forty years of age. 

Sex. — Ninety per cent, occur in women. More cases are found in 
autopsies on males, though more women are operated on. In America 
it is common among the negroes. It is very seldom primary (0.7 per cent.) , 
but is secondary to (a) lung, bronchial gland or pleural tuberculosis (in 
80 per cent.); (b) intestinal ulcers or mesenteric and retroperitoneal 
adenitis, especially in children (tubercle bacilli may pass the intestinal 
wall without localizing in it); (c) tuberculosis of the Fallopian tubes 
(which in turn, is secondary to bronchial adenopathy). Tuberculous 
peritonitis is hematogenous. 

It frequently complicates liver cirrhosis (though it is strange that 
tuberculosis should develop in any stasis), ovarian tumors or trauma, 
which disseminates infection from some quiescent focus. Sixty-two 
cases are reported in hernial sacs. 

Types. — A clinical description is difficult, for the disease may be 
acute or chronic, latent or stormy, circumscribed or diffuse; it may 
be marked by adhesions, free or encapsulated ascites or by large tumor- 
like masses; it may be obscured by coincident miliary tuberculosis, 
liver cirrhosis, exudative pleurisy or ulcerative phthisis, or may appear 
as a seemingly primary clinical fact. The unessential miliary tubercle, 
and the small, non-inflammatory tubercles over intestinal ulcers are not 
considered. Certain types may be described: 

1. The acute form begins with severe symptoms, fever, rapid pulse, 
vomiting, abdominal tenderness and pain, free peritoneal fluid, which 
shifts with change of position, and meteor ism from paresis of the gut. 
This type may resemble typhoid when the intoxication is more marked 
than the local signs. The peritonitic local signs may be sharply marked, 
but always less so than in suppurative peritonitis. Certain cases simulate 
appendicitis, ileus from tuberculous adhesions, or incarceration beneath 
bands; or in three cases precipitated by delivery, puerperal infection. 
Indicanuria, so frequent in other acute peritonitides, is usually absent. 
The ascitic fluid is usually lemon-colored, serous or slightly flocculent 
or hemorrhagic, and of a specific gravity of over 1.014; the leukocytes 
are usually mononuclear. In rare instances the acute peritonitis is 
suppurative; 26 cases are on record due to perforation of a tuberculous 
ulcer in the gut. In some cases the acute type is a terminal infection. 
Though commonly diffuse, there is sometimes acute local pain or cir- 
cumscribed effusion. Plastic adhesions occasionally modify the freedom 
with which this ascitic form shifts with alteration of posture. Acute 



TUBERCULOSIS 173 

tuberculous peritonitis comes more often under the care of the physician 
than of the gynecologist or surgeon. 

2. Subacute or chronic forms include: (a) The fibrinoplastic form, 
causing adhesions, may result from the acute form or may develop 
insidiously; symptoms and signs are usually lacking, or not distinctive. 
(6) The fibrinocaseous form is characterized by large solid masses, by 
fusion of tubercles. Between the recesses formed by the adhesions, 
pockets of exudate frequently occur, containing blood-stained serum, 
cold abscesses or cheesy material; the intestine is thickened and con- 
tracted, the mesentery deformed and the omentum shrunken, (c) The 
effusive form is marked by serous, serofibrinous, serohemorrhagic and less 
often by puriform or adipose exudate. 

These subtypes vary so much that the individual symptoms will be 
considered separately: 

Individual Symptoms. — 1. Adhesions and Retraction. — The infil- 
trated omentum gradually indurates and retracts above the navel as a 
fibrocaseous tumor-like mass ; it may often be palpated, even when there 
is much exudate, but becomes clearer after paracentesis; it has been 
mistaken for gastric carcinoma, enlarged liver or distended gall-bladder, 
especially in chronic forms with little fever; it is more suggestive of 
tuberculous than carcinomatous peritonitis. The walls of the gut are 
frequently so thickened that intestinal stenosis results; the gut may 
measure but one-half or one-third of its original length; it may be 
thickened, adherent or tumor-like. The entire peritoneal sac may be 
distorted (peritonitis deformans) and intestinal stenosis ensues. The 
mesenteric retraction (mesenteritis retrahens) modifies the physical 
findings, tympany and dulness; the mesentery may measure one inch in 
thickness. 

2. Ascites. — The abdomen is moderately enlarged by exudation 
and meteorism. Large exudates may cause widening of the abdominal 
veins because the cava is compressed, as in ascites (q. v.). The abdomen 
protrudes but its centre is not usually flattened nor its sides bulging as 
in the ascites of liver or cardiac disease, but it is often prominent in the 
median line, as in ovarian cyst; most of Lohlein's cases were sent to him 
with a diagnosis of ovarian cyst. Without adhesions, the dulness shifts 
with change of posture, with tympany over the supernatant gut and 
dulness over the settling fluid. The physical signs differ from common 
ascites in that the tympany is often on the right side, the mesenteritis 
retrahens pulling the small gut to the right. A tuberculous mass 
may dislocate the tympanitic intestines to the left, the median line or 
pelvis. In very rare cases the fluid may rupture into the bowel or ex- 
ternally through the navel. Dulness may indicate adhesions, thickening 
of the gut, caseous masses or enlarged glands. 

3. Meteorism. — Sudden paresis of the gut in the acute type or 
tuberculous tumors impeding peristalsis cause gaseous accumulations. 
Meteorism is one of the stigmata of tuberculosis of the mesenteric glands 
and then is often due to coincident peritonitis; in both conditions, but 
most often in children, the stools are fatty. 



174 BACTERIAL DISEASES 

4. Palpation. — A doughy sensation on palpation is usually referred 
to peritoneal adhesions or constricted intestine, but in some instances 
is due to early infiltration of the preperitoneal tissues. 

5. Other Symptoms. — In some cases the Beatty- Bright friction-rub 
can be elicited. Pelvic effusion is common in women, who also suffer 
from painful and disturbed menstruation. Fever is frequently irregular, 
sometimes continuous, remittent or hectic; it is most frequent in acute 
types or in acute exacerbations of chronic cases; the disease cannot be 
excluded by the absence of fever. Fever, pain and tenderness distinguish 
tuberculous encapsulation from simple ascites. Pain and tenderness are 
generally conspicuous, though less than in suppurative peritonitis and by 
no means constant. Emaciation is frequent, but often patients with tuber- 
culous peritonitis present a good color and robust appearance. Gastro- 
intestinal disturbances are frequent; the usual constipation is occasioned 
by impaired peristalsis; in some cases diarrhea is caused by toxemia. 
In rare instances there are icterus, splenic tumor, and other complica- 
tions due to special localizations of the process. 

Diagnosis. — Sometimes there are no just grounds for suspecting the 
disease. Importance attaches to tuberculous lesions in the lungs, pleurae, 
glands or Fallopian tubes. Multiple serositis is extremely suggestive. 
If another tuberculous lesion cannot be established, tuberculous peri- 
tonitis, which constitutes nearly all chronic peritonitides, is very probably 
present; malignancy must be considered. A positive tuberculin reaction 
does not prove that the tuberculous lesion is peritoneal. Inoculation 
may be made with fluid withdrawn by paracentesis. (See Pleurisy.) 
Exploratory laparotomy is justifiable, as simple abdominal section is the 
foremost therapeutic measure. 

Course. — The onset is usually insidious and the course, independently 
of therapeutic measures, shows spontaneous remissions. 
. Treatment. — Rest in bed, good hygiene and full feeding very often 
arrest the process (in 25 per cent, of cases). The tumors, exudate and 
adhesions may recede and no symptom reappear for months or years. 
Spontaneous recovery, first described by Bamberger was ignored until 
recent times. In 1864 Spencer Wells observed that healing may follow 
laparotomy. Experiment has shown that the tubercles heal by degenera- 
tion, vascularization and development of connective tissue. 

Operation gives various results, recovery occurring in 75 per cent, 
of 1300 cases. Operation in the first four months is contra-indicated, as 
the early exudate has strong bactericidal properties. Simple paracentesis 
is inferior to laparotomy. Lavage is superfluous. It is thought that the 
access of air or sunlight or manipulation is the potent curative factor 
in operative treatment ; the withdrawal of fluid allows the access of fresh 
serum with increased antitoxic properties. Operation, in the author's 
opinion, is clearly of great value; the free fluid is evacuated, detritus 
or pus removed and the (local) cause, as pyosalpinx, is excised, the 
percentage of recoveries rising to 71 to 92 per cent. Some writers believe 
that the tubercles which heal after operation were already in process of 
healing spontaneously. s (See Pleurisy for autoserotherapy.) 






TUBERCULOSIS 175 

VI. Tuberculosis of the Brain and Meninges. — Involvement may 
result from (a) the miliary tubercle (v. s.), (b) the solitary or conglomer- 
ate tubercle, which produces symptoms identical with those of brain 
tumor (q. v.), (c) the tuberculous abscess and (d) meningitis (in 4.7 
per cent, of adults dying with pulmonary phthisis). 

Primary cerebral tuberculosis is extremely rare, and in reported cases 
it is probable that microscopic foci elsewhere escaped detection. 

VII. Tuberculosis of the Eye. — Only 50 cases occurred in 141,000 
eye patients. The number of reported cases of conjunctival tuberculosis 
is 150, of which but 100 were proved tuberculous. 

VIII. Tuberculosis of the Alimentary Tract.— 1. Lips. — The lips are 
very seldom affected; lupus may invade them. Tuberculous ulcers 
are very painful and may be confused with cancer or chancre. 

2. Gums. — The gums are seldom involved, though tuberculosis has 
followed caries and extraction of the teeth. 

3. Tongue. — This is involved in 0.6 per cent, of cases. Tuberculous 
tumors sometimes break down into cold abscesses. Tuberculous ulcers 
develop on the dorsum or edges; they have rough caseous bases with 
uneven or undermined edges, and are almost never primary; syphilitic 
ulcers are differentiated by the therapy and Wassermann; cancer by 
adenopathy; and both, by the absence of bacilli and the results of 
inoculation. 

4. Pharynx. — Primary disease is most infrequent, and involvement, 
secondary to pulmonary or laryngeal phthisis, occurs in 0.3 per qent. 
only. The process begins in the lymphoid structures, which are 
infected by tuberculous sputum or food, or it extends by the lymph 
vessels from the larynx. Three-fifths of the cases are associated with 
tuberculous intestines, and one-seventh with oral tuberculosis. The 
cervical glands may be affected in acute, but rarely in chronic, cases. 
The ulcerations are usually superficial; when propagated from the 
larynx the most distressing dysphagia results. Retropharyngeal abscess 
usually results from suppurative lymphadenitis and osseous disease. 

5. Palate. — Ulceration occurs in 1 per cent, of phthisis cases; in 
coughing, bacilli come in forcible contact with the palate. Lubinski 
observed three instances among 16,000 throat cases. 

6. Tonsils. — The tonsils are diseased in 4 per cent, of phthisis cases; 
the process may stop at the tonsils, for they act as barriers to infection, 
or tuberculous cervical adenitis may develop. Their infection may be 
primary, and Dieulafoy holds that tonsillar infection may be followed 
by a descending tuberculous adenitis, which in turn infects the lungs. 
The lesions are more often miliary than caseous. 

7. Salivary Glands.— Of parotid disease 14 records exist. 

8. Esophagus. — No clear primary case is recorded, and Cone could 
collect only 48 secondary cases. Infection by contiguity, from the 
peribronchial glands, may occasion esophageal perforation, hemorrhage, 
diverticula or stenosis. Extension from the larynx or pharynx along the 
lymph tracts or from the spine or lung cavities is possible. 

9. Stomach.- — There are only 4 primary cases on record. Secondary 
disease is estimated at 0.4 per cent. Garre collected about 100 cases of 



176 BACTERIAL DISEASES 

tuberculous ulcer, of which 25 were operated upon for pyloric stenosis. 
The HC1 is inimical to gastric tubercle. Tuberculous ulcer of the stomach 
occurs from the sputum, invasion by contiguity or in few cases from 
hematogenous infection. 

10. Intestinal Tuberculosis. — It was first observed by Bayle (1810). 
(a) It is usually secondary to ulcerative lung tuberculosis from infective 
sputum; its frequency is 30 to 50 per cent. Tubercle bacilli may be 
swallowed without causing intestinal tuberculosis. Of ail intestinal 
ulcerations, tuberculous are the most frequent. Infection from the 
peritoneum, mesenteric glands or hematogenous infection is barely 
possible. (b) Primary intestinal tuberculosis is much more rare, occurring 
in only 0.1 per cent, of adult cases. The intestinal mucosa in children 
often allows of the passage of tubercle bacilli to the intestinal lymph 
glands without disease of the intestine itself. Koch denies infection 
by milk, and Behring affirms that it is the chief cause of tuberculosis. 

The ulcers are most frequent in (i) the ileocecal region and next in 
the colon, (ii) They always originate in the lymphadenoid follicles or 
Peyer's patches. Small tubercles fuse into large ones, which caseate and 
ulcerate; in exceptional cases the caseous nodes do not rupture but cause 
the peritoneum and mucosa to bulge out. (iii) The ulcers are irregular 
in shape and (iv) their disposition is ring-like around the gut (extension 
by the bead-like lymphangitis tuberculosa) ; rarely they lie in the long 
axis of the gut and are ovoid, incompletely corresponding to Peyer's 
patches, (v) They are single or multiple, and sometimes cover most of 
the large and small intestines, (vi) Their bases are rough or caseous 
and their edges infiltrated, which also invades the contiguous mucosa 
and submucosa. (vii) Localized adhesive peritonitis is a common issue 
when the process reaches the serosa; perforation occurs in 5 per cent, 
of cases, but is resisted by the muscular coat and by adhesions; it results 
in pericecal abscess and suppurative peritonitis. Stenosis of the intestine 
may also result, single, or less often multiple (129 cases collected by 
Arbuson, 1904). Eisenhardt saw v 10 complete and 26 incomplete recov- 
eries in 567 tuberculous ulcerations. Hepatic suppuration or steatosis 
may result. 

Symptoms. — The symptoms usually commence with catarrhal enteritis, 
pain and fever; diarrhea occurs in but half the cases of ulceration. 
They may resemble typhoid. The only pathognomonic finding is the 
tubercle bacillus, but this finding may result also from swallowed sputum. 
Rosenblatt's method of detecting the bacilli in the feces is to give laud- 
anum until the stools become hard; in the mucus on their surface, the 
bacilli are usually found on the first examination, for the hard feces 
apparently scrape the bacilli from the ulcers. Pus is often found. Girode 
called attention to the black stools, which are ominous, as they indicate 
malnutrition; the picture of dysentery is rarely observed; fatal hemor- 
rhage is infrequent. An appendicitic form may be noted, with recurrence 
and fistulse. In typhlitis tuberculosa there is great thickening in the cecal 
region, with a hard, slightly movable or totally adherent, vertical, tender 
tumor. The onset is usually insidious with recurrent pain, increasing 
intestinal stenosis and constipation alternating with diarrhea. Hemor- 



TUBERCULOSIS 177 

rhage is infrequent, fever is usually absent and emaciation is sometimes 
pronounced. Duguet described this condition in 1869, and, since it so 
fully resembles cancer or sarcoma, it attracted the especial attention 
of surgeons, Bassini, Bouilly and Billroth. Campiche collected 379 
cases, of which 25 per cent, died from the operation; 35 per cent, were 
well for months or years; and 40 per cent, ultimately died of tuber- 
culosis. The process usually begins in the mucosa (rarely in the serosa) 
and is marked by ulceration, villosities in the mucosa, great local infil- 
tration and hypertrophy of the bowel and destruction of the ileocecal 
valve. Patients may die of acute obstruction, or only after a chronic 
course of a decade or more; recovery by fibrosis is possible. 

In the rectum ulcers, lupus, tuberculosis cutis and periproctal abscess 
are sometimes seen. Fistula in ano occurs in 3 per cent, of phthisic 
subjects and rarely in other conditions; the idea that its excision excites 
phthisis is confusion of cause and effect. 

11. Liver. — The liver is involved less in adults than in children (38 
per cent.), but at all ages it is of pathological interest chiefly, (i) Large 
tubercles may develop in the liver, sometimes with peritonitis and 
perihepatitis, (ii) Miliary tubercles (in 80 per cent.) are of no clinical 
significance, (iii) Hanot maintains that there is a primary cirrhosis of 
the liver, associated with tubercles, fatty degeneration, tuberculous 
peritonitis and perihepatitis {v. page 167); at the most it is extremely 
rare, (iv) Tuberculous cholangitis begins in the bile vessels as small 
nodes; breaking down, they resemble cysts or abscesses. 

12. Spleen. — The spleen is involved in 45 per cent, of tuberculous 
children. Franke collected 29 cases of primary tuberculosis; 10 were 
operated on, with 7 recoveries. (See Diseases of Spleen.) 

IX. Tuberculosis of the Genito-urinary Tract. — Genito-urinary tuber- 
culosis was described by Morgagni and by Bayle, but first fully by 
Lichtheim, in the cadaver, and by Rosenstein, Babes and Smith, clinically. 
It is most frequent in the period of greatest sexual activity (twentieth 
to fortieth year), and 72 per cent, occur in males. 

Modes of Infection. — 1. Hematogenic Infection. — This is the most 
frequent variety. It occurs in 5 per cent, of cases of chronic pulmonary 
tuberculosis; 76 per cent, of cases are secondary to some pulmonary 
or peribronchial glandular focus, which very often is latent, so that most, 
seemingly primary, foci are secondary. Jani found tubercle bacilli in 
sound testes and prostates (an invasion in the death agony). 

2. Urogenic Infection. — Contrary to the old doctrine, hematogenous 
infection of the kidney descends to the lower urinary tract, not vice versa. 
Transmission is very rare by infected fingers, instruments, catheters or 
sexual intercourse. 

3. Infection by Contiguity. — The Fallopian tubes are diseased 
in a third to a half of the cases of tuberculous peritonitis. Jani found 
tubercle bacilli in the tubes in women dying of phthisis. The bladder, 
seminal vesicles and vasa deferentia are rarely invaded per contiguitatem 
from peritoneal, vertebral or rectal foci. 

1. Renal Tuberculosis. — The kidney in miliary tuberculosis is involved 
in 90 per cent., but without distinguishing symptoms. The common 
12 



178 BACTERIAL DISEASES 

clinical form is the caseous-ulcerative. Caseous nodes develop in the 
cortex, infection reaching it from the blood stream (in 90 per cent.); 
they often break down into cavities, form cold abscesses, undergo second- 
ary pyogenic infection or remain localized in one pole of the kidney. 
Tubercles also develop in the apices of the pyramids and pelvis of the 
kidney and form caseous infiltration and ulcers; Caspar, Walker and 
Israel proved that the process in 41 per cent, of cases descends from the 
kidney to the bladder. When the process is developed there is a tuber- 
culous pyonephrosis. The entire kidney may become a large sac of 
caseous material, detritus and lime salts — degenerescence massive. The 
kidney is often adherent to adjacent structures; its capsule is thickened, 
its removal strips off particles of renal substance and it is sometimes 
perforated, causing tuberculous paranephritis. The surface of the kidney 
may be smooth and normal, lumpy from caseous deposits or softened 
from diffuse ulceration. In exceptional cases spontaneous healing is 
possible. Whether one or both kidneys are diseased depends on the stage 
of the process, and is a most important matter when surgical interference 
is contemplated. Israel, in his celebrated observations, found one kidney 
involved in 90 per cent., and Pallet and Albarran in 85 per cent. (Natu- 
rally, in autopsy figures, bilateral disease is greater.) Compensatory 
hypertrophy of the sound kidney is frequent. 

Symptoms. — The symptoms are (a) urinary, (b) local and (c) general. 
These may be absent if the renal pelvis is intact. 

(a) Urinary. — The urinary symptoms are chiefly those of pyelitis 
(q. v.) . The urine is acid. Urination is often difficult (dysuria) or frequent 
(pollakiuria) , so that cystitis is at first suspected ; it is a safe rule always 
to consider the possibility of renal phthisis in every cystitis, in which the 
origin is not clear and the treatment unsuccessful, and in every acid, 
sterile, purulent urine. In 62 per cent, bladder symptoms are the first 
to appear ; they are reflex from the kidney lesion, or are due to complicat- 
ing cystitis, simple or tuberculous. Guy on describes an early polyuria 
in which the urine is clear, and a later polyuria in which it is turbid. 
Hematuria (q. v.) occurs in 66 per cent.; it may be severe or slight and 
its occurrence is more often early than late; its recurrence distinguishes 
the "hemorrhagic type"; it may last one month to four years. Pyuria 
occurs when the pelvis is invaded, but is absent if cortical foci do not 
communicate with the pelvis, or the ureter is occluded; the amount of 
albumin corresponds to the glistening, shrunken and poorly nucleated 
pus cells. Epithelial cells, sometimes caseous matter, elastic fibers and 
necrotic renal tissue are found. The sediment is often a crumbly, 
rapidly settling detritus; tubercle bacilli are found in 80 per cent., but 
must not be confused with the smegma bacillus (v. page 167); the anti 
formin method is most valuable (page 167), and inoculations settle the 
diagnosis. Sometimes bacilli in the urine are found in pulmonary 
tuberculosis without disease of the kidneys. Casts are very infrequent. 
Ureteral catheterization determines which kidney is involved. 

(b) Local. — Lumbar pain sometimes results from capsular tension; it 
is dull, or colicky, and reflected to the groins and testes, which may be 
retracted, as in renal colic; colic is due to the passage of caseous particles 



TUBERCULOSIS 179 

or blood clots; differentiation from calculous disease (q. v.) may be diffi- 
cult until tubercle bacilli are found. Tumor, in tuberculous pyonephrosis 
or hydronephrosis, is a small, tender enlargement, seldom of the size 
attained in calculous or other obstructive disease. The kidney is palpable 
in one out of five cases. X-ray examination frequently shows caseous 
foci or calcification. 

(c) General.- — General symptoms are hectic fever, malnutrition and 
other general toxemic symptoms (see page 155), tuberculosis in the 
lungs and foci in the testes. The heart almost never hypertrophies. 
In 60 per cent, of the cases operated on, the diagnosis was found correct. 
The course is chronic and remittent^ two, three or even five years being 
the usual duration; frequently there is prolonged clinical latency; re- 
covery from circumscribed lesions is possible; death results from tuber- 
culous generalization, less often from sepsis, perinephritis or amyloid 
degeneration, and rarely from nephritis or uremia; in Vienna tubercu- 
lous meningitis was present in 17 per cent, as against 6 per cent, in phthisis. 
The treatment is surgical, the first operation being performed by Simon 
(1871). The operative mortality of nephrectomy is 3 to 5 per cent., and 
the end result, in Legueu's and Chevassu's 1539 collected cases, was 75 
per cent, of recoveries. 

2. Ureter and Bladder. — The ureter is thickened, infiltrated, caseous, 
ulcerated and often stenosed; it is involved in 80 per cent, of cases of 
renal tuberculosis. Secondary involvement from the kidney may be 
limited to the ureter at its vesical ending. Bladder disease is almost 
invariably secondary per contiguitatem or from hematogenous deposits, 
as seen by means of the cystoscope. Israel noted tuberculous cystitis 
in 41 per cent, of cases of renal tuberculosis (v. s.), and Vignernon in 
50 per cent. Cystitis of long standing always suggests renal tuberculosis, 
even with gonorrheal or other antecedents. Diagnosis is based on the 
bacteriology and cystoscope. Rovsing cauterizes with carbolic acid and 
Caspar irrigates with bichloride. Surgical intervention is indicated. 

3. Male Genitalia. — The epididymis is more often involved than the 
testis, except in youth. (In early life testicular disease results from general- 
ized tuberculosis; one-half of Jullien's cases occurred under two years 
of age.) Sometimes there is no caseation, as in hyperplastic lymphadenitis, 
and even microscopic confusion with sarcoma is possible unless the bacilli 
are particularly sought. The process is bilateral in 50 to 75 per cent, of 
cases. Testicular tuberculosis is most often confused with syphilis 
(q. v.), though in the latter there is less pain and fever and more nodular 
enlargement. The seminal vesicles, vasa deferentia and urethra may be 
invaded and a rectal examination should never be neglected. Recently 
the prostate, "the cross road of the urinary and genital tracts," has 
attracted especial attention; its primary involvement is disputed by 
some, but the gland is affected in 65 per cent, of genital tuberculosis in 
the male. The lungs are invaded in primary genital tuberculosis in 70 
per cent, and the urinary tract in 56 per cent. Treatment is surgical. 
Carl Rose found but 8 records of tuberculosis of the penis (1911), aside 
from infection by ritual circumcision of which. 41 instances exist (Holt, 
1913). 



180 BACTERIAL DISEASES 

4. Female Genitalia. — Local tuberculosis occurs in 2 per cent, of 
pulmonary tuberculosis. Tuberculous tubes are found in 1.5 per cent, of 
abdominal operations (according to W. Williams, 8 per cent.). Nearly 
all lesions are due to small foci in the bronchial glands. The tubes show 
nodules, infiltration, caseation and ulceration; bilateral involvement is 
usual and its true nature may be apparent only under the microscope; 
tuberculous salpingitis may simulate tuberculous peritonitis; tubal 
disease may be found in very young children. The uterus ranks next 
and is involved secondarily. Ovarian phthisis is always secondary. 
Tuberculosis of the vagina, cervix, vulva and female urethra is most 
exceptional. 

Mammae. — Schley (1903) collected 65 cases of which 12 were primary; 
tuberculous lesions often cause nipple retraction, tumor formation or 
axillary adenopathy (66 per cent.). When cold abscesses, fistulse or 
ulcers form, the diagnosis is more definite. A chronic interstitial non- 
tuberculous mastitis was described by Bedor. 

X. Tuberculosis of the Upper Respiratory Tract. — 1. Nose. — The nose 
is seldom affected, because its irritation excites sneezing and increased 
secretion, inimical to the tubercle bacilli. Thrasher (1905) collected 
125 cases. In the rare primary form there are very few bacilli and an 
exuberant non-caseous growth, which may resemble sarcoma; there is 
little pain and the chief symptom is a chronic coryza. In the secondary 
form the bacilli are abundant; multiple caseation and ulceration occur 
as in other localizations; suppressed coughing, with the mouth closed, 
is thought to force germs into the nose. Nasal infection may occur 
by picking the nose, and is promoted by wounds, ulcers and various 
obstructive processes. Infection may spread by the lymph vessels, 
especially in children, to the cervical glands or even to the meninges. 
In 33 per cent, lupus affects the nose (Bender). 

2. Nasopharynx. — Primary involvement is infrequent. Secondary 
disease, late in phthisis, occurs in 20 per cent. ; it is promoted by coughing 
with the lips closed. The third tonsil may be affected; adenoids are 
tuberculous in 20 per cent. (Dieulafoy). 

3. Ear. — Tuberculous otitis media occurs chiefly in late phthisis (32 
per cent.). It is furthered by measles and scarlatina, is rarely primary, 
and often causes cervical lymphadenitis, and rarely, mastoiditis. 

4. Larynx. — Laryngeal phthisis is very rarely primary. Louis, in 
1825, asserted that it was secondary to lung disease, resulting from 
infection by sputum, which view still holds; hematogenous and lympho- 
genous infection is rare. Laryngeal tuberculosis develops in 25 per cent, 
of pulmonary tuberculosis in adults, and in 3 per cent, in children. 
Adjuvant factors are inflammation, fissure and syphilis. In 700 cases 
Krieg observed unilateral involvement in 39 per cent., of which 92 per 
cent, occurred on the same side as the lung lesion, not from lymphatic 
extension but from paresis of the vocal cord due to neuritis of the recurrent 
laryngeal nerve, and to stagnation of sputum on the paralyzed and 
anesthetic side. Unilateral disease usually becomes bilateral from contact. 

Symptoms. — In those tare and unfavorable cases in which the trouble 
begins with laryngeal symptoms, the cough is dry or brassy; it may 



TUBERCULOSIS 181 

develop under the guise of simple laryngitis. In cases following phthisis, 
the bronchitic hack becomes brassy ; in the last stages it becomes incom- 
plete, ineffectual or eructative, as the vocal cords cannot be apposed. 
Pain and hoarseness are followed by dysphonia, aphonia, dyspnea and 
distressing dysphagia. 

Forms. — (a) Most commonly the ulcers are found in the interarytenoid 
region, on the vocal cords, posterior wall of the larynx and arytenoids; 
they are not deep but are broad; their edges are "nibbled," and their bases 
pale and sometimes caseous. Particles aspirated into the lungs, cause 
tuberculous or suppurative foci. In diagnosis, syphilitic ulcers (q. v.) 
are more often single and redder, have more "cut out" edges, frequently 
show cicatrization, oftener involve the epiglottis and posterior surface 
of the arytenoids, and less often the vocal cords; show no tubercle 
bacilli, show no local reaction on tuberculin injection and respond to 
mercury, iodides and Wassermann test. Ninety per cent, of all laryngeal 
necrosis is tuberculous. Perichondritis may occasion sudden edema 
glottidis, urgent dyspnea and early death unless timely tracheotomy is 
performed, (b) In other cases the submucous tissues are infiltrated and 
the mucosa is hardened (pachydermous form); the true cords are less 
involved than other parts; if ulceration develops it is inconspicuous. 
(c) Caseous tumors are not frequent; they may precede the ulcerative 
form or occur independently of it. (d) The vegetative type exhibits small 
excrescences on the ulcers or on the intact mucosa. 

Treatment. — Pronounced lung changes exist and dysphagia occasions 
rapid emaciation. Besides general treatment (v. i.), local measures, 
as a rule, do not modify the process. Insufflations of boric acid, iodol 
and painting with 10 per cent, menthol, 10 per cent, carbolic acid or 20 
per cent, lactic acid solution (gradually increased to 80 per cent.), may 
relieve the local pain; gr. \ of morphine, hypodermically, and 10 per 
cent, cocaine, locally, for a time allow the patient to eat but finally fail 
to anesthetize the wide-spread ulceration. The patient may be able 
to draw up milk and water by a tube, when the head is turned over the 
edge of the bed. Caustics are injurious. In Casselberry's practice, 10 
recovered. 

XI. Tuberculosis of the Heart and Vessels. — (a) Pericardium: (v. 
Serous Membranes), (b) Myocardium: Raviart (1906) collected 185 
cases of myocardial tubercle; miliary granulations 41 cases, conglomerate 
tubercles 83, tuberculous infiltration 12 and tuberculous sclerosis 6 
cases, (c) Endocardium: Norris found endocarditis in 1.4 per cent, of 
over 11,000 phthisical necropsies; tuberculous endocarditis is vegetative, 
very rarely ulcerative or caseous; secondary infection causes some cases 
complicating tuberculosis. Pellegrini (1912) cites 120 cases of endocardial 
tuberculosis, of which 53 showed tubercle bacilli, {d) Few cases of 
primary disease of the vessels are reported; 18 cases of tuberculosis of 
the aorta were collected by Simmitsky (v. miliary tuberculosis) . 

XII. Tuberculosis of the Bones and Joints. — This topic properly 
belongs to surgery, but its relations demand consideration. Koch first 
demonstrated the tuberculous nature of caries, fungus joint lesions and 
tumor albus, and Damsch determined this relation by inoculations. 



182 BACTERIAL DISEASES 

Konig and Orth found that 80 per cent, of bone and joint tuberculosis, 
was clearly secondary to pulmonary, glandular, genito-urinary and other 
tuberculosis. Probably all cases are secondary to tuberculosis elsewhere. 
Infection is hematogenic in the majority of cases, far less often lympho- 
genic. Experimentation shows that trauma may determine localization 
in animals already infected with the Bacillus tuberculosis. Thirty-three 
per cent, of the cases occur in the first decade of life, and 50 per cent, 
in the first two decades. Tuberculosis in children involves the bones 
and joints in 22 per cent, of cases (versus 3 per cent, of adult phthisis). 
Bovine bacilli cause a certain proportion of tuberculous osteopathies. 

Localization. — Watson Cheyne estimates that the knee is affected 
in 16.5 per cent, of cases, the hip in 14.6, tarsus and ankle in 14.4, elbow 
in 6.3, skull and face in 5.5, sternum, clavicle and ribs in 5.2, pelvic 
bones in 3.5, femur, fibula and tibia in 3.5, spine in 2.3, shoulder in 1.5 
and scapula, ulna and radius in 1 per cent. Jaffe finds involvement of 
the spine in 20, foot in 21, hip in 13, knee in 10, hand in 9 and elbow in 
4 per cent. 

1. Bones. — The spongy epiphyses of the long bones are the particular 
seat of tuberculous osteomyelitis and periostitis, whence infection easily 
reaches the joints; the diaphyses and flat bones are seldom involved. 
Involvement of the fingers and toes, less often of the ulna, may cause 
bulging — the spina ventosa, seen oftenest at about five years of age. 

In the bone-marrow there develops a grayish-red granuloma which 
dissolves the bone (caries sicca) ; the trabecule necrose and are discharged 
through fistula? as sequesters or "bone sand," in a caseous, pus-like fluid. 
Even large foci may heal by granulating osteitis. Infection may remain 
semiquiescent until aroused by mixed infection or trauma. Cold abscesses 
are lined by granulation tissue. There may be local tenderness, stiffness, 
fever and nocturnal pain. Bore lesions are not incompatible with 
otherwise robust health. Landouzy's camptodactyly is a bending of 
the fourth and fifth fingers which can be flexed but not extended. 

2. Joints. — Involvement generally follows contiguous osseous disease. 
Very often there is synovial inflammation and proliferation; far less 
frequently there are isolated tubercles in a non-inflamed synovial sac. 
Serous or serofibrinous synovitis (or the rice bodies, corpora orzyoidea) 
may result from toxins in a neighboring osseous focus, without the actual 
presence of tubercle bacilli. The symptoms of onset may be acute or 
insidious. Pain, especially at night, contractures and fever may be 
noted. In the later stages of joint disease granulation tissue forms with 
large caseous deposits, hydrops, empyema articulorum or the tumor 
albus (so named because of the thickening of the connective tissue, the 
edema and glistening appearance of the periarticular structures). The 
joint is sometimes disorganized. Twenty-five per cent, recover under 
immobilization, iodoform injections, .T-rays, Bier's stasis, heat and sea 
air. 

Poncet first called attention to a tuberculous pseudorheumatism, which 
closely resembles rheumatism (rheumatisme tuberculeuse ankylosante) . 
Poncet maintains that 5 to 17 per cent, of active, and 20 per cent, of 
chronic phthisics have pseudorheumatism and 40 to 50 per cent, of 



TUBERCULOSIS 183 

patients with chronic deforming rheumatism are tuberculous. It is 
affirmed that the exuded leukocytes are of the lymphocyte type ; inocula- 
tions have proven positive in a number of cases, but toxemia is the most 
probable cause. It is most frequent in children. Lejars found one case 
of primary tuberculosis of the muscles. 

XIII. Tuberculosis of the Skin. — 1. Lupus. — Lupus, the most frequent 
form, in 66 per cent, of cases is located on the nose, lips and angle of the 
eye. It occurs with pulmonary tuberculosis in 21 per cent, and other 
tuberculosis in 62 per cent. It is typical granulation tissue with true 
tuberculous tumors, which contain few bacilli and often advances on one 
border while it cicatrizes on another. 

2. Scrofuloderma. — This granuloma appears as movable, painless, 
subcutaneous nodes, which later become cold abscesses (the so-called 
scrofulous gumma, gomme scrofuleuse) ; they discharge a milky fluid and 
leave a sharply marked granulating ulcer. 

3. Lichen. — Lichen scrofulosorum is often tuberculous; the eruption 
originates from the follicles and is constituted of thick, oily, epidermal 
cells removable without bleeding, and distributed in sharply marked 
groups of yellow-brown nodules as large as a pin-head. 

4. Tuberculosis Cutis. — Tuberculosis cutis verrucosa of Riehl and 
Paltauf is observed on the backs of the hands and fingers and in the 
interdigital folds, chiefly in butchers, cooks and horsemen. 

5. Postmortem Tubercles. — Laennec referred his pulmonary phthisis, 
though probably incorrectly, to a postmortem tubercle. Gerber suffered 
from tuberculosis of the axillary glands following a tubercle. They are 
observed in butchers, veterinary surgeons and pathologists, especially 
in those beyond middle life. 

6. Ulcers. — Tuberculous ulcers may develop from cuts by broken 
sputum cups, bites of tuberculous subjects, ants or flies, burns, tattooing, 
skin grafting, circumcision or vaccination. 

Treatment of Tuberculosis. — (A) Prophylaxis. — 1. Antibactllary 
prevention concerns the etiological factors in the dissemination of the 
bacillus. Cleanliness of the skin; disinfection of contaminated feces, 
urine or pus; confiscation of diseased meat; and regulation of dairies 
and inspection of cows are important; but the destruction of infective 
sputum is the prime indication. Tuberculous, pneumonic, grippal and 
other sputa must be destroyed. An appeal is made to the conscience 
or selfishness of tuberculous patients, setting forth the risks of auto- 
reinfection. Of all educators, Biggs, of New York, and Flick, of Phila- 
delphia, have rendered the greatest service. Patients should carry small 
spit cups, of which Dettweiler's and Major Appel's are the best; the 
sputum should be burned or boiled before it dries. Spittoons are danger- 
ous. The patient should sleep alone, and kissing must be interdicted. 
The bedclothes, linen and eating utensils should be steamed or boiled. 
Rooms should be cleaned with moist cloths and swept with the windows 
and doors open. The danger of swallowing sputum must be set forth, 
and the mouth washed out with some antiseptic before eating, though a 
few bacilli with the food are probably destroyed by the gastric juice. 



184 BACTERIAL DISEASES 

In Germany the reduction of mortality by 33 per cent, is clearly due 
to an awakened public intelligence. The dangers of overcrowding, 
public conveyances and foul air, are already impressed upon the public, 
yet public school ventilation remains a scandal. 

2. Governmental Prophylaxis, less promising in republican than 
in autocratic states, is important. It comprises: Education of the 
public by publication of the dangers and preventive measures in tuber- 
culosis; the establishment of sanatoria for the poor, among whom the 
mortality is four times, and the morbidity many times greater than in the 
rich; the building of separate wards for the hopelessly diseased; the 
reporting of the disease ; and the regulation of the air capacity of dwelling 
rooms, in tenements, factories and stores. Aside from great suffering 
and sorrow of thousands in every large community, there is an enormous 
economical waste in work and wages, an enormous cost in hospital care 
and a great loss in live stock. The sociological damage is apparent, as 
the ravages of tuberculosis involve the working years of life (15 to 60), 
while 94 per cent, of deaths from diphtheria occur under ten years. 

3. Individual Prophylaxis concerns increasing physiological resist- 
ance and promoting sound development in children. Weakly children 
should be brought up and taught in the open air, judiciously fed, watched 
during acute infections, sent into the country during vacation, taught 
moderation and later, should be informed as to the danger of alcoholism, 
sexual excesses and infections. Milk and cream should be pasteurized 
or better, boiled. 

(B) Hygienic Treatment. — The three great factors are fresh air, proper 
food and rest. Bodington (1839), in England, treated cases by fresh air, 
but to Brehmer (1850), in Germany, is due the credit of soundly estab- 
lishing the fresh-air treatment and the curability of phthisis. A few of 
his views are untenable, but many of them are the basis of the modern 
methods practised by McCormack, Driver, Dettweiler, Trudeau, Knopf 
and others. Patients were treated in sanatoria, and those at Nordrach 
and Saranac and many others, have given such excellent results that 
institutions of this class in America number almost three hundred. 
Results depend on (a) the extent of the disease; (b) the condition of organs 
other than the lungs, as the pleura, intestines, larynx and heart; and (c) 
the social status of the case. Trudeau brought about recovery in 31 
per cent, of all, and in 66 per cent, of incipient, cases; Rumpf followed 
97 per cent, of his cases : 70 per cent, of incipient cases were able to work — 
"the best test of a cure"; 55 per cent, of those in the second stage 
and 23 per cent, of those in the third, recovered. The chief value of 
sanatorium treatment is that the patient learns the lesson of living 
properly. 

1. Fresh Air. — This is the chief hygienic factor in treatment, at 
home, in sanatoria or in change of climate, (a) Treatment at home is 
especially important, as but 5 per cent, of tuberculous people are able to 
leave home. The patient should be carefully clothed and recline in the 
sun with the windows of his room open, or lie on a veranda, one-quarter 
to one-half the sunny hours, according to the season. At night the 
patient's bed can be brought to an open window, from which "a window 



TUBERCULOSIS 185 

tent" of canvas encloses the head and leaves him out of doors. Rain, 
snow, dampness and extreme cold are no contra-indications, nor are fever, 
cough and hemoptysis; but wind, dust and sudden variations in tempera- 
ture are to be avoided. Very thick clothing, so frequently observed among 
the poor, is unhygienic. Acute caseous and advanced types generally 
should be kept at home. Extreme care in disinfection is imperative 
lest the home become a menace to the family. For those unable to obtain 
sanatorium treatment, "classes" have proved of the greatest value 
(Pratt) . (b) Sanatorium treatment offers the advantage of strict discipline, 
systematic living and the constant regulation of the details of every- 
day life by a physician. Sanatoria should be located well outside of 
every large centre of population, (c) Change of climate was once con- 
sidered absolutely indispensable; now it is said "to be not without 
influence." No climate is specific but many offer advantages over 
the northern climate. High altitudes give purer air, stimulation of 
breathing, increase of the chest dimensions, growth of the muscles of 
inspiration, increase of metabolism and stimulation of the appetite and 
blood-making organs. Colorado, Arizona and New Mexico (4000 to 7000 
feet elevation) are excellent for opportunities to secure permanent 
occupation after recovery; because of the emphysema induced by 
altitudes, a return to the sea level should be avoided. St. Moritz, Les 
Avants and Davos (5200 feet elevation) offer a dry, clear, cold, still 
atmosphere, where patients may reside summer and winter; it resembles 
the climate of Colorado, Montana and northern Wyoming. There are 
also the Peruvian Andes and numerous other altitudes (see Solly's 
Climatology). High altitudes are best adapted to those with incipient 
lesions, slight cavity formation and little emaciation, or slowly pro- 
gressing or torpid cases. Slight fever and slight hemoptysis are not 
contra-indications; emphysema, weak heart, constant fever, great 
nervousness or repeated hemoptysis are contra-indications. Moderate 
altitudes (2000 to 2500 feet) best serve the majority of cases, as Asheville 
(2250 feet), the Adirondacks (2000 feet), Aikin (2250 feet), Summer- 
ville, Thomasville, etc. The climate of Minnesota, Nebraska and Dakota 
(1000 feet elevation) is cool and dry; dryness is more desirable than lack 
of variability. Moderate elevations do not induce emphysema, whence 
return to the sea level is easier. The sea level is best for the tuberculous 
aged, quiescent cases with great cicatrization or extensive damage, those 
with diabetes, albuminuria, nephritis, bone disease, marked anemia, 
repeated hemoptysis, emphysema or rapid softening, incurable forms, 
thin, nervous and exophthalmic subjects. Sea voyages are experimental; 
those with incipient forms, genito-urinary, glandular or osseous disease 
or open wounds are often helped. Moist, warm climates at the sea level 
are especially adapted to laryngeal disease — as the Bermudas, Florida, 
the Madeira or Canary Islands; patients with dyspepsia and diarrhea 
do well in Corsica, Palermo and Capri. Warm, dry climates, as southern 
California, Egypt, Algiers or the Riviera are good for catarrhal types. 
Climate alone, without reasonable hygiene, rarely benefits. Direct 
exposure of the body to the sun (heliotherapy) is advocated, especially 
in surgical tuberculosis. 



186 BACTERIAL DISEASES 

2. Nutrition. — Most physicians recommend 5 or 6 meals daily, but 
better results are often achieved by 3 meals, whereby the stomach is 
allowed rest. Feeding requires individualization. The staple diet is 
meat, eggs, milk, cream and butter, fish, well-cooked leguminous vegetables 
(advantageously given in soups), oil on salads, bread, pastries and 
cakes. If anorexia is of the nervous type, patients must be compelled 
to eat, but long hours in the fresh air usually stimulate the appetite. 
With habitually light eaters caution is necessary; beef -juice, milk and 
koumyss should be given; the amount should be gradually increased 
and other foods added. Wine, vermouth, fluidextract of condurango 
mIxv-xxx or strychnine, gr. -^ in solution, half an hour before meals, 
are valuable appetizers. Raw beef (zomo therapy) was recommended 
by Richet and Hericourt; fresh lean meat is cut, soaked in one-fifth 
its weight of water, pressed to extract the blood and fluid, and adminis- 
tered; it must be freshly prepared, as it soon becomes tainted. Raw 
eggs are often given between or just before meals, beginning with 1 and 
increasing to 4, three times daily, the taste being disguised by orange- 
juice. Fever does not contra-indicate full feeding. More than If quarts 
of milk induces gastric atony; it is given to advantage with bread, 
crackers or toast, in order to divide the curds; it may be peptonized, 
disguised with cocoa or cognac or given by the rectum (v. Gastric Ulcer) ; 
cream and butter are excellent substitutes for cod-liver oil, and buttermilk 
is indicated when the stomach is weak. Fats and carbohydrates are 
necessary to offset nitrogenous waste ; the dark form of cod-liver oil 
(v. i.), lipanin (94 parts olive oil and 6 parts oleic acid), malt, honey 
and cocoa are valuable. In overfeeding (sur alimentation) the tolerance 
of the stomach must be considered; Debove's method consists of gastric 
lavage followed by the introduction through the tube of three ounces of 
powdered meat, a quart of milk and three eggs. Alcohol, administered 
less often and in smaller amounts than formerly, is frequently indicated 
symptomatically (v. i.) ; small amounts of red wine or cognac and whisky 
in egg-nogs are very valuable as a food and tonic. Tobacco should be 
interdicted; in special cases a cigar or two daily may be allowed, but the 
smoke must never be inhaled. 

3. Rest. — Rest is one essential in Dettweiler's therapy. Patients 
should lie in the bright sunshine and fresh air, and active mental occu- 
pation should be carefully avoided. Exercise destroys tissue, induces 
anemia and irritates the heart; it is distinctly contra-indicated by fever, 
emaciation, hemoptysis, rapid pulse, nausea and coughing. "Too 
many cases of phthisis walk into their graves." Late in the treatment 
graduated exercise may be taken. Pulmonary gymnastics and pneumatic 
differentiation are clearly injurious. Hardening and exercise should be 
obtained by quick, dry rubs with a large, coarse towel, after w r hich rapid 
partial, and then general, wet rubs may be instituted; hydrotherapy 
is shunned when there is any tendency to hemoptysis. 

(C) Specifics. — As yet there is no specific for tuberculosis. 

Tuberculin Therapy. — (i) Theory of Action. — Tuberculin is an endo- 
toxin and not a toxin. Its injection causes an increase in antibodies 
(opsonins, agglutinins and precipitins) and an increased tolerance of the 



TUBERCULOSIS 187 

tuberculin; unhappily, however, increased tolerance to tuberculin is 
not identical with immunity, as is demonstrated clinically at autopsy 
and in animals. The immune substances may be antitoxic but possibly 
not bacteriolytic. In treatment it is not specific but merely accessory, 
(ii) The indications are: Incipient subjects who are well nourished, 
without fever and come to a stand-still after some improvement, (iii) 
The contra-indications embrace malnutrition, rapid wasting, profound 
toxemia, pronounced fever, acute phthisis, rapid heart action, nephritis 
and great nervousness. * (iv) Dosage is solely empirical, since there is 
no scientific gauge of tolerance (Wright's opsonic index and other methods 
are open to error). Carelessly used, tuberculin is dangerous. Of the "old 
tuberculin" (O. T.); the initial dose should be 0.0000001 gm.; the initial 
dosage for the "bacillus emulsion" (B.E.) is 0.00000001 gm., increasing 
gradually toward the decimal point, every three days at first, and later once 
a week between doses. The maximum dose of O. T. is 0.0001 and B. E. 
0.0005; the course is 5 months, interrupted when coryza, cough, indiges- 
tion, fever, emaciation or hemoptysis intervenes, (v) Results: Trudeau 
conservatively states that "tuberculin immunizes, prolongs life, causes 
the bacilli to disappear from the sputum, aborts commencing infection 
and also the smouldering fires of chronic infection." The subject is still 
sub judice and as one writer puts it, "a chaos of personal impressions." 

(D) Expectant or Symptomatic Treatment. — 1. Fever. — Rest, digest- 
ible food, fresh air and change of climate are indicated in great preference 
to drugs. Strong wine may be administered as the fever begins to rise; 
arsenic is recommended, but no remedy in safe doses controls fever. 
Quinine disturbs the digestion. Sponging is efficacious. 

2. Cough. — A slight morning cough, removing secretion, needs no 
restraint, but, if excessive, it begets coughing by congesting the lungs, 
and its consecutive exhaustion, insomnia, aspiration and vomiting 
necessitate interference. Fresh air and avoidance of dirt, dust and 
smoke are most beneficial. Rest, especially after eating, should be en- 
forced. The cough is somewhat under the control of the will, as Galen 
knew; the comment on its absence, especially at the table, is universal 
among observers of sanatorium methods,- slow breathing, with the head 
slightly thrown back, or the sipping of warm water, with 10 grains of 
salt, before meals often aids in suppressing the emetic cough. Creosote 
discovered by Reichenbach, in 1832, is not specific, but often increases 
the appetite, modifies abundant secretion from the bronchi (by which 
the drug is in part eliminated), and relieves the cough. Administration 
in the fluid form is best, beginning with one drop, well diluted, after 
meals, and increasing to ten drops; full dosage often irritates the stomach 
and kidneys; it should not be given in febrile cases or in hemoptysis. 
Creosote may be administered in milk, water, gentian or sherry wine: 

R- — Creosoti 5iss 

Glycerini Sss 

Tr. gentianse co §iv 

M. et S. — One teaspoonful after meals, well diluted. 

1$ — Creosoti 5iss 

Mucilag. acacias . §iij 

Pulv. althsese q. s. 

M. et fac pilulas 10°. 
S. — One after meals. 



188 BACTERIAL DISEASES 

Guaiacol carbonate is better tolerated and is cheaper: 

1$ — Guaiacolis carbonatis . . . 5iij 

Strychninse nitratis, 

Arseni trioxidi . aa gr. iss 

Sparteinse sulphatis gr. xlv 

M. et fac chartulas 40. 

Sig. — One powder after meals. 

Cod-liver oil, first used by Hughes-Bennett, is usually given in full doses 
which disturb digestion; the first dose should be 10 drops and the amount 
gradually increased. It is most valuable in tuberculosis of the glands 
and bones. Eructations can be avoided by administration one hour 
after meals, when the food leaves the stomach. The oil is readily absorbed 
because of the bile contained; it is possibly alterative but is not superior 
to butter or cream. Kit may be floated on whisky, beer or milk, and 
gulped down. Its taste may be partly disguised by using syrup of 
orange, capsules, or a "chaser" of whisky. Opiates may be used, 
such as paregoric; codeine gr. J with aq. laurocerasi and glycerin aa 
Tfl,xv and syr. tolutani 5 j q. i- d.; heroine gr. T V q. i. d.; even morphine 
sulp. gr. J with ac. hydrocyanici dil. TTlij; myrtol gr. ij, a.m. and p.m.; 
terpin hydrate gr. ij-v, t. i. d.; and ol. terebinthinseniij. (See formulae 
under Bronchitis.) 

1$ — Tr. belladonnse . 3ss 

Spts. chloroformi §iss 

Mucilag. acacise §j 

Aquae q. s. ad. giij 

M. et S. — One teaspoonful after meals, or as indicated. 

Expectorants are to be avoided because of their nauseating tendencies. 
Tr. benzoin co., 1 per cent, phenol, and creosote may be vaporized. 
The nasopharyngeal mucosa may be painted with iodine, potas. iodide 
and glycerin in proportions of 1, 10 and 100; or 20 per cent, menthol 
applied locally (v. Laryngeal Tuberculosis). 

3. Sweats. — The room should be cool at night, the bed not too heavily 
covered, and the body protected by a flannel night-gown. A glass' of 
cold milk, with 5ij of cognac, given at bedtime, is often beneficial or 
morphine when sweats are associated with cough and insufficient oxy- 
genation. Atropine gr. yj-g- to -gV> and camphoric acid gr. xv to xxx, 
at bedtime, are superior to aromatic sulphuric acid TUx to xx, agaricin gr. 
yV to iy> t r - nucis vomica? Tfl,xxx, picro toxin gr. -^ and muscarin Vf[v 
of a 1 per cent, solution. 

T$ — Quininae sulph 3ss 

Calcii hypophosphitis 3ij 

Extr. nucis vomicae gr. v 

M. et fac pilulas 20. 

S. — One after meals. 

4. Hemoptysis. — Exertion, loud talking or singing and excesses in 
alcohol, venery, coffee or tobacco, must be shunned in all cases. It 
is well to warn patients of the possibility of hemoptysis, in order to 
prevent undue excitement, if it appears. Effusive pleurisy should not 



TUBERCULOSIS 189 

be tapped in recent bleeding from the lungs, as thoracocentesis has pro- 
duced fatal hemoptysis, The indications are absolute physical and mental 
rest, the semirecumbent posture and silence; massage and stimulants are 
contra-indicated; no physical examination should be made except by 
auscultation, as percussion is obviously dangerous; and a hypodermic 
of morphine should be given to lessen cough, quiet the heart and allay 
the excitement attending most hemorrhages. As the tonus of the pul- 
monary vessels is beyond regulation, ergotin, tannic acid and other 
hemostatics are useless, though digitalis and fresh suprarenal extract 
gr. ij-v are sometimes efficacious. Salt 3 j is a popular remedy and is 
supposed to act by stimulating the vagus. An ice-bag should be placed 
over the heart and one over the lung, if rales are heard. Deep breathing 
seems to lessen bleeding. Calcium lactate gr. xv t. i. d. for two days is 
valuable. Amyl nitrite, recommended by F. Hare, is given at midnight, 
when the vasomotor centre is regaining its tone, lost during sleep. 01. 
terebinthinae 1Uij-iij is considered the best drug by Frantzel. In 
severe or recurrent hemorrhage, bandaging of the extremities (Hippo- 
crates), to lessen the return flow of blood, or injection of horse serum 
may be indicated. As a last resort in hemoptysis, or in cavity forma- 
tion, artificial pneumothorax has been advocated (Morton, 1833) . l 

5. Pain. — Pleuritic pain is treated by adhesive straps; if muscular 
it is treated by codeine, fomentations or phenacetin. 

6. Dyspnea. — If due to stagnant secretion, change of posture aids 
in its evacuation; if asthmatic, iodide gr. iij is indicated, but with care 
lest it congest the lungs; if cardiac, digitalis or strychnine is indicated. 

7. Cardiac Weakness. — Rest, an ice-bag over the precordia, cham- 
pagne, camphor, strychnine or digitalis are in order. 

8. Insomnia. — The patient should have fresh air night and day, a 
light, early evening meal, a glass of beer, porter or some whisky on 
retiring. Bromides, codeine and morphine are beneficial. 

9. G astro-intestinal Symptoms. — Nervous anorexia is relieved by 
fresh air, forced feeding and guaiacol (v. s.). Dyspeptic symptoms neces- 
sitate a scant diet and feeding by rectum. In gastric atony, frequent 
meals of small volume, limitation of fluids and strychnine are indicated. 
For gas formation or pain the following are indicated; phenol Ml j; resorcin 
gr. iij; bismuth gr. x; extr. belladonnas or spts. chloroformiTflxx. Pyrosis 
may be corrected by sod. bicarb, and magnesia carb. aa gr. xxx. Hyper- 
acidity demands a milk diet, belladonna, Carlsbad water and alkalies; 
anacidity is relieved by easily digested foods and hydrochloric acid. 
Vomiting is caused by the cough, overfeeding, overmedication or irrita- 
tion of the pharynx (Lugol's solution locally, or gargles 1 to 10 of pot. 
bromide); small doses of carbolic acid are most successful (v. Typhoid). 
Constipation (q. v.) is treated by the usual measures. Diarrhea may be 
dyspeptic, toxemic, ulcerative or amyloid; the following are indicated: 

1 Nitrogen gas is injected, under manc-metric control, no gas being injected till the column 
oscillates several centimeters with each inspiration (whereby it is claimed that gas embolism, 
subcutaneous emphysema and pulmonary perforation are avoided) ; 300-700 c.c. may be 
injected. Contra-indications are bilateral involvement, dry or effusive pleurisy, cardiorenal 
disease or great debility. In all probability, the revival of this method will result in a 
repetition of the former fiasco. Some 3000 cases have been treated, with some fatalities. 



190 BACTERIAL DISEASES 

tannic acid gr. v; opium gr. j; lead acetate gr. ij; camphor gr. ij; 
tannigen gr. vij-xv, or bismuth 5j (see Typhoid). 

10. Anemia. — This is benefited by fresh air, change to a high altitude, 
full diet, iron in small doses and arsenic. 

11. Sexual Symptoms. — Intercourse must be forbidden in incipient 
as well as in advanced cases. Three years after recovery marriage may 
sometimes be allowed; it is generally less injurious to men than to 
women. Tuberculous parents may rear healthy children, but tuber- 
culosis ("scrofula") is common. In 66 per cent, of pregnant tuberculous 
women the prognosis is bad, and laryngeal tuberculosis is almost in- 
variably fatal within a short time. In severe cases abortion may be con- 
templated; Martin and Schauta advise abortion, but in 70 per cent, 
of cases abortion does not alter the clinical course. 

12. Treatment of Other Complications. — (v. s.) 



LEPROSY. 

Definition. — A chronic incurable contagion, caused by the Bacillus 
leprae and characterized clinically by nodules, which are observed ex- 
ternally and internally in many organs; or by perineuritis leprosa, which 
causes sensory, motor and other symptoms. 

Distribution. — The home of leprosy is Egypt, where it existed 2400 
or even 4620 B.C. The leprosy of Leviticus probably includes other 
diseases. It prevailed in India 700, and in China 400 years B.C. 
Just before the Christian era, Pompey's soldiers brought leprosy to 
Italy, whence it spread over Europe and the Crusaders at the end of 
the thirteenth century further disseminated the disease. In Europe there 
were 20,000 asylums, but many cases were probably syphilis; the disease 
has steadily decreased since the sixteenth century. It is estimated that 
at present there are 3,000,000 cases in the world. Cases are found in 
Europe, Asia, Africa and America (New Brunswick, Nova Scotia and 
British Columbia) ; in the United States (California, Louisiana, Minne- 
sota, North Dakota, Florida; in 1912 there were 146 lepers in this 
country, of whom half were native born). 

Bacteriology. — The Bacillus leprce was found by Hansen (1871) and 
fully described by Neisser (1879). It is a fine, narrow rod, measuring 
J to f of a red cell, and closely resembles the tubercle bacillus mor- 
phologically and in its staining properties; both bacilli contain fat. 
Inoculation is the surest differential criterion. In the internal viscera 
it may exceed the dimensions attained in the skin and mucosae five or 
six times. It is motile and has been cultivated. It is found in the 
typical nodes and infiltrations of the skin and upper mucosae, fresh 
maculae and recent nerve disease, sebaceous and hair glands, lymph 
glands, bloodvessels, blood during fever (metastatic distribution), 
and in practically all the viscera, secretions and excretions. Strickler 
found it in the nasal secretion in 96 per cent, of the nodular, 96 per cent, 
of the mixed, and in 66 per cent, of the nervous type. It corresponds 
to all of Koch's criteria; i. e., it is always present in leprosy; it can be 



LEPROSY 191 

cultivated, and has been inoculated in mice, guinea-pigs and monkeys; 
the value of successful inoculations on criminals under sentence of death 
has been justly criticized, for these cases developed in a leprous com- 
munity. Leprosy is contagious only by long and intimate contact with 
lepers. The nodular is far more dangerous than the anesthetic type. 
Infection may be direct or indirect and chiefly through the skin and 
nose, and possibly the genitalia. Extension occurs more by the lymphatics 
than the bloodvessels. Only 4 per cent, of children of leprous parents 
acquire the disease. More cases occur in colored than in white races, 
more in men than in women, more in the poorer than in the upper and 
middle classes and largely between the ages of fifteen and thirty. 

The incubation is at least three to five, sometimes twenty years. 

Symptoms. — Visceral involvement is seen in every type; the main 
types are nearly always somewhat blended. 

1. Nodular Type (Lepra tuberculosa). — The prodromal toxemic symp- 
toms indicate an infection already established, but escaping recog- 
nition; they are depression, formication, sweats, pains, vertigo, digestive 
disturbance and temperature. After months or years, macula? appear 
on the face and extremities; they may disappear, leave pigmentation or 
metamorphose into nodules, which are present in 75 per cent, of all 
cases. The nodule or leproma, is a granuloma similar to the tubercle 
or gumma, highly vascular and formed of a scanty reticulum, in which 
lie emigrated leukocytes, small epithelioid cells and the larger multi- 
nucleated lepra cells of Virchow, which contain close clumps of bacilli. 
The nodes by fusion form gelatinous, glistening and yellowish-red infil- 
trations. The nodes vary from the size of a millet seed to a hazel-nut or 
walnut; in the skin they are dark red and later yellowish-brown, glisten- 
ing, vascular, slightly desquamating and at first soft but later harder. 
Sensation is always disturbed in their vicinity. They are most conspicuous 
on the face and hands, but also appear on the extensor surfaces and 
very seldom on the soles, palms, scalp or penis. The forehead, nose, 
cheeks, chin, lips and ears are thickened, the nose becomes flatter, the 
eyebrows, lashes and beard are shed. The eyes are involved in over 
90 per cent, of the cases; the expression is leonine (leontiasis) , or, as the 
ancients called it, faun-like (satyriasis). The nodes grow and extend 
slowly, and the lymph vessels and glands become enlarged and tender. 
Sometimes the progression is intermittently acute, with fever and an 
eruption resembling erysipelas. They often necrose and ulcerate. At 
the same time or later, nodules which are prone to early ulceration and 
infiltration occlude the nose, roughen the voice, distort the larynx and 
throat, and impede mastication, swallowing or respiration. Cicatrization 
of the face causes added deformity. 

2. Nervous Type (Lepra nervorum, anesthetica, mutilans). — The 
most common prodromes are fever, neuralgia, paresthesia, hyperesthesia 
and cerebral congestion. Macula? develop on the face, trunk or limbs; 
they are pale or dark red, slightly raised, growing peripherally and 
paling centrally and present a glistening or powdered aspect. Histo- 
logically they are identical with the nodules, but contain fewer bacilli, 
contain no large cells and tend more toward fibrous change. Their 



192 BACTERIAL DISEASES 

distribution is asymmetrical, like that of the underlying nerve lesions; 
they are often oversensitive, sometimes pigmented (lepra nigra) or 
leukoderma-like (lepra alba). 

Sensory disturbances are due to lesions in the nerve trunks, which 
are the seat of a perineuritis and interstitial neuritis which slowly com- 
press the nerve fibers. The connective tissue and the bacilli differentiate 
this from the parenchymatous neuritides. Unlike ordinary neuritis, 
leprous neuritis affects the sensory more than the motor filaments. There 
is an irregular dissociated anesthesia in which the perception of pain 
and temperature is usually more dulled than other forms of sensation, 
mostly in the peripheral branches in the arms and legs. Sensation may be 
perverted or retarded and sudden anesthesia is considered rather char- 
acteristic. Pain may be slight or agonizing, as in a personal case of ten 
years' duration. The nerve trunks are palpable and tender in many cases; 
in the case cited the ulnar nerve was thicker than a lead-pencil; the 
auricular nerve is felt in 90 per cent. Motor weakness and atrophy 
are less common and rarely extreme; the oral, sometimes the masticatory 
and ocular muscles are paretic; ulnar and peroneal implication causes 
the " claw-hand" and "claw-foot"; facial paralysis occurs in 9 per cent, 
of cases. The tendon reflexes are often increased, sometimes normal 
or decreased; there is often fibrillation and increased myotatic irrita- 
bility. Trophic changes include edema, glossy skin, " mal perjorant" 
(26 per cent.), loss of hair or nails, bone resorption, rheumatoid swellings, 
ankylosis and pigmentation. Great trophic changes mark the lepra 
mutilans. 

3. Mixed Type. — This is a combination of the nodose and anesthetic 
types. In all developed forms the internal tissues are invaded: the liver, 
spleen and lymph glands are enlarged; the lungs show peribronchial 
foci, cavities or induration; and the intestine is infiltrated. The sexual 
functions are decreased or lost. Infantilism results in cases developing 
before puberty. Cachexia, sensitiveness to cold, low temperature and 
heart weakness develop. 

Course and Prognosis. — The course is slow and progressive, the outcome 
invariably fatal. The nodular type covers eight to twelve years, the 
anesthetic form fifteen to twenty years, but either variety may endure 
seven decades; 38 per cent, of cases die of leprosy (exhaustion, diarrhea, 
cardiac weakness), 22 of chronic nephritis, 17 of lung disease (oftener 
leprous than tuberculous), 10 of diarrhea (leprous infiltration of the gut), 
and the remaining 13 per cent, die of erysipelas, sepsis, amyloidosis and 
intercurrent disease. 

Diagnosis. — The diagnosis is based on the history of residence and 
exposure which is often suppressed by the patient, on the macules or 
leukoderma found in 90 per cent., on the anesthesia, amyotrophy and 
multilation, and on the finding of the bacillus in the nasal secretion, 
nodes and macules. In some reports, a positive Wassermann is given. 

Treatment. — 1. Prophylaxis. — All suspicious cases should be registered 
and all clear cases sequestrated. 

2. Therapy. — Few drugs are helpful, (a) Gurjun oil 5 ss— ij in 
water or lime-water; (b) chaulmoogra oil, in milk, beginning with a few 



ACTINOMYCOSIS 193 

minims and increasing to 3j _ iij; (c) salves of 5 per cent, pyrogalloi or 
10 per cent, chrysarobin ; (d) Calamette's antivenin, 20 to 30 c.c; (e) 
arsenic, nastin, salvarsan, carbon dioxide snow and x-rays are recom- 
mended. 



NON-BACTERIAL FUNGUS INFECTIONS. 

ACTINOMYCOSIS. 

Definition. — A chronic infection caused by the actinomyces (literally 
"ray fungus"); mostly sporadic in cattle and occasionally in man; 
and characterized by chronic inflammation in the mouth, head or neck, 
lungs or intestines or abdomen. 

History. — Von Langenbeck (1845) and Davaine (1850), observed 
the peculiar sulphur granules in the pus. Bollinger (1877) first scien- 
tifically described the fungus in cattle, and J. Israel (1878) found the 
parasite in human cases, but to Ponfick (1879) is due the credit of 
identifying the bovine and the human types. 

Etiology. — Statistics in Berlin, Breslau and Vienna show large numbers 
of cases; there are more in Scotland, Denmark, Italy and Russia than in 
America, where up to 1902, 100 cases were observed. Seventy per cent, 
of the cases occur in males and 33 per cent, between twenty and thirty; 
82 per cent, between ten and fifty. The fungus enters chiefly by the 
mouth, in which ragged teeth, abrasions, etc., favor its access. Israel 
and Lord believe it inhabits the tonsils and carious teeth. Though little 
is known of it outside of the body, it probably exists in the intestines of 
herbivora. Most cases occur in young cattle at dentition and 89 per 
cent, in the last half of the year, when the ingested grain is dry. 

Bacteriology. — The parasite, classified as a streptothrix is found in 
small granules which measure 0.15 to 0.75 millimeters, usually ovoid 
or "radiate" when squeezed under the cover-glass. The younger forms 
are transparent, sago-like, whitish-gray bodies which may be easily over- 
looked; the older sulphur-like granules consist of threads and coccoid 
bodies which some consider spores. Clubbing is considered a degenerative 
change. The threads divide and branch. The fungus is therefore 
pleomorphic. It stains with the usual dyes and Gram's method. Cul- 
tures are successful in 50 per cent, of the cases, by mixing the granules 
with softened gelatin and bouillon. The colonies are thick, folded, 
membranous, resistant and at first have a mucoid or crystalline appear- 
ance. Infection is very rarely direct either from animals to man or from 
one person to another. The virulence is therefore of low grade. 

Forms. — Incubation averages four weeks. Clinically there are three 
main forms: (1) That of the head and neck; (2) the lower digestive 
tract; and (3) the respiratory tract. 

1. Head and Neck. — This form constitutes 50 per cent, of actinomy- 
cosis. The atrium is the mouth and throat. The fungus is surrounded 
by a massive accumulation of round cells which soon degenerate centrally. 
13 



194 NON-BACTERIAL FUNGUS INFECTIONS 

The connective-tissue reaction is marked and the proliferation shows 
numerous round or polygonal cells with large nuclei — the epithelioid 
cells. Giant cells also form. The process is considered chronic inflam- 
mation by Bostroem, and by Israel an infective granuloma, resembling 
the tuberculous or syphilitic process. The destiny of the granulations 
is modified by the resistance of the tissues and by the animal diseased: 
(a) In man the granulation wall melts into a mucoid, creamy fluid, 
in which there are oil, fibrin, blood, pigment and actinomycotic cocci 
and threads; the "cold" abscess is formed by the fungus itself which, 
unaided by pyogenic organisms, burrows to the surface by circuitous 
fistula?; it discharges a 'thin, puriform secretion like that of tuberculous 
glands but contains the sulphur-like grains, (b) In cattle and horses 
the granulation tissue is more effectually limitative and develops hard, 
board-like or ligneous tumors ("lumpy jaw," "wooden tongue"); sup- 
puration and miliary dissemination are less, and calcification is more 
frequent than in man. In human subjects the infiltration may involve 
the neck, face, tongue, pharynx, tonsils, larynx and thyroid gland. 
There is frequent inflammation of the soft tissues, especially submaxillary 
or submental infiltration and superficial invasion of the bones. In a 
few cases the maxillae may be primarily invaded. Sarcoma and caries 
may be simulated. It may spread regionally to the base of the brain 
and meninges; along the spine causing vertebral erosion; and behind 
the sternum with mediastinal infiltration. 

Symptoms. — The fever is irregular. Pain and tenderness are not 
marked, for the process is indolent or chronic. In 26 cases of involvement 
of the tongue, its forms were a hard tumor, localized abscess or diffuse 
suppuration; it causes less pain and adenitis than does cancer. Dys- 
phagia accompanies retropharyngeal involvement, edema occurs in laryn- 
geal localization and other local interference such as venous obstruction 
is frequent. The writer observed trismus and severe unilateral trifacial 
neuralgia from a primary focus at the base of the skull, recovering 
after operation. Besides the above regional invasion, hematogenous 
extension by metastasis may occur in this type as well as in the others 
to be described later. Trauma may initiate generalization. Unlike 
tuberculosis, extension to the lymphatics, or general dissemination by 
them, is unusual. In the head-and-neck form the mortality is 10 per cent. 

2. Digestive Tract. — The digestive tract ranks next in frequency 
of infection (25 per cent.) ; 50 per cent, occurs in the region of the ileum, 
cecum and appendix (perityphlitis actinomycotic^) ; of 200 instances of 
inflamed cecum, 4 per cent, were actinomycotic. Local pain, tender- 
ness, induration and adhesions follow the primary lesion in the intestine, 
which in rare instances remains superficial (enteritis actinomycotica super- 
ficialis). Small nodes develop in the submucosa, followed by softening 
and the development of small ulcers, the undermined edges and uneven 
bases of which resemble tuberculous ulcers. Secondary pyogenic infec- 
tions are frequent. The ulcers may cicatrize or fuse into larger ulcerations. 

Symptoms. — The signs were those of appendicitis in 150 cases on record. 
Colic and vomiting are often present and constipation is more frequent 
than diarrhea. Extension of the process downward involves the iliac 



ACTINOMYCOSIS 195 

bone and occasionally the hip, bladder, ovaries, vagina or rectum; the 
ray fungus is voided in the urine and feces; and anteriorly, preperitoneal, 
suprapubic or muscular infiltrations occur, with external fistula?. The 
process then extends backward into the retroperitoneal cellular tissue, in 
which it may burrow around the kidneys or into the chest — perineph- 
ritis, peripsoitis, parametritis or peripleuritis. In rare cases, freely mov- 
able operable tumors may develop. Vascular metastases may occur; liver 
abscess is the most frequent development, and is secondary, though some- 
times apparently primary (40 cases reported). In 70 per cent, death 
results from exhaustion, mixed infection or amyloidosis. Diagnosis is 
made from the yellow granules or microscopic recognition of the 
fungus, 

3. Respiratory Tract. — Respiratory involvement is less frequent 
(20 per cent.). It is (a) secondary to regional extension from the neck 
or abdomen, or to infarcts, or, still less frequently, (b) primary in the 
lungs (very rarely as a fibrinous or actinomycotic bronchitis). Most 
often it invades the alveoli. The lower lobes, its usual seat, show a gray 
hepatization with the ordinary actinomycotic changes. Fusion of the 
usually small foci may involve large portions of tissue, but demarcation 
is usual in the lung. The clinical picture varies: (i) In some instances 
cavity formation is obvious, with hectic fever, a harassing cough and 
malnutrition; the sputum is puriform, sometimes fetid and stained 
with altered blood like raspberry jelly and often reveals the actino- 
mycosis rays, (ii) Induration may occur from cicatricial development. 
(iii) Pleurisy, peripleuritis, pericarditis or mediastinitis may be the 
dominant finding. There may be much luxation of the intrathoracic 
contents, with dyspnea, dilatation and hydrops. Penetration may occur 
through the chest wall with characteristic discharge from the sinuses 
which run along the spine and iliopsoas muscle, or into the abdomen. 
Hematogenous generalization occurs as in other forms. In 25 per cent, 
of cases the ray fungus is seen in the sputum and tuberculosis is excluded 
by absence of tubercle bacilli and elastic fibers; differentiation may be 
impossible. The course is usually subchronic (averaging under a year), 
less often chronic (two or three years) and very rarely acute. Only 6 
recoveries are reported. 

4. Other Localizations are rare; 23 primary skin cases are reported. 
They may resemble lupus or tubercle. Primary brain lesions niay 
simulate brain tumor or cause cortical epilepsy. Very few cases of 
primary genito-urinary infection are recorded. The lachrymal duct or 
middle ear is very rarely the primary focus. 

Diagnosis. — Similar fungi may cause difficulty in diagnosis (v. i.). 
Treatment. — 1. Prophylaxis. — Care is necessary in regard to picking 
the teeth with straws. Thorough cooking of cereals is essential. 

2. Surgical Extirpation. — A sharp spoon is used to clean accessible 
foci and fistula?, which are then packed with iodoform or sublimate 
gauze. Injections of bichloride of mercury (0.5 per cent.) are recom- 
mended. Recurrence is frequent in abdominal types. 

3. Potassium Iodide. — In cases inaccessible to the knife, potassium 
iodide is excellent. It is not parasiticidal, but large doses soften the 



196 NON-BACTERIAL FUNGUS INFECTIONS 

tissues, prepare operable cases for surgical measures, inhibit growth 
and minimize metastasis; 53 per cent, of bovine cases recover under its 
use. Rydygier injects large quantities of a 1 per cent, solution into 
the affected tissues. Tuberculin, vaccine therapy and the internal use 
of copper sulphate, J to 1 grain are recommended. 

NOCARDIOSIS. 

J. H. Wright describes nocardia as an acid-fast, branching strep tothrix, 
differing from actinomycosis in that it does not occur in compact struct- 
ures, does not radiate or form club-bearing granules and never is local- 
ized about the mouth and jaw. Wright collected a dozen cases in which 
the lesions and symptoms resembled pulmonary tuberculosis or septico- 
pyemia (abscesses in the skin, brain, etc.). The prognosis is unfavorable, 
although iodides sometimes help. 

SPOROTRICHOSIS. 

Schenk (1896) discovered the Sporotrichum Schenkii, a fungus with 
branched mycelia and numerous spores. Over 200 cases are reported, 
largely in farmers, in wiiom trauma probably opens the way for cutaneous 
infection. Its toxin produces little fever. The serum exhibits specific 
agglutination. Infection follows the lymphatics. The hard nodules 
may resemble a chancre; other hard nodes produce subcutaneous ab- 
scesses; still others resemble cutaneous gumma or tuberculoma his- 
tologically and clinically. Lesions may appear in the mucosae or general- 
ization may ensue with lesions in the bones, joints, muscles, lungs, etc., 
by way of the blood stream. Surgery and iodides are indicated. 

OIDIOMYCOSIS. 

Coccidioidal granuloma is a specific, subacute or chronic infectious 
disease. Twenty-four cases have been recognized in various parts of the 
western hemisphere, most of them in California. The histological changes 
in the lesions closely resemble those of tuberculosis. Differential diag- 
nosis depends on finding the specific microorganism, Coccidioides im- 
mitis, a species of mould belonging to the Ascomycetes. In the animal 
body it exists as spheres enclosed in doubly contoured capsules and 
multiplies by endogenous spore formation. As to blastomycosis, caused 
by the Cryptococcus dermatidis, Brown and Cummins point out well- 
defined differences in the pathogenicity of the two diseases, coccidioidal 
granuloma being always and often rapidly fatal in man, while blasto- 
mycosis is commonly not so, except for the systemic cases. The clinical 
and pathological aspects of coccidioidal disease are those more closely 
resembling tuberculosis, as there is a greater predilection for the lym- 
phatic system than in blastomycosis, and cutaneous lesions are likely 
to be more ulcerative. There appears but one reported case of coccidioidal 
disease in the female sex, whereas there have been many of blastomycosis. 



SYPHILIS 197 

Iodides have temporarily benefited many, and apparently cured a few, 
blastomycosis patients, whereas they have had no effect on the rapidly 
progressive lesions and toxemia of coccidioidal granuloma. Morpho- 
logically, in pus and solid tissues they are differentiable by the endo- 
sporulation in the one and budding in the other. Generalization may 
occur in the bones, joints, meninges, etc. Iodides, x-rays, radium and 
vaccines are indicated. 

MYCETOMA. 

Madura foot, first described by Kaempfer (1712), is largely seen in 
India; seven American cases are reported. Infection of the foot occurs 
usually in those going bare-footed — by the Streptothrix madurse; its 
varieties are the red, black and yellow. A nodule on the sole forms, 
softens, ruptures, and by extension leads to enlargement of the foot, 
sinus formation and involvement of all structures of the part, muscles, 
bones, etc. Amputation is required. 

ASPERGILLOSIS. 

Aspergillus fumigatus infection may occur as a primary or secondary 
disease. As birds, cattle or even dogs may be affected, the disease may 
occur in pigeon-feeders or in hair-sorters, from rye-flour dust employed 
to remove grease from the hair. Bronchopneumonic patches develop, 
from which induration or necrosis ensues, resembling phthisis and gener- 
ally ending fatally. 



PROTOZOAN INFECTIONS. 

SYPHILIS (POX, VARIOLA MAGNA, LUES VENEREA). 

Syphilis is an ancient disease, as indicated by syphilitic bones belong- 
ing to the stone age. Nusi King described syphilis in China 2600 B.C. 
The first clear outbreak occurred in 1494 among the troops of Charles 
VIII. Fracastorius in 1530 called the disease Siphilus (a shepherd smit- 
ten with the disease by Apollo because of blasphemy) . A full account 
of this disease will be given because of its collossal importance. 
Metchnikoff's historical sketch distinguishes three epochs: First, the era 
of superstition, in which the only discovery was mercury; the second 
empiric period concerned the clinical pathology and the differentiation 
of gonorrhea and chancroid; the third dates from 1905, since when the 
cause, experimental inoculation of syphilis, its serodiagnosis and the 
cultivation of the treponema have been determined. 

Definition. — A specific chronic infection, caused by the Treponema 
(Spirochete) pallidum, and found in man only, either hereditary or 
acquired by inoculation, in the seat of which a primary lesion or hard 
chancre develops, followed in two or three months by secondary lesions 



198 PROTOZOAN INFECTIONS 

in the skin and mucosse. After months or years, tertiary lesions or 
gummata develop in the viscera, bones and skin, followed in some in- 
stances by the so-called parasyphilitic manifestations, as tabes dorsalis, 
dementia and aneurysm. 

Stages According to Ricord. — The Primary Stage. — (1) Incubation 
lasts until the chancre appears, when syphilis is already a general disease ; 
(2) the chancre develops, the lymph vessels and adjacent glands enlarge, 
and there is a period of latency, the second incubation. 

The Secondary Stage. — (1) Symptoms prodromal to the eruption, 
as fever or anemia, develop and then (2) the eruption appears on the skin 
and mucosse, with headache, "rheumatism," iritis, or sometimes jaundice, 
albuminuria and splenic tumor. 

The Tertiary Stage. — This may follow very closely upon the second- 
aries or appear with them (syphilis maligna and hereditary forms) 
but usually is not manifest for three or four years (even fifty or sixty). 
Tumor-like gummata occur in the skin and viscera, especially in the 
liver, scrotum, brain and cord. Unlike secondary manifestations, they 
are asymmetrical, persistent, recurrent and less contagious. There is 
a close histological resemblance between the primary, secondary and 
tertiary lesions. 

The quaternary or parasyphilitic stage of Fournier, Sigmund, 
Lancereaux and Baumler is not included in Ricord's division. In this 
group of affections, the spirochete is also found, as in paresis. 

I. Acquired Syphilis. — Etiology. — 1. Transmission by Sexual Inter- 
course. — This causes the great majority of cases, but the term lues 
venerea is often inaccurate and unjust since syphilis may occur in 
the innocent (syphilis insontium); in certain districts in Russia 70 
per cent, of syphilis is innocent. In 1905 Schaudinn and Hoffmann 
described a treponema or spirochete pallida, so named because of the 
difficulty in staining it. It is long, delicate, thread-like, refractile, ac- 
tively motile, pointed at its ends and twisted like a corkscrew; it measures 
4 to 20 ix in length; it lies free and not in the cells; it resembles the 
spirochete of relapsing fever and is a flagellated protozoon. It is present 
in all cases, stages, types and tissues of syphilis."* It has been inoculated 
in monkeys from man, from monkeys to rabbits and then to monkeys 
again through many generations. With Giemsa's stain the spirochetes 
are a delicate violet and the leukocyte nuclei deep red. The spirochete 
refringens, found in the mouth, ulcers, smegma and venereal warts, is 
differentiated by its being more quickly stained, its greater size and, 
particularly, by its broader and more wave-like undulations. (See 
Plate VII.) It was cultivated by Schereschewsky but first by Noguchi 
in pure cultures, thus fulfilling all of Koch's postulates. 

The sound skin and mucosas resist infection, and hence a raw surface, 
erosion or wound is necessary for infection. Syphilis not only has a 
certain choice of place in its inoculation, but persists with peculiar 
obstinacy in certain localities, notably about the genitalia, breasts, 
axillse, navel, toes, angles of the mouth, tongue, iris, palate or tonsils, 
because of irritation by secretions, clothing, trauma, smoking, etc. 
These foci are of great moment in the recrudescence of the disease. 



PLATE VII 






V 



r 



\ 



Spirochetes of Syphilis. (Simon.) 
a, S. refringens; b, S. pallida. (Stained with Giemsa's stain.) 



SYPHILIS 199 

Syphilis is called a disease of cities; though more common in cities, 
syphilis very frequently escapes recognition in the country. 

2. Accidental Infection. — Accidental infection occurs in surgical 
practice, skin-grafting, postmortem infection (2 cases of personal 
observation), ritual circumcision, nursing, vaccination, kissing (as in the 
epidemic recorded by Shamberg), from use of pipes, in shaving, by 
scratches, from instruments used in glass-blowing, or from catheters. 
Bardinel describes infection of over 100 women by one midwife. 

Symptoms. — 1. Primary Stage. — After an incubation of two or three 
weeks, the initial lesion occurs (the ulcus durum, Hunterian ' chancre or 
initial sclerosis). Multiple lesions occur in 25 per cent. The induration is 
usually oval, always sharply localized, of variable or even cartilaginous 
hardness, freely movable, and usually papular and copper-colored. Hard- 
ness is the most constant characteristic of the chancre, which heals only 
when the hardness disappears. It is most characteristic in the third or 
fourth week, when the adjacent glands enlarge. Retrogressive ulceration 
or necrosis is frequent. The ulcer is round, elliptical, slit-like or irregular; 
it is hard, painless, with even surface, seldom with elevations or excava- 
tions; it has no areola, but a smooth, glistening base with thin secretion 
containing the spirochete. Contact ulcers around the corona are hard. 
The sclerosis may resemble herpes; an herpetiform chancre becomes 
indurated in about sixteen days, while simple herpes lasts but three or 
four days; herpes may be the atrium for syphilitic inoculation. If the 
sclerosis occurs on a mucous surface there is little elevation; maceration 
and bleeding readily occur, (a) The genital sclerosis in men occurs on 
the urethral orifice; in the fossa navicularis; on the glans, often as an 
erosion, and difficult to diagnosticate because of the hardness of the 
glans; on the corona, circular and hard; on the (broken) frenulum or 
in the sulcus coronarius, usually with much induration, giving the " split 
pea" appearance, one-half lying on the glans and the other half on the 
prepuce; on the prepuce, often with phimosis; or on the dorsum, (b) 
The genital sclerosis in women occurs mostly on the labia; on the labia 
majora, as large, readily ulcerating contact ulcers with inflammatory 
edema; on the labia minora as small, hard and circumscribed nodes; 
on the prepuce as hard fissures; in the urethral orifice with induration 
felt from the vagina; on the posterior commissure, as erosions, which 
are especially prone to infect during coitus; on the hymen relics, as 
fissures, or large, hard ulcers reaching into the vagina; rarely in the 
vagina, because of its paucity in glands and its thick epithelium; in 
the vaginal portion of the cervix, usually in women who have been 
pregnant, in which location it is difficult to differentiate from erosions. 
(c) The perigenital sclerosis occurs on the scrotum, mons veneris or inner 
thigh, (d) Extragenital scleroses (5 per cent, of chancres) are especially 
dangerous in mid wives, physicians and wet-nurses. They occur on the 
scalp, conjunctiva, nose, eyelids, lips, tongue and tonsils (from sexual 
perversion), cheeks, fingers, arms and mammae. In rare cases of accidental 
syphilis the chancre may not be found. Among 9058 extragenital 
chancres, 1863 occurred from vaccination, 745 from cupping or phle- 
botomy, 179 from circumcision, and 82 from tattooing (Bulkley). 



200 PROTOZOAN INFECTIONS 

The primary sclerosis is inoculated from an individual with a chancre 
or secondary syphilis; Williams reports 41 infections from gummata. 
When the sclerosis is recognized, the blood is already infected. 

Histology of Chancre. — The round cells increase the vessel walls tenfold, 
and the vessel lumen is narrowed from pressure and endothelial pro- 
liferation, even to obliteration, when ulceration ensues. Epithelioid 
and giant cells, and proliferation of the connective tissue in and about 
the vessels are noted. The Spirochete pallida is present. 

Coukse. — Usually induration disappears in thirty to ninety days, 
generally with scar formation. In exceptional cases (1) relics of the 
sclerosis may be found after years (even 50) due to permanent vascular 
injury; (2) acute or (3) phagedenic inflammation sometimes intervenes. 
Chancre and chancroid are separate affections — the dualistic doctrine of 
Bassereau, Layroyenne and Ricord. 

Diagnosis. 

Chancre or Sclerosis — vs. — Venereal Ulcer or Chancroid 

Incubation: two or three weeks. Three days. 

Form: indurated erosion, ulcer, nodule. Pustule, ulcer, etc., without induration. 

Number: single in 75 per cent., rarely sue- Often multiple at beginning or successively 

cessively inoculated. inoculated. 

Depth: superficial, flat, rarely deep excava- Through entire cutis or mucosa; "punched- 

tions. out" appearance. 

Border: gradual descent. Abrupt, sharp, indented, undermined. 

Surface: red, livid. White, gray. 

Induration: marked, cartilaginous, sharply No basal induration; not sharply outlined; 

outlined, movable, sometimes thin, last- merges gradually into adjacent tissue; 

ing weeks or months. short duration. 

Secretion: scanty, serous; autoinoculation Rich, purulent; autoinoculation easy; 

difficult; spirochetes. Bacillus cancri mollis, pseudodiphtheria 

bacilli or staphylococci. 

Pain: little. Much. 

Destruction: rarely phagedenic. More often phagedenic; diffuse. 

Reinfection: extremely rare. Frequent. 

Lymph glands: regional, i ndolent, swelling Often absent or acute inflammatory swell- 
hard, painless, movable; rarely pus for- ing; often pus formation, capable of 

mation. autoinoculation. 

Nature of the disease: constitutional. A local infection. 

Wassermann reaction: positive soon. Negative. 

Mixed infection may occur, whence the now abandoned idea of the 
unity of all venereal ulcers; the practical lesson from this doctrine is 
diagnostic reservation in doubtful cases. 

Lymphangitis syphilitica is marked in 70 per cent. The lymph vessels 
may become as thick as a lead-pencil, bulging at their valves (bubonulus), 
hard, painless, and narrowed in their lumen from endothelial proliferation. 
They are best seen on the dorsum penis. Resorption occurs in three to 
eight months. Lymphangitic edema is particularly suggestive in women 
when the initial lesion cannot be found. Local lymphadenitis is present 
in 97 per cent, of cases, appears in three or four weeks, and in six weeks 
reaches the contralateral inguinal, iliac and lumbar groups, in seven 
weeks the cubital glands, and just before the secondary eruption, the 
other glands. 



SYPHILIS 201 

2. Secondary Stage. — Secondary symptoms appear in eight weeks. 
(a) General infection. Fever occurs in 20 to 33 per cent. It is far more 
common in secondary syphilis ("fever of syphilitic invasion") than in 
primary or tertiary. It often just precedes the eruption, mostly in the 
pustular variety. It may be continuous, remittent or intermittent, 
resembling typhoid, malaria or phthisis. Other toxemic symptoms are 
anemia, headache, nocturnal bone-aches, neuralgias, palpitation, night - 
sweats, polydipsia, digestive disorders, synovitis and icterus; swollen 
tonsils, spleen or liver, and albuminuria may occur as prodromata. 

(h) The exanthem is polymorphous, sharply marked, frequently grouped 
in a circular arrangement and without pain or itching; it is highly 
infective and is copper-colored, a fact recognized in the fifth century; it 
appears where other eruptions are rare, as on the forehead or nasolabial 
fold; recurrent crusts may develop on an infiltrated basis. The most 
frequent form is the macule, next the papular syphilide, and then types 
resembling pustules, varicella, pemphigus or impetigo. In folds or damp 
parts of the skin mucous patches appear, as at the angles of the mouth, 
the groin or perineum. 

(c) The enanthem on the mucous membranes is observed on the tongue, 
lips and cheeks (mucous patches), often with pharyngitis. 

(d) The lymphatic enlargement becomes general. "Rheumatism," 
bone-aches, iritis, etc., are treated under special symptomatology. 

Late secondary symptoms occurred after two to thirty years in 5.8 
per cent, of Fournier's 19,000 cases ("recurrent syphilis"). 

3. The Tertiary Stage. — This develops in 10 per cent, of luetics 
and is characterized by the gumma which occurs in many tissues. It 
is not known what determines tertiary development; in 2396 tertiary 
lesions, 78 per cent, of the cases were not treated at all, 19 per cent, 
moderately and only 3 per cent, well treated (Fournier). The topical 
symptomatology of gumma will be described below. The gumma may 
be microscopic, or an inch or more in diameter. On section it is usually 
hard, grayish-yellow, homogeneous, centrally caseous and peripherally 
fibrous. Tertiary syphilis, particularly of the viscera, may be attended 
by fever. In 30 per cent, of tertiary syphilis, no evidence of earlier lesions 
can be found. 

Special Symptomatology of Syphilis. — Lues affects different tissues 
variously : Some organs are very vulnerable, as the liver or brain ; other 
organs are comparatively invulnerable, as the spleen or bone-marrow, 
in which the parasite may linger for years without causing particular 
trouble; and in still other tissues, if affected, the parasite dies off rapidly. 
(These facts have a bearing on the Wassermann reaction, v. i.). Gen- 
eralization of the parasite occurs chiefly in the early septicemia, and its 
localization in a given tissue, governed perhaps by the strain of parasite, 
seems to inhibit somewhat its localization in other tissues. 

1. The Skin. — The macular (roseolous) syphilide is the most frequent 
secondary eruption. The spots are hyperemic at first and later somewhat 
infiltrated; the macule develops rapidly, lasts eight to ten days, varies 
from a lentil to a dime in size, and comes out more clearly by chilling 
the skin, and after administration of mercury (Herxheimer reaction). It 



202 PROTOZOAN INFECTIONS 

occurs mostly on the trunk. The face, hands and feet are usually free 
except in severe cases. It is symmetrical, mostly on the flexor surfaces, 
more frequently recurrent than any other variety and prognostically 
favorable. 

The papular syphilide presents various forms: (a) The small miliary 
lichen syphiliticus usually develops on the forehead, chin, nose, shoulders, 
buttocks, back and flexor surfaces of the extremities. At first red, it 
rapidly becomes brownish-red. Fine scales or crusts may form, which 
on falling, leave a lacquered appearance. Recurrences are infrequent. 
It must be differentiated from psoriasis, the development of which on the 
scalp, ear and extensor surfaces is not observed in syphilis, where the 
scales are smaller, thinner and less glistening. On the palms and soles 
differentiation may be difficult, but in syphilis the centre of the papule 
is likely to be sunken, (b) The large papular syphilide is often associated 
with fever, constitutional disturbance or synovitis, and may occur on 
all parts of the body, as the corona veneris on the forehead, around the 
nose, dorsum of the hand, furrows of the chin and neck or the junction 
of the skin and mucosa; its polymorphism is pronounced, as psoriasis 
palmaris, rhagades, onychia or verrucose forms, (c) The condyloma 
latum or mucous patch is the papule altered by secretions or excretions, 
and is found about the genito-anal region, axillae, etc. It is the most 
important syphilide in the propagation of syphilis; it is flat, dirty, ill- 
smelling, and produces a spirochete-laden secretion, (d) The pustular 
syphilide includes the acne form, the varioloid, varicelliform and 
impetiginous forms; a brown pigmented scar usually results. 

The general characters of secondary eruptions are: (i) Their circular 
form and circular groupings; (ii) slow evolution; (iii) symmetry of dis- 
tribution; (iv) polymorphism; (v) induration; (vi) copper-color; and 
(vii) diffuseness. 

Gummata of the skin are asymmetrically disposed; are cutaneous 
or subcutaneous, involving deeper structures; are non-infective; are 
prone to develop at the site of secondary involvements; occur in the 
skin more than in all other localities combined; are promoted by in- 
complete mercurial treatment, vicious habits and constitutional diseases ; 
and are seen in 10 per cent, of cases, most frequently in the third year 
after infection. Small gummata may resorb by fatty degeneration, but 
the larger ones caseate, ulcerate and leave a kidney-shaped scar with 
deformation. Gummata are differentiated from malignant ulcerations 
by the absence of adenopathy, by their slow growth, painlessness and 
multiplicity, and by the results of therapy. In gumma, ulceration is more 
rapid than in lupus; it is deeper, less sharply marked, redder and less 
symmetrical; recurrence after cicatrization is less frequent; the scars 
are less flat and smooth, and the bacteriological findings of lupus are absent. 

Leukoderma syphiliticum is observed after macular or lenticular 
syphilides as white spots with peripheral brown pigmentation, mostly 
on the face and neck; it occurs in 4 per cent, of syphilitic men and 45 
per cent, of syphilitic women and fades in a few years. 

The hair falls out except from the crown of the head, during the second- 
ary stage, proportionately to the intensity of the eruption. It is greater 



SYPHILIS 203 

in poorly nourished cases, and its regrowth is usually good. In the bald 
areas, there are no broken hairs. 

Onychia syphilitica occurs particularly in women. The nails may 
hypertrophy, fall out or fail to grow. Peri- or paronychia rarely causes 
pain, ulceration or suppuration. 

2. Lymph Glands. — The inguinal glands are first enlarged because 
they are nearest to the most common genital chancre. Adenopathy of 
any particular group is not pathognomonic of syphilis. The posterior 
cervical glands are involved more than the anterior. Next in frequency 
are the axillary, epitrochlear and pectoral. Dietrich observed that 99 
per cent, of healthy individuals have palpable glands. Inflammation, 
pain and suppuration, from mixed infection occur in but 3 per cent. 
In extragenital sclerosis, other glands are enlarged first, e. g., the an- 
terior cervical, from chancre of the lips. The glands are freely movable 
and are not usually larger than a hazel-nut, but occasionally become 
massive, resembling Hodgkin's disease. 

3. Gastrointestinal Tract. — On mucous membranes the eruption 
(enanthem) is less frequent and is less polymorphous than the exanthem, 
with which it is synchronous. 

Mouth. — This is more involved than any other part except the skin and 
recurrence is very frequent, (a) Erythema may occur as diffuse or cir- 
cumscribed, dark red macular, especially on the cheek, pharynx, uvula, 
palate and swollen tonsils — the acute syphilitic angina; it ceases sharply 
at the border of the soft and hard palate. Infiltration or fissures, with a 
slightly granulated and vesicular appearance may develop. Erosions 
may last long in users of tobacco and alcohol. 

(b) Mucous patches, which are papules modified by moisture, develop 
with the exanthem, mostly on the tonsils, cheeks and lips. They are 
elliptical or irregular, flat or slightly elevated, circumscribed patches, 
of variable color. On the lips they may measure 6 to 17 millimeters. 
The course is usually chronic; the patches swell, become granular, 
ecchymotic and often ulcerated. On the tonsils they may simulate 
diphtheritic patches, and in smokers a cure cannot be effected until the 
habit is stopped. They are the most important syphilide because so highly 
contagious. 

(c) Chronic a,ngina is of a granular appearance, accompanied by hyper- 
emia, edema and erosion, a gray coating on the swollen tonsils, and the 
appearance of pharyngitis granulosa. 

(d) Pachydermia, ichthyosis and leukoplakia occur on the mucosa 
of the cheeks, and on the angles of the mouth, lips and tongue, but 
are not always syphilitic. They are swellings with fissures, are gray in 
color, irregular, vary in shape and size and are thick and scar-like. They 
occur especially in users of tobacco and alcohol. Leukoplakia in tobacco 
users usually occurs on the tongue, lip or palate, while in syphilis it is 
mostly on the cheek. Psoriasis linguae presents elliptical, red, flat spots, 
with thread-like coating; fissures are frequent on the edges of the tongue, 
from the use of tobacco and from bad teeth. 

(e) Gummata of the oral cavity occur without glandular swelling. 
Gummata of the tongue are most frequent, occurring (a) as a diffuse 



204 PROTOZOAN INFECTIONS 

glossitis with later cirrhotic shrinkage or (b) as circumscribed nodes or 
ulceration, without pain or adenopathy. Gummata of the palate or 
pharynx are mostly multiple. They are frequently diffuse, deep 
or phagedenic; they destroy the uvula, produce adhesions, obliterate 
the posterior nares or Eustachian tube, stenose the pharynx or draw 
the tongue back, stenosing the respiratory passages or reaching the 
spine or brain. In the tonsils they may erode the carotid or palatine 
artery. Differentiation is required from tuberculosis and epithelioma 
in which the glands are usually involved. The diagnosis ex juvantibus 
and Wassermann test are important. 

Esophagus. — Strictures result from deep gummata, ulcerations in the 
larynx, or extension from the bronchial glands. Differentiation is 
required from tumor of the mediastinum, aneurysm, carcinoma, round 
ulcer and cardiospasm. Diverticula may result. 

Stomach. — (a) Acute catarrhal gastritis in the secondary stage is 
usually toxemic — rarely organic. (b) Chronic gastritis is more com- 
mon, in part explaining the anemia and malnutrition and differing 
from vulgar gastritis only in the influence of treatment. Amyloid and 
glandular wasting are infrequent, (c) Ulcers of the stomach may 
result from syphilitic arteritis; Garre collected 30 cases, (d) Gummata 
are rare. They begin in the submucosa, are usually multiple, leave 
radiate scars and differ from the ordinary round ulcer in that they are 
not funnel-shaped, have undermined edges and are broader at the base. 
(e) Hemorrhages from the stomach are most rare and Hay em's case is 
almost unique. They may result from cardiac, splenic, hepatic or renal 
lesions. 

Intestines. — Little is known of small intestine syphilis in the adult. 
(a) Acute catarrhal enteritis may induce icterus; it resists treatment 
other than specific, (b) Chronic enteritis in the syphilitic newborn, is 
manifested by the viscid meconium. Obstinate diarrhea and stenosis 
may follow, (c) Ulceration may result from enteritis in secondary 
syphilis or from gummatous, diphtheroid and amyloid changes in the 
tertiary stage. Meschede collected 54 cases of ulcer in the small intestines. 
They occur around the axis of the intestine and are characterized by 
spirochetes and productive inflammation which prevents perforation 
but leads to stenosis, (d) Intestinal amyloid disease is associated with 
amyloid liver, spleen and kidneys. The gut is pale, smooth, waxy, 
thick and rigid and there are obstinate diarrhea, stinking stools and 
hydrops. It is most frequent in the small intestine and is essentially a 
vascular change. Amyloidosis in general occurs in 67 per cent, of tuber- 
culosis and in 21 per cent, of syphilis. 

Rectum. — Ulceration may occur in papules or fissures near the anus. 
Rectal disease is usually secondary by contiguity, (a) Irritative proctitis 
is usually chronic, attended by evacuations of pus, itching, tenesmus and 
external excoriations. (6) Syphilitic ulcers are tertiary. They occur 
high up, extend to the colon and often produce stenosis. Perforation 
is rare. The periproctal tissues are invaded. Fistulse may develop, but 
the symptoms are less marked than in cancer or tuberculosis. The feces 
are covered with mucus and blood. Diarrhea from catarrh of the colon, 



SYPHILIS 205 

myositis of the sphincter, involuntary evacuations, burrowing of pus and 
sepsis necessitate a long course. Tuberculous ulcers rarely occur in the 
rectum alone, and are marked by the tubercle bacillus. In dysentery 
the involvement is higher up, colic is more frequent, diarrhea is more 
profuse, and the resulting stenosis is higher in the intestine. In car- 
cinoma, age, cachexia and local appearances are suggestive criteria; 
the stricture is higher and adhesions are more common. 

Pancreas. — Acute svphilitic pancreatitis, interstitial inflammation with 
cirrhosis (rarer in acquired than in hereditary syphilis) and gumma 
are recorded. The peritoneum sometimes participates in syphilitic dis- 
ease of the organs it envelops, e. g., perisplenitis, perihepatitis, etc.; it 
is extremely rare as an independent gummatous peritonitis. 

4. Spleen. — (a) Acute splenic tumor occurs in 31 per cent, of acquired 
and 61 per cent, of congenital syphilis, (b) Interstitial splenitis occurs 
chiefly with syphilitic liver, marked by increased size, hardness and 
pain from perisplenitis, (c) Gummatous splenitis is very rare, (d) 
Amyloidosis occurs very frequently as the "sago" spleen, which is not 
necessarily very much enlarged; or as the diffuse amyloid spleen, which 
causes considerable swelling. 

5. Liver. — Syphilis of the liver occurs pathologically in two main 
forms, interstitial and gummatous, which are often associated with 
perihepatitis, amyloid or fatty change, and sometimes with parenchy- 
matous changes, as acute yellow atrophy, (a) Interstitial hepatitis 
(syphilitic cirrhosis) is twice as frequent in congenital as in acquired 
syphilis. The volume of the liver is increased in children, and sometimes 
decreased in adults. The surface is uneven, with furrows or nodules; 
the edge is thin, indented and sharp, whereas in other cirrhoses it is 
rounded. Perihepatic adhesions to the colon or abdominal wall are 
frequent, and clinically evidenced by lessened respiratory excursion. 
Connective-tissue forms in Glisson's capsule, follows the branches of the 
portal vein into the liver (peripylephlebitis), and shows as bands of 
grayish tissue. The liver cells are degenerated or destroved by fibrous 
tissue or obliterating endarteritis. The atrophy is most marked anteriorly 
and in the left lobe. The connective tissue is not only perilobular, but 
reaches more into the lobules than in alcoholic cirrhosis. In acquired 
syphilis the liver is not equally or completely diseased, whence protruding 
granules of sound tissue are noted. New bloodvessels from the hepatic 
artery develop in the connective tissue and thrombosis may occur in 
the portal vein and its radicles (pylephlebitis). 

Symptoms. — The enlargement is at first insidious — without pain 
or ascites. The abdominal veins may be distended; the urine is often 
dark and albuminuric, possibly icteric. The splenic tumor results from 
hyperplasia, stasis or amyloid degeneration. Ascites is less frequent and 
less early than in alcoholic cirrhosis. Icterus develops in 33 per cent. 
More bile is present in the stools than in ordinary cirrhosis. Gastro- 
intestinal dyspepsia and vomiting of blood are not infrequent. This 
form develops more often in men; is promoted by alcoholism; runs a 
chronic course; and its prognosis is better than in non-syphilitic cirrhosis, 
since relative, even spontaneous recovery is possible. When the liver 



206 PROTOZOAN INFECTIONS 

shrinks death results from intercurrent pneumonia, cholemia or hemor- 
rhagic diathesis. 

(6) Gummatous hepatitis (syphilitic hepatitis par excellence) is more 
frequent than the first form, and occurs oftener in acquired than in 
congenital syphilis. The gummata are either miliary, or large nodes 
which may fill the abdomen; they vary from 1 to 50 and may be super- 
ficial or deep. The surface of the liver is smooth, warty, or adherent 
to the diaphragm or colon. The liver is distorted, mammillated or 
lobulated (hepar lobatum). Deep, irregular, radiating furrows are fre- 
quent, resulting from cicatrized gummata, affecting either lobe and 
mostly on the anterior surface near the suspensory ligament or on the 
edge. In congenital syphilis gummata are often observed at the hilum, 
in the wall of the portal vein or near the bile vessels. 

Symptoms. — Gummata are frequently latent, i. e., are discovered 
only at postmortem. Considerable pain occurs in the shoulder, as well as 
pain on motion or tenderness on pressure in the epigastrium or hypo- 
chondrium. Pain is due mostly to perihepatitis; a friction-rub is heard 
when the inflammation is fresh; adhesions and loss of respiratory ex- 
cursion result, in older cases. Icterus is infrequent and results from 
gummatous compression of the bile ducts, perihepatitis or cicatrices. 
The liver usually shows furrows and nodules. Early enlargement is more 
frequent than in alcoholic cirrhosis; ultimate shrinkage has been observed. 
Ascites is rare except from syphilitic cirrhosis, amyloid liver or cardiac 
insufficiency, and is usually terminal and often associated with albumin- 
uria. Splenic tumor is infrequent, except from gummata or amyloid 
degeneration in the spleen, coincident liver cirrhosis or gummata at the 
porta hepatis. Hemorrhages and inflammations of the serous membranes 
are not infrequent. 

Diagnosis. — This depends upon other evidences of syphilis; it is often 
difficult. Syphilis of the liver may remain stationary for a time and in 
general a longer course is expected than in alcoholic cirrhosis. In thirty 
instances of apparent cirrhosis, the Wassermann reaction was positive 
in twenty-two. Gummata and cancer may be confused; age is only a 
relative criterion, yet most cases of liver syphilis occur under the fortieth 
year; ascites, icterus, enlarged liver and cachexia may occur in both 
diseases, occasioning doubt and confusion. The nodules of syphilis are 
usually small but may be larger than those of cancer. Rapid growth 
is an indication of cancer; more constant size, of syphilis. Albuminuria 
and splenic tumor are more common in syphilitic liver; in 66 per cent, 
of hepatic syphilis, occult bleeding and marked gastro-intestinal symp- 
toms may simulate malignancy. The safest rule is always to think 
of syphilis when cancer seems the obvious diagnosis. The lungs are 
compressed in cancer more than they are in syphilis. The smooth edge 
of the liver, signs of fresh hepatitis, and lack of respiratory excursion, 
indicate syphilis. Riedel found similar symptoms in syphilis and gall- 
stones, such as pain, fever and tenderness. Fever is not uncommon in 
hepatic syphilis, which may then be easily confused with liver abscess 
(q. v.), malaria, tuberculosis, typhoid or septicemia: there may be pain, 
tenderness, rigors, sweats and leukocytosis, which, with the fever, readily 



SYPHILIS 207 

lead to diagnostic errors; the Wassermann test is invaluable. (See 
Differential Table of Diseases of the Liver.) 

Amyloid liver (q. v.) is most frequent in the tertiary or quaternary 
stage of acquired syphilis; it is rare in the liver alone. 

Syphilitic pylethrombosis (see Pylephlebitis). 

Icterus is attributed to swelling of the portal lymphatics, early 
hepatitis, cholangitis, injury to the liver cells or to gastroduodenal 
catarrh. 

Devic and Beriel summarized 21 instances of hepatic hemorrhages, 
due to infarction or luetic endarteritis. 

6. Kidneys. — (a) Albuminuria occurs in recent syphilis from toxemia 
or in the later ulceration from vascular changes. It is usually transitory 
and nephritis rarely follows it, but the later in the disease that albu- 
minuria appears, the poorer is the prognosis. Energetic (not moderate) 
mercurialization may produce albuminuria and cylindruria. (6) Parox- 
ysmal hemoglobinuria occurs relatively often after mercurial therapy, 
(c) Acute parenchymatous nephritis is focal and cortical. It is early, 
toxemic and rare. The albuminuria is intense. When it develops late 
from ulceration, the prognosis is unfavorable; anemia, vomiting or other 
symptoms of acute nephritis may be present, but uremia is rare, since 
it is a focal disease, (d) Chronic parenchymatous nephritis may follow 
syphilis (0.5 per cent.), (e) Chronic interstitial nephritis differs from the 
ordinary form in its disseminated focal involvement, which leaves scars. 
Polyuria is rarely great, casts and albumin are present in greater amount, 
and the course is more rapid than the ordinary course of three to seven 
years, because of marantic, amyloid and other visceral changes. It occurs 
at an early age when arteriosclerosis is rare. There is said to be no cardiac 
hypertrophy. (/) Miliary or large gummata are found in the cortex 
chiefly, usually multiple and unilateral. They coexist with amyloid 
kidney and chronic parenchymatous nephritis. The symptoms are 
indeterminate, (g) Amyloid kidney, q. v., under diseases of the kidney. 
(h) Syphilis is an occasional etiological factor in glycosuria. The supra- 
renals are rarely involved, except in congenital syphilis; fatty degenera- 
tion, gummata, inflammation and amyloid changes in the Malpighian 
bodies have been recorded — in Addison's disease. 

7. Circulation. — Heart. — (a) Syphilitic myocarditis originates in 
coronary arteritis; interstitial foci occur as infiltration along the small 
vessels, especially in congenital syphilis, into the intermuscular septa, 
and areas of myocardial, fatty degeneration, with spirochetes. It in- 
volves the front or apex of the left ventricle, or the interventricular 
septum. In congenital syphilis it occurs in the right more than in the 
left heart. Resulting changes are cardiac hypertrophy, aneurysm of the 
heart, Dittrich's heart stenosis (conus stenosis) or amyloid change. 
Only 97 (62 perfectly clear) cases of myocardial gummata are recorded 
(Stockmann, Goldf rank) . Gummata may attain great dimensions in the 
interventricular septum. The disease is often latent until, in 50 per cent, 
of the cases, sudden death results, largely in persons between thirty and 
forty years of age; myocardial alterations often occur in the secondary 
stage. The heart action may be incompetent or irregular, and there 



208 PROTOZOAN INFECTIONS 

may be dyspnea, angina pectoris, heart-rupture or cerebral embolism. 
Hydrops is rare. 

(6) Syphilitic pericarditis is invariably a complication of myocardial 
syphilis, occurring over the large vessels or anterior surface of the heart. 
The symptoms are those of disordered compensation or myocarditis, 
its invariable associate. 

(c) Syphilitic endocarditis may cause valvular disease (v. i., Aorta). 
Endocardial gummata may occur. 

Bloodvessels. — Endarteritis syphilitica, known to Morgagni and Pare, 
causes wide-spread, often irreparable or fatal complications, (a) The 
usual fibrous form is the obliterating endarteritis of Heubner (see page 211) ; 
the wall is thick and opaque, the intima and elastic tissue hyperplastic 
and the lumen eccentric. When the muscular coat is not involved, 
thromboses occur; when both the muscular and elastic coats are diseased, 
aneurysms result. It may begin one year after infection, (b) Gum- 
matous arteritis or periarteritis is very rare, (c) General arteriosclerosis 
involves the vessels more widely than does the syphilitic arteritis which 
is largely localized in the aorta, coronary and brain vessels and exception- 
ally in the other vessels. 

Aorta. — Syphilitic aortitis is oftenest seen in the ascending aorta, 
its arch and thoracic segment, and the lower part of the abdominal 
aorta. The early stages show gray, gelatinous patches of productive 
cellular inflammation and spirochetes in the intima; older foci are 
grayish- white, round or oval, elevated and stellate plaques. The process 
sometimes becomes deep and calcification occurs in the intima with 
thrombosis. It may involve the aortic valves. Three-quarters of cases 
of pure aortic insufficiency (q. v.) result from luetic aortitis, and two-thirds 
react to Wassermann's test. (See Aneurysm.) Its origin may be (a) 
in the intima, (b) in the adventitia and media together (mesaortitis) 
or (c) in the intima and adventitia (vasa vasorum) . It ultimately involves 
all the walls in varying degrees. The resulting; loss of elasticity and 
resistance promotes aneurysm. Symptoms of aortitis, as precordial 
pain, paroxysmal dyspnea or substernal dulness may begin soon after 
the secondary stage, to reappear after one or two decades as typical 
aneurysmal signs. The author believes 90 per cent, of aneurysms are 
syphilitic. Syphilitic aneurysms may be single or multiple and usually 
occur in the arch, and sometimes also in the abdominal aorta or its 
branches. Aortitis occurs in 98 per cent, of paretics, and in 50 per cent, 
of syphilitics. Only 6 cases of gummata are on record. 

Pulmonary Artery. — Occlusion of the pulmonary trunk, its compression 
by scars and valvular gummata are very rare. Syphilitic aneurysm of 
the pulmonary artery is not known. 

Vein Syphilis. — Thirty-three cases of phlebitis were collected by 
Roussy. Periphlebitis originates in the adventitia, especially in heredi- 
tary syphilis. Gummata exist in the veins or involve them secondarily. 

Blood. — Oligocythemia and oligochromemia occur most markedly 
when the glands are widely involved. The anemia disappears under 
administration of mercury, to reappear if too much be given. A count 
as low as 1,700,000 may be observed. The hemoglobin is reduced 15 



SYPHILIS 209 

to 30 per cent. The " Justus test/' based on a 10 to 20 per cent, reduction 
in the hemoglobin after a large inunction or injection of mercury, in the 
florid secondary stage, is suggestive of syphilis. The white cells are 
increased, especially the lymphocytes; the eosinophiles are increased 
but not constantly. Myelocytosis may develop in the tertiary stage. 
The blood contains the spirochetes and by way of the blood, syphilis becomes 
a sepsis. The Wassermann test (v. Diagnosis). 

8. Respiratory Tract. — Nose. — (a) An initial nasal lesion is described 
(only 95 cases recorded), (b) Acute rhinitis is much rarer in adults than 
in the newborn; it is characterized by its persistence, erythematous 
papular foci, hemorrhagic erosions and fetor, (c) Gummata usually 
develop late, though they have been seen in the seventh month; they 
begin in the floor and septum, periosteum, bone and secondarily in the 
cartilage. The diffuse necrosis involves the cartilaginous and membran- 
ous septum and cartilages of the alse; sequestra may be blown from the 
nose. Septal perforation may develop and a long course is usual, with 
discharge of pus and crusts; the bone is often denuded and may crepitate 
on palpation. The deformed "saddle-back" nose is due to loss of the 
triangular cartilage and vomer. Differentiation must be considered 
from noma, tuberculosis, carcinoma and the perforating ulcer of Zucker- 
kandl (beginning as a hemorrhage and due to streptococcic or staphyl- 
ococcic infection). The diagnosis is best made by Wassermann's test 
and ex juvantibus. 

Larynx. — (a) Catarrhal laryngitis occurs with the eruption, with 
redness, swelling, coughing and hoarseness, (b) Papular laryngitis is 
often associated with ulceration, infiltration and nodes. The epiglottis 
is involved^ Stenosis of the glottis results if ulcers invade the submucous 
tissue, (c) Gummata of the larynx are usually multiple, and vary from 
the miliary size to that of a pigeon's egg; sometimes a diffuse infiltration 
occurs. They may produce dysphonia, dysphagia, dyspnea, hemorrhage 
or suffocation. They always leave stenosis or deformity. 

Diagnosis. — In cancer the glands are usually enlarged, the growth is 
harder than in syphilis and the microscopic examination may be final. 
Syphilis and tuberculosis may occur together; the syphilitic ulcer 
usually begins near the epiglottis, is rounder and larger and has 
sharper edges, a redder border and a whitish-yellow coating of its 
deeper base, while the tuberculous ulcer is less red, less infiltrated and 
less deep. 

(d) Perichondritis. — Any cartilage may become excoriated, necrosed 
and surrounded by edema. Syphilis causes 13 per cent, of cases of 
glottis edema; tuberculosis, 9 per cent. The prognosis is always grave, 
yet the lower the necrosis, the worse is the prognosis, for deformity and 
stenosis occur, with dyspnea or dysphagia. 

(e) Syphilitic vegetations, due to irritating secretions, are sessile or 
pedunculated and cause dysphonia or even suffocation. 

Trachea. — The trachea is red, swollen, sometimes ulcerated. Tracheal 

stenosis, resulting from healing gummata, is usually angular and involves 

mostly" the middle third. The symptoms are inspiratory dyspnea on 

exertion or on lying down; cyanosis; and a cough resembling pertussis, 

14 



210 PROTOZOAN INFECTIONS 

with sanguinopurulent sputum, which may contain fragments of cartilage. 
The diagnosis is made by the laryngoscope. 

Bronchi. — (a) Acute bronchitis may be a secondary symptom. 

(b) Chronic bronchitis accompanies laryngeal, tracheal or bronchial 
affections. Phthisis may be suggested. The breathing is disproportion- 
ately disturbed by irritation of the vagus by enlarged bronchial glands. 

(c) Kidney-shaped ulcers may cause stenosis or perforation into the 
vessels, mediastinum or esophagus; in Conner's 128 cases of bronchial 
and tracheal syphilis, 56 per cent, affected the trachea alone; gummata 
occurred in 15 per cent.; ulcers in 44 per cent., frequently with severe 
hemorrhages; cicatrices and stenoses in 40; and bronchiectasis in 20, 
peritracheitis in 6, and pulmonary syphilis in 7 per cent. 

Lungs. — Syphilis may simulate pulmonary tuberculosis. Patients 
with tuberculous signs should be searched for syphilis. 

(a) In the white pneumonia of hereditary syphilis, the lung is firm, 
heavy, airless and grayish-white, the chief changes being infiltrated 
alveolar walls, desquamated, swollen epithelium and spirochetes in the 
air cells and miliary foci about the arteries. 

(b) Diffuse infiltration differs from tuberculosis in that it rarely occurs 
in the apex; in Grandidier's 30 cases the right middle lobe was affected 
in 27. The lung is red, hard, large, airless and smooth on section and 
later becomes gray, uneven and nodulated. Connective-tissue infiltration 
occurs about the vessels, impinging upon the air cells. Necrosis, fatty 
change, caseation and later, cavities may result from vascular occlusion. 
Disproportionate dyspnea is present. Temperature may occur with or 
without ulceration. 

(c) Gummatous pneumonia may occur alone or with diffuse infil- 
tration. Gummata develop largely in the lower lobes near the hilum. 
Differentiation from tuberculosis is often difficult and both lesions may 
occur together. Durness and other signs of consolidation or cavity for- 
mation often result. The sputum is mucous, purulent, profuse, blood- 
tinged, stinking, and contains masses of tissue but no tubercle bacilli. 
The course is usually chronic, and advanced cases may heal with appro- 
priate treatment; Brambilla (1777) described a supposedly phthisical 
patient, who, by mistake, took mercury and recovered. Tuberculosis 
occurs more frequently in the upper, syphilis more often in the lower 
or middle lobes. Rise of temperature is more frequent in tuberculosis. 
In syphilis, actual hemorrhage is rare, as the vessels are obliterated, and 
night sweats are infrequent. 

(d) In syphilitic interstitial pneumonia the lung may be tabulated 
(pulmolobatus) like the tabulated liver; marked induration dilates or 
distorts the bronchi; diagnosis is impossible. 

(e) Syphilitic pleura disease occurs chiefly with lung lesions. 

9. Nervous System. — Syphilis of the nervous system occurs eight 
times more frequently in men, mostly between the years of twenty-five 
and forty, and after trauma; in brain workers or those debilitated by 
worry or excesses; or in children as perhaps the first symptom of parental 
disease. 

In 20 per cent, of cases there is no history of chancre. It occurs where 



SYPHILIS 211 

the secondaries have been light and ineffectually treated. Syphilis 
occurs in the brain in 16.5 per cent, of syphilitics and more often than 
in other viscera, excepting the liver. 

Fifty per cent, of brain syphilis occurs ivithin three years after infection. 
Formerly described as occurring many years after infection, cerebro- 
spinal syphilis may develop as early as five weeks after infection 
(especially in those advanced in years). Nervous symptoms in the 
secondary stage as headache, neuralgia, increased reflexes or fleeting 
paralyses, are partly toxemic but largely anatomic, as is demonstrated 
by the pleocytosis (over ten cells in the cell count), lymphocytosis, 
Wassermann and globulin reactions of the cerebrospinal fluid. 

In general, the symptoms are marked by: (a) variability and incon- 
sistency, due to alternate regression and recurrence in the lesions; 

(b) incompleteness, as partial paralysis or disturbance of consciousness; 

(c) the symptoms are partly tumor-like, partly vascular, or partly in- 
flammatory; they are partly meningeal, partly basal or cortical, and rarely 
occur in the centre of the brain except from secondary vessel lesions and 
gummata. Syphilis produces no symptom not produced by other disease. 

Types. — 1. Syphilitic arterial disease is the most frequent form, and 
aside from neuritis paralysis, the most frequent cause of syphilitic paralysis. 
As prodromal disturbances, headache is usual; vomiting, vertigo, psychic 
changes, convulsions, hemianopsia and aphasia may occur; choked disk 
is rare. Thrombosis and obliteration of the vessels are gradual in onset 
and intermittent — e. g., involving the leg and, in a few hours or days, 
the arm — and the multiple softening in 95 per cent, of cases occurs in 
the distribution of the Arteria fossae Sylvii. 

Course. — The first attacks are mild ; the later are more severe, and occur 
with somnolence, bilateral, alternating or crossed paralysis, general or 
rarely Jacksonian convulsions, or with partial aphasia, mental changes 
or progressive bulbar phenomena. 

In diagnosis the ordinary arteriosclerosis in over 90 per cent, of cases 
occurs in late life, its progress is slower, the changes are more disseminated, 
all coats of the vessels are involved, its fatty and calcareous changes lead 
more often to widening than to obliteration, and hemorrhage is more 
characteristic than softening; whereas in syphilitic endarteritis the onset 
is more acute and headache more conspicuous, encephalomalacia occurs 
at a younger age (see Brain Embolism), the changes affect chiefly the 
aorta and cerebral vessels, the intima is principally involved, calcareous 
and fatty changes are rare and obliteration is usual; the hemiplegia 
occurs by "instalments," associated with meningitis, apathy, dementia, 
somnolence or delirium; and finally the symptoms are more diffuse. 
The Wassermann test and spinal puncture are final. Without treatment, 
the average duration is one to three months. 

Multiple aneurysms of the basilar, Sylvian and carotid trunks are 
generally tertiary, but occasionally secondary; their rupture produces 
symptoms of apoplexy or meningeal hemorrhage. Otherwise hemorrhage 
is rare in brain syphilis. 

While softening is usually ischemic (non-inflammatory), encephalitis 
syphilitica may rarely cause disseminated softening or indurated sclerosis. 



212 PROTOZOAN INFECTIONS 

2. Basal gummatous meningitis, the best-known type, and the next 
most frequent form, begins in the dura, especially about the optic chiasm, 
interpeduncular spaces or cavernous sinus; less frequently in the fossa 
of Sylvius and the cortex; pathologically it consists of fibrinous exudate, 
granulation tissue, gummata and cicatrices. 

General Symptoms. — Headache is the most important and early 
symptom (in 75 per cent.). It is paroxysmal, is increased at night, sharp, 
boring and deep-seated. Other symptoms are projectile vomiting, vertigo, 
somnolence, semi-intoxication, motiveless activity, nocturnal automatism 
or dementia, alternating with delirium, epileptic attacks or paralytic 
seizures; the symptoms may resemble those of uremia, meningitis or 
typhoid. Between attacks, cerebration may be normal. Epilepsy 
may be typical or unilateral, frequent or violent. Polydipsia, diabetes 
insipidus from disease in the third ventricle, or diabetes mellitus, of which 
Oppenheim collected 20 cases, may occur. Fever may be present. 

The cranial nerves, especially the second and third are often affected. 
Involvement of successive branches is most characteristic (85 per cent.) ; 
80 to 90 per cent, of nerve 'involvements result from syphilis of the brain, 
tabes or less frequently, general paralysis and brain tumor, (a) The 
third nerve is involved in 65 per cent, of these cases — "the sign of 
syphilis." (6) The optic nerve is diseased anatomically in 82 per cent, 
and clinically in 40 per cent, of cases; choked disk (10 per cent.) is 
almost always bilateral (see Plate IV). Simple atrophy, with complete 
blindness (in 6.6 per cent.), is most frequent in tabes and next most 
frequent in brain syphilis and general paralysis. Amaurosis is common 
and often unilateral. Hemianopsia is homonymous. Temporal heterony- 
mous hemianopsia is very often syphilitic; the nasal form is rarely so. 
Eye changes, due to meningitis, bone disease or gumma are susceptible 
to treatment, (c) The fourth, sixth and fifth nerves are next in frequency 
of involvement. The fifth is unilaterally affected, and more in its sensory 
than motor branches. The olfactory nerve is rarely involved. The facial 
nerve may be paralyzed, nearly always unilaterally and peripherally. 
The eighth nerve is sometimes involved, and the resulting Meniere 
complex is ominous. The vagus or hypoglossus may be affected. 

With the above changes (i) gummata may grow into the pons, crus or 
medulla, and cause hemiplegia and crossed paralyses, as hemiplegia 
plus oculomotor paralysis (Weber's paralysis); plus facial paralysis 
(Gubler's paralysis) or plus abducens and trigeminus paralysis (Leyden's 
paralysis) ; or (ii) arterial phenomena are often noted, syncope, apoplecti- 
form attacks, encephalomalacia, hemiplegia, hemianesthesia and hemi- 
anopsia, usually as later symptoms. Syphilitic meningitis is typically 
subacute with remissions and exacerbations, and lasts rarely more than 
half a year. 

Differential Diagnosis. — Carcinoma and sarcoma at the base of the 
brain, involving the meninges, run a continuous progressive course, 
with definite localization, while in syphilis the course is intermittent, 
localization varies, and, vascular changes are often marked. In tuber- 
culous meningitis there is less development of connective tissue, vascular 
changes are rarer, the nerves less frequently involved, the course more 



SYPHILIS 213 

acute, febrile and progressive, and remissions less frequent and less 
marked. Mental obscurity is more marked, sudden and stationary. 
The initial irritation is followed by later paralysis, while paralysis may 
occur at once in syphilis. Tuberculous meningitis usually occurs before, 
and syphilis after, twenty years of age. Other syphilitic or tuberculous 
foci, the Wassermann reaction, lumbar puncture and the results of 
therapy determine the differentiation. Spirochetes have been found 
directly in the cerebrospinal fluid only five times. Differentiation from 
Quincke's serous meningitis is not difficult. The multiple nerve root 
affection of Kahler, involving the seventh and third cerebral and the 
cervical and dorsal nerve roots causes neuralgia and paralysis. Periodic 
paralysis of the third nerve is rhythmic in its attacks, usually involves 
the entire nerve, occurs in young children especially, and with attacks 
of migraine. 

3. Syphilis of the convexity is a meningo-encephalitis, with circumscribed 
symptoms like cortical tumor or with diffuse manifestations. 

General Symptoms. — Headache is usually the first and most common 
manifestation. Focal Jacksonian attacks occur with mono- or hemiplegia, 
develop by starts or "instalments" and occur without an aura. Ninety 
per cent, of convulsions in those over thirty years of age, not uremic or 
alcoholic, are syphilitic (Fournier). The symptoms are more diffuse 
than in vulgar epilepsy. The convulsions may number even 400 in 
twenty-four hours. Aphasia is frequent, usually of the transitory motor 
type and occurs less often from gumma than from vascular disease. 
Diffuse meningo-encephalitis may resemble an acute psychosis or de- 
mentia. Convexity syphilis recovers more frequently than other 
forms. 

4. Gummata, the least frequent variety, occur usually in the meninges, 
sometimes in the central ganglia, cerebellum, pon or crus. The symptoms 
are those of brain tumor, except that there is often regression, either 
spontaneous or therapeutic. Cortical gummata, producing cortical 
epilepsy and monoplegia, require differentiation from cortical tumor 
(q. v.) in which the pressure symptoms, and slow pulse are more marked; 
the disk changes follow focal signs and the process advances less by 
epochs; while in syphilis the pressure symptoms are more diffuse and 
rapidly extensive; the disk is involved when coincident basal meningitis 
occurs; cortical paralysis is often associated with Jacksonian epilepsy 
(v. s.); the symptoms are more undulatory, the Wassermann test is 
positive, and treatment is successful. 

5. Cerebrospinal syphilis produces suggestive spinal symptoms: (a) 
their asymmetry, (b) their less-pronounced character, (c) their variability, 
(d) meningeal and nerve-root symptoms, (e) the cerebrospinal fluid 
issues under pressure and exhibits pleocytosis (the normal number of 
lymphocytes being 4 to 6), Wassermann's reaction and globulin, and (/) 
response to mercury and iodides. Syphilis is never a system disease 
(Gowers). Syphilis of the cord is six times less frequent than brain 
syphilis. 

The most frequent and chracteristic form is meningo-encephalomyelitis. 
While the symptoms may be strictly spinal, cerebral meningo-enceph- 



214 PROTOZOAN INFECTIONS 

alitis is frequently found anatomically. Heubner's arteritis is not noted. 
Brain changes may mask the spinal symptoms. The meninges are most 
involved in the cervical and upper dorsal regions, as evidenced by pain, 
stiffness or girdle sensation; while the cord itself is mostly affected in the 
lower dorsal region, and therefore causes weakness in the legs, paresthesia, 
sphincter disturbance and decubitus. Intercostal neuralgia, nocturnal 
pains in the extremities, spastic paraparesis, hemiparaplegia, triplegia, 
Brown-Sequard's syndrome, increased reflexes and sensory disturbances, 
are some of the symptoms of cerebrospinal syphilis. Erb laid special 
stress on the spastic paraplegic type. The so-called syphilitic myelitis 
is often only softening — myelomalacia. Gummata of the cord and 
perineuritis gummosa of the nerve roots are uncommon. 

In cerebrospinal syphilis, tabes and dementia, the lumbar puncture 
is important (v. s.). 

Prognosis of Brain Syphilis. — Only half of the cases recover. The 
later the disease, the worse is the prognosis. The prognosis is more favor- 
able in meningeal, i.e., extracerebral involvement, when nerve symptoms 
or epilepsy are dominant, or when early and thorough treatment is 
instituted. The prognosis is less favorable in specific endarteritis, 
bulbar forms, diffuse involvement, in great psychic alteration and in 
extragenital infections and hereditary syphilis. Recovery is rarely 
complete and recurrence is possible. 

6. Syphilis of the peripheral nerves may cause facial and trigeminal 
paralysis, even in the secondary stage. The most frequently affected 
spinal nerves are the occipital and auriculotemporal. But 6 reports of 
luetic multiple neuritis exist in the literature. 

10. Eye and Ear. — Syphilis explains 3 per cent, of all eye diseases 
and 3 per cent, of all syphilitics have eye disease. The uveal tract is 
most involved; next in frequency come the retina, optic nerve and eye- 
muscles; the lens suffers only from uveal tract disease. The lids are 
not often involved (chancre, condyloma and gumma). 

Conjunctiva. — Twenty-two scleroses have been observed, as well as a 
few gummata; catarrh occurs in the secondary stage. 

Cornea. — The cornea is frequently involved: (a) As parenchymatous 
keratitis, which is mostly observed in congenital syphilis, and occurs even 
in the third generation; in acquired syphilis it occurs in but 2 per cent, 
of cases. "Hutchinson's triad'' in congenital syphilis consists of keratitis, 
notched teeth and congenital or early acquired deafness. The cornea is 
diffusely clouded and milky (the ground-glass cornea), and on close exami- 
nation shows patches or streaks of inflammation; (b) as keratitis inter- 
stitialis, circumscribed or punctate; (c) as gumma, which is infrequent; 
(d) as keratomalacia, observed in the congenital variety. 

7m. — Of all inflammations of the iris, 75 to 90 per cent, are syphilitic. 
The symptoms are those of other iritides — ciliary injection, discoloration, 
slow reaction and synechia or occlusion of the pupil. It is plastic, or 
exudative with tiny papules; iritis with nodules, if not traumatic, is 
strongly indicative of syphilis. Iritis is usually secondary, rarely tertiary. 
Without cyclitis it is rare in congenital syphilis. Atropine should be 
administered early while mercury is being given, for expectant treat- 



SYPHILIS 215 

merit results in severe lesions and recurrence. Ciliary involvement is 
usually secondary, rarely tertiary. Injection and exquisite tenderness 
are characteristic. 

Choroid. — The choroid is involved in the secondary period, perhaps 
following iritis or cyclitis. Its several forms terminate with the same 
appearances — exudative choroiditis with small, oval or irregular yellowish, 
bluish or rose-colored spots. Both the spots and pigment lie behind the 
retinal vessels, which branch over them in the ophthalmoscopic picture 
(Plate VI). Disseminated choroiditis consisting of spots of pigment 
especially in the peripheral eye-ground, usually indicates syphilis. When 
recurrent, with inflammation of the retina and choroid, blindness may 
result. The vitreous humor is rarely involved without lesions of the uvea. 
It results in opacities or dust-like bodies; in the absence of myopia it 
rather indicates syphilis. 

Retina. — The retina is involved chiefly in its anterior layers, be- 
coming cloudy about the disk, with opacity of the nerve and blurring 
of the disk outlines. The course of the arteries is lost or broken and 
the veins are tortuous and engorged. Most cases of idiopathic retinitis 
are syphilitic. Nodules, either papules or gummata, constitute the 
specific retinitis. Recurring retinitis, commencing at the macula, is of 
great importance. Retinitis with pigment formation occurs mostly in 
congenital syphilis. The optic nerve is usually involved with the retina, 
and anywhere from its central origin to the disk. Sometimes the change 
is simple blue atrophy; again the appearance is nearly normal, or again 
choked disk occurs. The causative lesions are gumma in the brain, 
syphilitic inflammation of the intracranial tract or basal disease. Neither 
its syphilitic nature nor its location can be diagnosticated by the 
ophthalmoscope. Amblyopia or amaurosis may result from transitory, 
circulatory, or permanent organic changes. Hemianopsia is often 
central, results from lesion in the optic tract and, in most cases, is 
transitory. 

Eye Muscles. — The eye muscles are involved as frequently as is the 
iris; more than half the paralyses of the eye muscles are syphilitic. 
Ocular paralyses may be (a) peripheral; (b) intracranial as at the base 
of the brain; or (c) central (nuclear, fascicular and cortical). The 
following lesions occur: syphilitic meningitis, basal gummata, periostitis, 
cellulitis of the orbit, diffuse arterial disease, nuclear disease, polien- 
cephalitis and gummata of the hemispheres or cortex. Other causes as 
tabes, general paralysis and tumor, must be considered. Thirty-six 
to 50 per cent, of nuclear paralyses are syphilitic. Syphilis frequently 
produces progressive paralysis of all the muscles of both eyes. Total 
paralysis of the oculomotor is rare; if it occurs, the lesion is usually at 
the base, is rarely orbital, or may be nuclear, especially if one twig 
after another become involved. If it is partial, it is usually nuclear, 
rarely neural or muscular. Ptosis is highly suggestive of syphilis. Ab- 
ducens and trochlear paralysis may occur. Ophthalmoplegia interna, 
involving the sphincter iridis and the ciliary muscle, produces mydriasis 
and paresis of accommodation; 36 per cent, of all mydriases are syphilitic 
and nuclear. Ophthalmoplegia externa may occur with facial paralysis, 



216 PROTOZOAN INFECTIONS 

involving the orbicularis palpebrarum, or with trigeminal paralysis 
involving the sensory filaments of the eye. 

Orbit. — Periostitis is indicated by deep tenderness over the eye-ball 
or edge of the orbit; by pain on movement of the eye; more rarely 
by blindness, exophthalmos and thrombosis. Periosteal gummata are 
often mistaken for tumors. 

Ear. — Four instances of primary sclerosis on the external ear have 
been noted; 33 per cent, of children with hereditary syphilis are deaf; 
otosclerosis is specific in 25 and nervous deafness in 50 per cent. 
Condylomata, mastoid periostitis or gumma, sclerosis or gumma of 
the Eustachian tube, may be observed. 

11. Genitalia. — Some chancres occur in the urethra; gummata have 
been observed in the urethra and bladder (23 cases) . 

Penis. — Gummata, at the site of the primary lesion or elsewhere, 
often are confused with chancre, chancroids or carcinoma. 

Testes. — (a) Diffuse interstitial orchitis occurs with great pyriform 
swelling and flattening of the epididymis; it is often nodular, due to 
periorchitis or gummata. Serous effusion and synechia occur. Absorp- 
tion of this sarcocele syphilitica may result. The connective tissue 
is increased and the canals are compressed, fatty and infiltrated with 
round cells (b) Gummatous orchitis is less frequent, and usually involves 
one testis. Great symmetrical or irregular swelling may occur, and 
frequently the entire testis is firm and studded with gummata, single or 
multiple, hard, irregular, painless nodules. The testes sclerose and 
atrophy. The symptoms develop gradually or after trauma. The scrotum 
is infiltrated, nodular and red. Perforation is frequent, with a crater-like 
opening and irregular edges. Oligospermia, azoospermia or impotentia 
does not always follow, because islets of functionating tissue frequently 
remain; syphilis has been inoculated into rabbits from the sperma. 
Differentiation is required from gonorrheal orchitis, which is more acute, 
painful and involves the epididymis first; plastic orchitis, resulting from 
stricture and traumatic orchitis; also from tuberculous disease, which 
is often bilateral or occurs in several foci, and frequently involves the 
cord, vesicles, epididymis and often causes perforation with pain, fever 
and prostration, in which case tubercle bacilli may be detected. Sar- 
coma is harder, develops more rapidly, is more nodular, produces 
lancinating pains and frequently affects the glands, epididymis and 
cord, which are less often involved in syphilis. Carcinoma, which 
requires differentiation from interstitial orchitis does not respond to 
specific treatment. 

Vas deferens and prostatic involvements are rare. 

Vagina. — Chancres are relatively rare, because of the thick epithelium 
and the paucity of glands; secondary eruptions are rarely observed. 
Gummata occur infrequently. 

Vulva. — The vulva is very frequently the seat of secondary lesions, 
upon which tertiary lesions may develop, which may extend to the urethra 
or bladder. Enormous swelling, resembling blisters, is a common result 
of lymphatic involvement. Gummata are readily differentiated from 
carcinoma and tuberculosis. 



SYPHILIS 217 

Cervix. — Chancre occurs in 5 per cent, of cases. Scars may result 
from gummata, with stenosis and sterility. 

Uterus. — Syphilitic endometritis is frequent; metrorrhagia may respond 
only to mercury. Virchow described a papular and a tuberous variety. 
Endometritis may produce sterility. In clear cases of metritis large 
tumors disappeared under specific therapy. Specific or simple peri- 
metritis is secondary to rectal disease. Placental involvement and 
abortion are discussed under Congenital Syphilis. 

Tubes and Ovaries. — Salpingitis, oophoritis and gummata have been 
described. 

12. Bones, Joints and Muscles. — Periostitis produces pain, tender- 
ness and swelling, which is hard at first, and later is elastic even to fluctu- 
ation. It occurs especially on parts subject to trauma, as the head, ster- 
num, ribs, tibia or clavicle. Fugitive pains occur with the secondary 
eruption, but the pain of periostitis is fixed, rarely migrates, is boring in 
character, appears at night — dolores nocturne — and disappears at 1 
or 2 o'clock in the morning with sweating, but otherwise resembles the 
common types of periostitis. In 28 per cent, it occurs in the frontal or 
temporal bones, and forms circumscribed, smooth, elastic and immovable 
tumors. On the ribs, it occasions pain on coughing or neuralgia over the 
sternum. Tibial nodes occur in 16 per cent, of cases. Osteophytes 
develop. Periosteal changes last for ^.ve or six weeks. 

Gummata of the bones, the first well-studied form of gummata, largely 
occur on the exposed parts as: (a) Diffuse subperiosteal infiltration, 
which causes molecular destruction of the bone. Sequestra may form, 
especially in the femur ; osteophytes in the diaphysis sometimes resemble 
arthritis deformans, (b) Circumscribed gummata, the more important 
form, develop in the periosteum, as elastic, immobile, not especially 
tender tumors which afterward soften and, perhaps fibrose and calcify. 
Gummata of the cranium are attended by dull pain, especially at night; 
grow slowly ; are at first soft, and later have a wall-like, hard edge. They 
rarely ulcerate except from pyogenic infection and often disappear 
spontaneously, leaving an elevated periphery and a deeper centre. They 
are often mistaken for supra-orbital neuralgia or migraine. Tuberculous 
ulcers rarely occur in this location. Meningeal symptoms may develop 
(perforating type) . Gummata at the base, where periostitis is infrequent, 
occur chiefly in the middle fossa and involve the nerves or bloodvessels. 
Diffuse gummatous infiltration develops very slowly, with little pain, 
possibly with ulcerative exposure of the bone and is diagnosticated with 
difficulty. In 1914 Hunt collected 100 instances of luetic spondylitis; 
only 44 per cent, recovered, due to its late recognition; the affection is 
cervical in 70 per cent., rarely dorsal, very rarely lumbar, and affects the 
bodies of the vertebra? less than their processes and arches, in contra- 
distinction to tuberculosis. Pain and immobility are observed. The head 
is held in the hands, if the atlas is involved ; death results from ulceration, 
pressure on the medulla or luxation (10 per cent.). The humerus, radius 
and carpus are infrequently involved. The phalanges may be involved, 
usually one finger only, spina ventosa, the parts being swollen but soft, 
with periosteal thickening, shining appearance and rarely pain or ulcera- 



2i8 PROTOZOAN INFECTIONS 

tion. The clavicle, from its exposure to trauma, is very frequently 
involved ; the course is slow and often painless. Ulceration of the sternum 
is frequent; of the ilium and sacrum, rare. 

Joints. — (a) Acute synovitis occurs alone or with periostitis at the time 
of the eruption; pain alone may be observed or the swelling is poly- 
articular, with tenderness, nocturnal pain, immobility, temperature, 
and involvement of the muscles and tendons. The knees are most 
frequently involved and, according to Fournier, more than three joints 
are never affected. This luetic pseudorheumatism may last weeks or 
months and does not involve the heart. In 100 acute arthritides among 
negro laborers on the Panama Canal, Baetz found 63 per cent, syphi- 
litic and 28 per cent, gonococcic. (b) Chronic synovitis or arthritis 
is usually monarticular, indolent, afebrile, painless, and affects chiefly 
the knee and elbow, (c) Joint disease of late syphilis originates in the bone 
or cartilages (tumor albus syphilitique) , and affects chiefly the knee, elbow 
and ankle. The central portion of the cartilage is involved, and not its 
edge, as is the case in arthritis deformans, probably due to osseous gummata 
and most frequent in congenital syphilis. The onset is slow, with moderate 
pain and swelling; no temperature is observed. There may be a close 
resemblance to tuberculous lesions ; tuberculosis is usually inflammatory, 
incipient syphilitic lesions non-inflammatory; in syphilis, sequestration 
and ulceration are infrequent; therapy and the seroreaction are the 
final tests. Syphilis is most prone to attack the periosteum, gonorrhea 
the joint, and pyogenic organisms the bone. The writer has repeatedly 
seen lues simulate arthritis deformans. 

Muscles. — Early involvement may occur from toxemia or myositis. 
The latter is a diffuse or circumscribed infiltration, which possibly 
eventuates in muscular contractures, especially in the arm and finger 
flexors, sphincter ani, masseters, deltoid and sternomastoid. The course 
is subacute or chronic, depending on treatment. Gummata cause con- 
fusion with neoplasms; they may be as large as the fist, single or multiple, 
usually with a firm connective-tissue capsule; they involve the long 
muscles of the arms and neck, especially at their attachments. The 
course is long, and regression may occur with induration and atrophy 
(arterial disease and central nervous lesions). Myositis ossificans is 
rare. The tendons may be involved, partly from changes in the bones or 
muscles, (a) The early irritative, acute bursitis or tendosynovitis is 
sometimes confused with rheumatism. It occurs most frequently in 
sewing women and washerwomen. There is more tension than pain. 
■(b) The gummatous form, occurring in the flexor tendons, is character- 
ized by indolence, painlessness and benignancy. Churchman collected 
26 cases of bursitis (1876-1908). 

13. Mamivle. — (a) The diffuse infiltration, syphilitic mastitis, with 
swelling, occurs largely in the secondary stage, and often resorbs spon- 
taneously, (b) Gummatous mastitis is deep-seated and is not very sensi- 
tive. Rapid growth may be observed with central necrosis, fluctuation 
or external ulceration. It requires differentiation from adenoma, fibroma 
and carcinoma; it is frequently bilateral, without cachexia or adenopathy, 
but possibly with gummata elsewhere, (c) 206 cases of mammary 



SYPHILIS 219 

chancre are recorded (Dimey). There is a reversion to the abandoned 
idea that milk may convey infection. 

Diagnosis of Syphilis. — Differentiation has been treated under the 
primary chancre, secondary manifestations and special visceral pathology. 
The last ten years have brought within our reach special, we may say 
absolute, diagnostic helps for the careful diagnostician, and yet there 
is a tendency to leap at once to laboratory diagnosis and to disregard 
the frequently characteristic clinical physiognomy of the disease. 

I. The Treponema. — In the initial induration, the detection of the 
parasite is invaluable, employing the dark-ground illumination. Doubt- 
less cultural methods soon will be available for practical use. 

II. The Wassermann Reaction. — Elaborate studies of this compli- 
cated test, discovered in 1906 by Wassermann, Neisser and Bruck, 
have shown its presence in 85 to 95 per cent, of syphilitics; in the chancre 
stage, it appears in 90 per cent, usually in six weeks; in the secondary 
stage, in 95 to 100 per cent, (in 80 per cent, when no outward signs are 
present); in the tertiary stage, in 96 per cent, (in 57 to 65 per cent, 
of cases showing no obvious symptoms); in the quaternary stage, in 
95 to 100 per cent, of general paresis, in 75 per cent, of tabes and in about 
66 per cent, of cases of aortic leakage, aneurysm (95 per cent, of those 
under forty years of age) and aortitis. In general, Wassermann' s 1982 
cases of syphilis gave the reaction in 90 per cent, of manifest lues and in 
50 per cent, of cases without obvious symptoms. A positive reaction is 
sometimes encountered in leprosy, frambesia, trypanosomiasis, scar- 
latina, etc. 

The positive reaction is the most common symptom of syphilis, but 
it is only a symptom and may be lacking ; much less significance attaches 
to a negative reaction, which, in general, is encountered in 10 per cent, of 
cases undoubtedly syphilitic. A positive reaction denotes the survival 
in the body of some living spirochetes, and 99 per cent, of positive re- 
actions are absolutely diagnostic of lues. Mercury and arsenic, pre- 
viously administered, vitiate the reaction, as does also alcohol (taken 
within twenty-four hours of the test). The best results follow the 
original unmodified Wassermann technique. The practical bearings of 
the test are immense, e. g., upon the questions of immunity, which is 
merely latency of the disease, reinfection, familial diseases, heredity, 
congenital lues, prostitution, marriage, life insurance, and treatment, 
all of which are discussed later. To mention but a few instances: 
Letulle found positive reactions in 43 per cent, of chronic obscure diseases 
and in 25 per cent, of chronic nephritides, Dean in one-sixth of 330 
idiots, etc. A Wassermann on the spinal fluid may be positive in nervous 
lues when one on the blood is negative; the former is important diag- 
nostically and also therapeutically, since a test of the spinal fluid 
should be negative before a case may be declared cured. 

III. Noguchi's Luetin Test. — Luetin prepared from strains of spiro- 
chetes, sterilized from pure cultures, is injected as a fine emulsion 
in doses of 0.05 c.c. intradermally. Luetin (the antigen) elicits a cuta- 
neous reaction or allergy comparable to v. Pirquet's test. The positive 
reaction, obtainable only in syphilis, begins as a small erythematous area 



220 PROTOZOAN INFECTIONS 

surrounding the point of injection, usually within twenty-four hours. This 
area may remain without further change for several days or may become 
papular or pustular, according to the severity of the reaction, which 
reaches its height in four or five days. In some cases a slight rise in tem- 
perature occurs, lasting a day or so, and accompanied by malaise, loss of 
appetite and diarrhea. The reaction is sometimes torpid, coming on 
after ten or more days as a pustular eruption. Noguchi concludes: 
(1) The luetin reaction is specific for syphilis. (2) The reaction is present 
in the majority of cases of tertiary (100 per cent.), latent (96 per cent.) 
and hereditary syphilis (96 per cent.). (3) It is less constantly present 
in secondary untreated and primary cases (50 per cent.). (4) In treated 
secondary cases the reaction is present in most instances, especially 
when treated by salvarsan. (5) In general paralysis and tabes dorsalis 
a positive reaction was obtained in 60 per cent, of cases. (6) In certain 
cases of tertiary and hereditary syphilis there may be a considerable 
inflammatory reaction at the site of injection of the control fluid, and 
as strong as at the luetin inoculation site. The Wassermann reaction is 
more constantly present than the luetin reaction in primary and second- 
ary syphilis, especially when only a slight amount of treatment or none 
was given, but the luetin reaction is more constantly present than the 
Wassermann reaction in cases of tertiary and latent syphilis. Through 
the treatment the Wassermann and clinical symptoms gradually are made 
to disappear, while the luetin reaction becomes more distinct. 

IV. Diagnosis ex Juvantibus. — v. i. Therapy. 

Immunity. — Syphilis confers immunity, but this is neither absolute 
nor life-long, because (1) reinfection may occur; of 356 instances in the 
literature, only 132 stand criticism (F. John, 1909); (2) in hereditary 
syphilis, a later infection may be acquired (27 cases known) ; (3) a sound 
child of syphilitic parentage may acquire syphilis (29 cases reported); 
and (4) apes have been reinoculated. Gitting's case with a second chancre, 
occurring while the Wassermann was still positive, may have been a 
recurrence. In general, immunity means only latency of the luetic 
virus. 1 

Abnormal Course of Syphilis. — Of special importance is malignant 
syphilis (syphilis precox, acute or galloping syphilis, synonymous with 

1 Levaditi holds that during the period of incubation before the primary sore the parasites 
invade the body, causing the development of immune bodies, as manifested by a refractory 
condition of the skin to further infection; this resistance becomes well developed at the 
onset of secondary lesions. During the secondary stage the lesions are chiefly inflamma- 
tory, with evidence of great resistance by the tissues, which suffer little injury, despite the 
presence of great numbers of parasites. In the tertiary stage, the resistance to infection is 
highly developed, and the lesions show great tissue destruction produced by comparatively 
small numbers of parasites. 

Levaditi suggests that the resistance of the host to the invading organism developed 
during the primary stage may hold the parasites in check for a time, until they acquire a 
certain degree of immunity of their own to the antibodies of the host; they then enter 
the blood and set up a generalized infection, characteristic of the secondary stage; in 
reaction to infection, greater quantities of antibodies are formed, suppressing the parasites 
to a large degree, although not destroying all of them. The tissues themselves may become 
hypersensitive, i. e., a few spirochetes cause extensive local necrosis, characteristic 
of gumma ta. Gummata, then, are produced by parasites, which are refractory to the 
antibodies of the patient and develop in tissues which have grown sensitized. Iodides 
operate by rendering the tissues less sensitive or anaphylactic. 



SYPHILIS 221 

early tertiary development). The cause may be increased virulence of 
the spirochete, or decreased physiological resistance, as in tuberculous, 
alcoholic and other cachexia?. Early ulceration, grave general symptoms 
and hemorrhage are noted. 

Prognosis. — On pregnancy the disease exerts a malign influence and 
mercury is less universally successful (v. Congenital Syphilis). Exan- 
thematous diseases may cause syphilis to disappear temporarily. The effect 
of coincident measles and smallpox is unfavorable. Chronic -diseases, 
as tuberculosis, often induce ulceration and early tertiary symptoms. 
Trauma; in the treatment of fractures and in plastic operations in 
syphilitics, mercury is indicated. Wounds may become the seat of 
specific ulceration. 

In life assurance the outlook is uncertain; Leser's figures indicate that 
33 per cent, of luetics ultimately die of tuberculosis, paralysis or aneurysm; 
other main causes of premature death are cardiac disease, nephritis, 
dementia, tabes, thrombosis and suicide; the chief contributing causes 
are poverty, worry, overwork and alcoholism. 

Congenital Syphilis. — Syphilis descends only to the first genera- 
tion; among the 115 cases recorded in the second generation, many are 
doubtful. 

It was formerly held that a child might acquire syphilis from the 
father, from the mother, or that mother and child might be infected 
simultaneously. Hutchinson still adheres to the possibility of paternal 
lues transmitting the disease. The Wassermann reaction and the presence 
of spirochetes have revolutionized our conceptions of congenital syphilis. 
According to Colles's (or Beaume's) law the syphilitic child is held to make 
the mother immune to infection; she cannot be infected from her in- 
fected child; and can nurse her syphilitic child without danger. In such 
cases, Fournier held that the mother is already syphilitic, and in 381 
cases, 76 per cent, gave a positive Wassermann reaction, whence it is 
probable that all such mothers are luetic, the syphilis being latent. 
Prof eta's law held that (apparently) sound children of syphilitic parentage 
possess an immunity against syphilitic infection; Wassermann 's re- 
action proves that these children have syphilis. 

The more recent the parental syphilis, the greater the probability 
of fetal infection; in tertiary syphilis of the parents, the child may escape. 
Thus the first product of conception may be aborted, the second macer- 
ated fetus prematurely delivered, the next die at birth or shortly after- 
ward, the next viable though infected, and finally, as the toxemia Avears 
off, even sound children. Only 28 per cent, of conceptions in syphilitic 
mothers result in full-term infants, and of these 85 per cent, die within 
the first year. Women who habitually abort, show the Wassermann 
reaction. 

It is possible that excessive emphasis has been placed upon the sig- 
nificance of abortion per se; infectious abortion is common among mares 
and cows and is due to a small bacillus (Bang, 1895). Infection from the 
mother is carried to the fetus by way of the placenta, in the fetal portion 
of which, and usually also in the umbilical cord, spirochetes are found, 
although but seldom in the maternal portion of the placenta. Significant 



222 PROTOZOAN INFECTIONS 

also is the heavy placenta whose weight compared with that of the syphilitic 
child is 1 to 5, 4 or 3 (normally 1 to 6). In the placental villi end- and 
periarteritis occur, which may cause, by vascular occlusion, placental 
necrosis and adherence. Similar changes in the umbilical vessels may 
destroy the child. When the macerated fetus is examined, the spirochete 
is found in 84 per cent., most often in the adrenals, next in the liver and 
lungs in the vicinity of the vessels, and often in the heart alone. The ovary, 
testicle, -and epididymis contain the spirochete. In living children 
the spirochete was found in the vesicles in cases of pemphigus. A differ- 
ence exists between the congenital syphilis with signs at birth, and the 
hereditary type, which develops later (possibly very late, syphilis hered- 
itaria tarda). Even when specific lesions are absent, pathological cell 
degeneration, rhachitis, slow intelligence, neuroses, psychoses and a high 
percentage of mortality to all diseases may result. 

Symptomatology. — The primary, secondary and tertiary stages are 
not discrete and lymphatic infection does not precede that of the 
entire organism. Secondary and tertiary manifestations may occur 
synchronously. The symptoms are recognizable at birth or after a few 
days or weeks, and almost always within the first three months. 

Appearance. — The atrophic child presents a rather characteristic 
appearance, with relaxed yellowish-gray skin, poorly developed hair, bent 
or undeveloped nails (onychia) and "the little old man" appearance 
described by Trousseau, but not pathognomonic of lues. The palms 
and soles are lacquered, the voice and muscles are weak and the child 
does not nurse well. Such children, especially when several are born in 
succession, point to syphilis. 

Pathognomonic Symptoms. — The exanthem is polymorphous, but 
varieties, often severe, occur which are absent or infrequent in the 
adult, such as pemphigus, hemorrhages, furuncles and diffuse infiltration 
of the skin. The macula? are dirty, brown-red, often confluent, and occur 
on the face, body, extremities and genital regions. The papules occur 
principally in the folds of the joints, axillae, groins and gluteal region 
and tend to recur and ulcerate; papules of various ages coexist with 
desquamation, though never with condyloma, which is always a sign of 
acquired syphilis. Psoriasis of the hands and soles of the feet is common. 
Pustular lesions occur in severe syphilis and are prognostically unfavorable. 
They occur in the immature fetus; pemphigus is a subtype of the pustule; 
gangrene and necrosis may occur. The copper-colored syphilitic infil- 
tration, especially on the nates and lower extremities, may be mistaken 
for erysipelas. Coryza ("snuffles") is very characteristic and almost 
invariable, the secretion being bloody and purulent, with crust formation, 
and spirochetes in 20 per cent. Fissures occur about the mouth, with an 
infiltrated base and cicatrix formation. Papular eruptions occur in the 
mouth, especially on the tongue and the palate, with a tendency to 
necrosis ; atrophy of the base of the tongue occurs in most cases. Rhagades 
occur about the infiltrated genital and anal regions. 

Teeth. — Erosions, furrows and notches may develop. The teeth are 
small, often irregular and poorly developed. Hutchinson held that 
the semilunar curving on the free edge of the upper middle permanent 



SYPHILIS 223 

incisors was pathognomonic of tardy congenital syphilis, appearing 
at the seventh year, but Hutchinson s teeth occur in other affections, 
and are expressions of constitutional derangement only. Later the 
lateral borders of the teeth become curved; the teeth may become 
peg-like or the notches grind off even. The other associates of Hutchin- 
son's triad — deafness and the ground-glass cornea — are discussed on 
pages 214 and 216. Blue sclerotics are accounted symptomatic of con- 
genital lues, and Heine found optic neuritis in 82 per cent. The Wasser- 
mann test is positive in 90 to ICO per cent.; it may be absent at first, to 
appear as the clinical signs develop; in one series it was positive in 298 
out of 300 cases. 

Bones. — As in adults, there may be periostitis, tophi or perforated 
palate. Osteochondritis occurs especially in the lower end of the femur; 
the diaphysis and epiphysis may be separated. There is (a) overgrowth 
of the cartilage of the diaphysis which produces the wavy line of white 
cartilage cells; (b) the line of cartilage cells becomes thick and foci 
of decalcification occur; (c) the cartilage is as prominent as in rickets, 
the part nearest the bone being soft. The immobility of the leg may 
suggest paralysis (Parrot). 




Fig. 14. — Notched teeth. Malformation of permanent teeth found in hereditary syphilis. 

(Jonathan Hutchinson.) 

Viscera. — Diffuse infiltration is much more frequent than gummata. 
There are characteristic changes in certain organs which are rarely 
involved in acquired syphilis, e. g., in the thymus, umbilical cord, 
pancreas, lungs, intestines and adrenals. The liver and spleen are greatly 
enlarged ; the Spirochete pallida is found in these viscera in vast numbers, 
even in the macerated fetus. To conserve the classification, these changes 
have been described under Special Symptomatology. Fournier de- 
scribes enlargement of the peripheral veins. Vascular changes are 
especially marked, as in the umbilical vessels, with a tendency to hemor- 
rhage — syphilis hemorrhagica neonatorum. Hemorrhages in the skin, 
mucous membranes and viscera, may be profuse, especially in the liver 
and lungs, where the circulation is precipitately altered after birth. 
Levaditi found spirochetes in the foci of hemorrhage. Some vessels may 
be thickened or infiltrated (disease of the vasa vasorum). 

Acquired Syphilis in Children vs. Hereditary. 

Less mortality and less malnutrition. Marked. 

After third month (are exceptions). Before third month. 

A primary lesion occurs. Absent. 

Lymph glands enlarged. Absent (from accidental causes only). 

Usual sequence of primary, secondary and Snuffles, anemia, diffuse pigmentation, 

tertiary symptoms. Secondary lesions, pemphigus, involvement of soles and 

then tertiary, palms, epiphyseal changes, etc. Second- 
ary and tertiary together. 



224 PROTOZOAN INFECTIONS 

Syphilis hereditaria tarda develops its first symptoms, mostly between 
the tenth and eighteenth years (rarely before the tenth year). The 
symptoms are those of infantilism, in regard to puberty, bone develop- 
ment, teeth, hair and brain. 

Treatment of Syphilis. — Prophylaxis. — The sexual instinct is even 
stronger than that of self-preservation. Irregular intercourse is promoted 
by class differences, lack of barriers among the ignorant and destitute, 
and the struggle for existence which makes early marriage impossible. 
Prostitution, hidden or open, is the basis of syphilis. In prostitutes, 
condylomata last years and repeatedly recur about the genitalia; the 
Wassermann test is found in all women who have been prostitutes over 
three years. Continence is the sole prophylactic measure. Enforced 
medical inspection is ineffectual. American sentiment is against licensed 
prostitution, which, besides, does not regulate men or hidden prostitution. 
Licensing also teaches the young that immorality is safe. Many 
infections are acquired under the influence of liquor {Sine Baccho 
friget Venus). Where ethical considerations fail, an appeal to fear may 
be effectual. Metchnikoff comments upon the remarkable fact that 
diseases conveyed by insects are rapidly becoming preventable, whereas 
diseases like syphilis and tuberculosis conveyed by rational human 
beings, are not. Efforts to educate the public will doubtless avail much; 
syphilis, however, must be presented as an infection and dissociated 
from ethics and retribution. 

The curse of the disease lies in its long course, the involvement of vital 
viscera, its transmission to the wife and offspring whose mortality and 
morbidity are enormous, and its wide dissemination (13 per cent, of 
the population acquire the disease, and 1,650,000 persons are infected 
annually) . v 

Marriage should be forbidden for at least three, better four, years or best,\ 
till the sero-test remains negative. In cases of doubtful infection of the 
wife or husband, both should be treated. Inunctions should be given / 
the pregnant mother. The physician should never countenance employ- 
ing a healthy wet-nurse for the syphilitic child. Circumcision is thought 
to lessen chances of infection. Blue ointment, applied before intercourse, 
is prophylactic. 

1. Initial Lesion. — Early mercurial treatment is indicated, but only 
when the diagnosis is certified by a typical chancre and spirochetes. 
Mercury is indicated in all stages of syphilis, for abortive treatment as 
well as that of the established disease. Local treatment includes the 
use of antiseptics, iodoform, mercurial plasters, iodoform in suppository 
(rectum or vagina), bichloride washes (mouth) and calomel for condy- 
lomata (calomel 6 parts, boric acid 3, and salicylic acid 1 part). 

2. Secondary Stage. — In the secondary stage mercury is a specific 
against the spirochetes. The teeth should be cleaned first, and bad 
teeth filled. Calomel acts especially on the lesions of the mouth and is 
prone to salivate. Mercury may disagree (v. i.) in tuberculous, cachectic, 
alcoholic or anemic subjects, in bleeders and in cases of galloping syphilis, 
in which latter iodides may be better than mercury. Mercury must be 



SYPHILIS 225 

used with great care in nephritic subjects. During and after a course of 
mercury, tobacco must be interdicted because it perpetuates syphilitic 
sores in the mouth for years, even decades. ^Moderation in all matters 
of life is enjoined upon the patient. 

Methods of Administration. — 1. By Mouth. — Ninety-five per cent, of 
cases are thus treated in this country, whence some account of this 
method is appropriate despite the fact that it is uncertain and unwise, 
and syphilides, gummata, tabes, general paresis and aortitis often develop 
after oral administration, but rarely after systematic inunctions, (a) 
Calomel (hydrargyri chloridum mite) is especially adapted to children 
under three years of age with hereditary syphilis; gr. J to \ t. i. d. It 
is insoluble, and is probably converted by the alkaline carbonates in the 
intestines into the gray oxide which is absorbed with the fats, (b) Blue 
mass (massa hydrargyri), gr. | to 1, is less irritant to the stomach than 
calomel, but produces salivation oftener than any other mercurial. 
(c) Hydrargyrum tannicum oxydulatum (50 per cent, mercury) is non- 
irritant, produces less diarrhea and is easily assimilated; gr. 1 to 1J 
plus pulv. opii gr. y 1 ^; (d) The hydrarg. iodidum flavum or protiodide is 
mild, insoluble and analogous to calomel. 

]$ — Hydrargyri iodidi flavi gr. xv 

Extr. opii gr. v 

Extr. gentianse q. s. 

M. et ft. pilulse no. lx. 

S. — One after meals. 

(e) The soluble sublimate or bichloride is irritating (hydrarg. chloridum 
corrosivum) ; it is not prone to salivate, is absorbed by the intestine 
and stimulates the liver. Mercury, administered internally, produces 
more irritation and is less likely to be absorbed, but patients are more 
apt to persist in this form of treatment. Mercury internally was first 
used by Benedictus (1525). 

2. Inunctions. — Rubbings must be thorough and given where the skin 
is soft (flexor surfaces). Mercury is absorbed by the lymph vessels. 
The skin must be bathed daily. A simple diet should be given; as a 
rule, mercury somewhat loosens the bowels. The rubbing requires 
twenty to thirty minutes. Hairy regions, the axillae, navel, nipple and 
areas of accidental eczema, psoriasis, etc., are to be avoided. If the hair 
on the body is redundant, the skin should be shaved. The occasional 
mercurial dermatitis is often due to decomposition of the fat in the 
inunction. On the first day the inunction should be given on the abdomen, 
on the second day on the chest, on the third on the calf, then on the thigh, 
forearm, arm, etc. After inunction, the part is enveloped in cotton. 
If an attendant gives the rubbing, his hand is protected by a rubber 
glove. Written instructions should always be given to the patient. 
4 Twenty to thirty inunctions should be given for the macular and 
papular types; more than thirty, for all pustular or ulcerating eruptions, 
but not more than forty should be given continuously. Inunctions must 
be interrupted for diarrhea or stomatitis. Salivation is not desirable, 
nor is it a sign that enough mercury has been given. The unguentum 
contains 50 per cent, of mercury, and the more elegant oleatum but 
15 




226 PROTOZOAN INFECTIONS 

25 per cent., which should be considered, as about 3ss of mercury should 
be incorporated daily. 

1$ — Unguent, hydrarg giv 

Div. in dos. equal, no. xxx. 

Dent, ad cartam ceratam. 
S. — One as directed daily. 

In children, mercurial ointment may be applied on a binder and 
allowed to remain for days. Children stand relatively large doses but 
women may endure only half the adult dose. The advantages of inunc- 
tions are as follows: They cause almost no digestive disturbance; they 
are especially good in children; they are the most rapid and effective 
method, and are attended by the least general ill-effects The disad- 
vantages are publicity, troublesomeness and dirtiness, but these, however, 
are only relative objections. Inunctions were first used by the Galenists. 

3. Injections. — Their advantages are prompt action and exact dosage. 
Intravenous injections may be imperative in cases with coma and other 
urgent symptoms. The disadvantages are the risk of embolism, slough- 
ing and pain; once given, their action cannot be regulated or decreased. 
The soluble salts are best: 

1$ — Hydrarg. chlorid. corrosivi 1 . 00 

Sodii chloridi 10 . 00 

Aquae dest . . . . . 100 . 00 

One c.c. daily equals 0.01 gm. or gr. -J- of HgCl 2 ; forty injections con- 
stitute a course. The succinamide is less irritating (hydrargyri succin- 
amidum, grain -J-) ; the best preparation is the insoluble basic salicylate 
of mercury — grain j to nix of albolene, injected two or three times a 
week. Insoluble preparations are painful; ten deaths followed injections 
of gray oil (Grancher) ; since 1906, Riehl collected 90 fatalities from in- 
jection of insoluble salts. Mercury may first make the eruption clearer 
(Herxheimer's reaction). 

4. Baths. — 3ij-iij of HgCl 2 to the bath are useful for skin lesions, as 
syphilitic psoriasis. 5. Fumigations are impracticable. 

As a working rule, mercury should first be given two months and 
stopped one month, through the first year, i. e., two-thirds of the time; 
in the second year, about half the time, with intervals; in the third year, 
one-third of the time. The Wassermann test is used to control the 
therapy; the positive sero-test lessens under mercurialization and recurs 
when therapy is intermitted. To convert a positive into a negative 
reaction requires very energetic, repeated treatment (v. i. page 229). 

Mercury is incompatible tvith nearly everything. Coincident anemia 
is treated by iron, strychnine and arsenic. Syphilitics tolerate mercury 
well, in large doses, and for a remarkable period. Considering briefly 
the action of the drug; in the smallest doses it is tonic, and increases 
the number of red cells. Back of the tongue near the epiglottis and in the 
folds of the pillars, a white, cloudy film may develop (perhaps due to the 
organisms of Vincent's angina). In larger doses there develops a symp- 
tom-complex known as salivation, of which peculiar fetor is first noted ; then 



SYPHILIS 227 

sore teeth, red, swollen, spongy and bleeding gums, and increased saliva, 
follow. Njhe drug is never given beyond this point. In still larger doses 
the tongue becomes swollen, the gums inflamed and the teeth loose; 
the greatly increased saliva is viscid and stringy; the salivary glands 
intumesce; eruptions appear, resembling eczema, scarlatina, measles 
and more rarely, purpura and pemphigus. Fever, albuminuria and 
dysenteric passages may be noted (the kidneys cannot excrete more than 
10 mgm. of mercury a day without irritation). Severe salivation results 
in loss of teeth, necrosis of jaw, ulceration of the mouth and contiguous 
parts, marked changes in the blood and profound exhaustion. The 
treatment consists of potassium chlorate as an antiseptic mouth wash 
and astringents, as tr. myrrh and tannic acid. 

3. Tektiaky Stage. — The resolvent action of iodides is little short 
of miraculous. They were introduced by Welch, of Ireland, and popular- 
ized by Ricord in France. They are sometimes used in the secondary 
stage, especially in febrile cases, secondary osseous and nervous mani- 
festations, and weakly persons with a marked macular eruption. They 
act more slowly and far less specifically on the spirochetes than mercury, 
though they aid in absorbing gummata or infiltrations, and rendering 
the tissues less sensitive to the spirochete (v. s. Immunity). .Jheir use 
should be intermittent and alternative with mercury." Mercury is con- 
jointly employed in all tertiaries, particularly when organs of great 
importance are involved, such as the larynx, brain and eye. 

The therapeutic tests for syphilis are cure with mercury and iodides 
and tolerance by the patient of very large doses. Regarding their diag- 
nostic value the influence of the drugs must be unequivocal and a positive 
Wassermann be converted into a negative reaction. Before negative" 
conclusions are drawn, it must be remembered that loss of tissue, e. g., in 
arterial occlusion and paralysis from brain softening, cannot be restored. 

Sodium iodide is milder, produces less iodism, is less bitter, and has 
less effect on metabolism than potassium iodide, which, however, is 
better than other iodides, though it irritates the stomach and bowel, 
and depresses the muscles and motor nerves. 

The following proportions for a single ordinary dose may be em- 
ployed; the mercury becomes mercuric iodide: 

1$ — Potassii iodidi gr. xv (gm. 1) 

Hydrargyri chloridi corrosivi gr. -^ (gm. 0.002) 

Tincturse opii Tflij (gm. 0.13) 

Syrupi aurantii corticis 5ss (gm. 2) 

M. et S. — After meals in a glass of water. 

Large doses of iodide are given in urgent cases, 5j~ij t. i. d., to break 
down more rapidly the new-formed granulation tissue. Enormous 
doses are unnecessary and not without danger (v. i.). Fournier warns 
against their intemperate use — "iodide debauches." Iodide dissolves 
in its own weight of water; hence one minim of a saturated solution 
equals one grain of iodide. Iodides are eliminated as the sodium salt; 
nine-tenths is eliminated in a few hours. If the stomach is intolerant, 
iodides may be given in nutrient enemata. It is best disguised by syr, 
sarsaparillse co. 



228 PROTOZOAN INFECTIONS 

Iodism is often produced by small, but usually ceases with larger, doses. 
It is obviated by intermittent administration, by daily baths, by flushing 
out the kidneys, the inactivity of which is the usual cause, by giving 
aromatic spirits of ammonia, arsenic or belladonna. Iodism is likely 
to occur in renal disease. Its leading characters are: Increased secretion 
from the eyes, nose, mouth, salivary glands, bronchi, stomach, bowels, 
skin and kidneys (i. e., from all organs concerned in the elimination of the 
drug). The eyes, throat, larynx and salivary glands swell. The writer 
once nearly suffocated from edema of the pharynx and uvula after inges- 
tion of 10 grains of iodide for a cold. Pulmonary edema and albuminuria, 
or even nephritis, may develop; 3ss induced edema of the larynx. 
Gastric irritation and nervous depression, mental derangement or 
excitement; acne, hemorrhages, blebs and telangiectases in the skin; 
cachexia, anemia, and hyperthyroidism especially in goitrous subjects; 
emaciation, wasting of mammse and testes; fever, increased pulse and 
neuralgias are also symptoms of iodism. 

p Iodides are continued for two months and their use then remitted for 
one month and so on. After years, iodides and mercury are given for 
one month twice a year, e. g., in January and July. 

*" Salvarsan. — Ehrlich (1909) introduced this arsenical preparation as a 
spirillicide, with the hope that one massive dose would result in complete 
curative sterilization. It was welcomed as our first, scientific discovery 
in therapy, destroying all spirochetes in all stages and forms of the disease, 
acting most rapidly in its production of antibodies and operating in other 
spirilloses — as relapsing fever and Vincent's angina, as well as in other 
types of parasitic disease. Its indications were: (i) primary lues, in 
which its best results were claimed; (ii) secondary and tertiary lues, 
particularly in malignant types and (iii) types refractory to mercury; 
(iv) hereditary syphilis; and (v) parasyphilitic lesions, without optic 
atrophy. Its contra-indications included: (i) organic diseases of the heart 
(hypertension, aneurysm, etc.), of the lungs (tuberculosis) and of the 
kidneys (severe nephritis); (ii) cachectic states, as severe diabetes; 
(iii) when arsenic had been administered previously, or there was idio- 
syncrasy to it; (iv) optic neuritis or atrophy; (v) severe nervous lesions, 
as general paralysis; and (vi) profound hereditary syphilis and preg- 
nancy. The early results were striking in rapidity of action, marked 
tonic effects, the remarkable healing of ulcerations in the mouth, genitalia 
and skin, coertion of malignant and pustular forms, relief from pain 
and the amenability of the occasional cases resisting mercury; its speci- 
ficity in apes (experimental syphilis) and in human syphilis on the clinical 
lesions and on the Wassermann reaction. The initial optimism was 
soon followed by complications; deaths, sudden or slower; and prejudice 
pro and contra. Local complications were necroses at the point of intra- 
muscular injection (20 per cent.), all bloodvessels obliterating and the 
arsenic being but slowly dissolved. Given intravenously, thrombophle- 
bitis often occurred. General reaction was common, with fever, leuko- 
cytosis, chill, head and backache, nausea and vomiting, local pain and 
tenderness, rapid pulse and respiration, even with dyspnea, collapse, 
bladder irritation, anxiety and other developments, suggesting anaphyl- 



MALARIA 229 

axis. The fever was not wholly due to bacteria in the distilled water 
nor to the saline of the infusion. Paralyses (facial, polyneuritis, etc.) 
developed; these neurorecidives, specially of the cranial nerves, were 
attributed to the disease (Benario) or to the drug (Finger). Finger 
observed 44 neurorecidives in 500 salvarsan injections as against 5 in 
over 2000 mercurial treatments. 

Deaths from hemorrhagic encephalitis, nephritis, cardiac failure, etc., 
have run into hundreds published and probably many more unpublished. 
Then salvarsan therapy was "modified"; first given intramuscularly 
and then intravenously, it was next given both ways; then it was pre- 
ceded and followed by mercury ; now neosalvarsan comes, with its milder 
local action and solubility, but with its quota of accidents and deaths; 
and salvarsan instead of sterilizing the body with one dose, is giveu many 
times, once a week for 6, 8 or more doses. Adrenalin recently is advocated, 
to prevent and cure untoward effects. 

One may not state now what is the value of salvarsan. It is certainly 
no more a cure than mercury; it does not replace mercury and even 
demands its cooperation; it entails a far greater mortality; it entails 
a surgical procedure with its attendant expense; and it is less penetra- 
tive than mercury which becomes part of the tissues as an albuminate, v 
whereas u _6Q6^-remains a foreign body. When are we justified in using it? 
If used, the writer's personal preference is for the intramuscular injection, 
in oil, and repeated; it rarely kills in this form. It is most valuable^/ 
early before the Wassermann test develops; when mercury fails; in 
malignant types; and where special prophylaxis is imperative. The 
intraspinal injection of salvarsanized serum is recommended by Swift 
and Ellis in lues of the nervous system, since the choroid plexus blocks 
the blood to the spinal fluid circulation. 

Control by the Wassermann Reaction. — With some exceptions, treatment 
by mercury, iodides or arsenic is measured by the turning of a positive 
into a negative reaction. Salvarsan leads in the early effects; in later 
syphilis mercury and salvarsan are alike. After one course of mercury, 
the reaction becomes negative in 50 per cent.; after 8 or more, in 90 per 
cent.; it takes several or many intravenous injections to effect the same 
result. Jonathan Hutchinson held that even mercury pills caused a 
negative reaction in 70 per cent. Mercury, though slower in action, 
remains the remedy for the practitioner. 

A syphilitic should nevek be dismissed or be given any guarantee 
of the extinction of the disease (Ricord). 

MALARIA. 

Definition. — An acute infection caused by the Plasmodium malarias, 
inoculated in man by the mosquito and characterized clinically by 
(1) paroxysms of intermittent, quartan, tertian or quotidian fever, or 
by (2) remittent or subcontinuous fever, and sometimes by (3) per- 
nicious, or chronic cachectic forms. 

History. — Malaria, known to Hippocrates and Celsus, is the most 
completely investigated of all diseases, in that (a) its cause is known; 



230 PROTOZOAN INFECTIONS 

(b) its prophylaxis is exact, since the discovery of infection by the mos- 
quito; (c) the stages of the disease can be followed in the blood; and 
(d) there is a truly specific therapy. 

Etiology. — Men are more exposed to infection; such occupations as 
sewer and railroad building, ditching and night work, especially, are pre- 
disposing factors; 32 per cent, of the French soldiers in Madagascar 
in 1895 acquired malaria; reduced physiological resistance, exposure, 
excesses and alcoholism predispose to infection. Negroes have a relative 
immunity. Epidemics may occur, as during the building of the Paris 
boulevards. Indirect causes, as climate, the warm season, moisture, 
rain, swampy localities, bad air (mal-aria) and impure drinking-water 
are causes only in so far as they relate to the breeding of the mosquito. 
In Africa, severe forms of malaria are found everywhere except in its 
lower part and in the Sahara. In the far East its chief seats are India, 
Burma, Assam, Faral and the East Asiatic coast; Asia Minor, Japan 
and the East Indies. In Europe, lower Russia, Italy, Hungary, the 
Balkans and Greece are most affected. Malaria was probably the cause 
of the decadence of ancient Greece. Malaria also abounds in the northern 
three-fourths of South America. In the West Indies, severe types prevail. 
In the United States, malaria seldom develops on the Pacific coast, in 
the Northwest, the dry West and the Lake region. Even in the South 
it is becoming less frequent. 

Direct Cause. — The malarial parasite, described by Laveran, in 1880, 
and Marchiafava and Celli, in 1885, is a red-cell parasite, a hemocyto- 
zoon. The biology of the Plasmodium malaria concerns (A) its life in 
the human blood, and (B) its life in the mosquito. Various species 
are recognized because (1) their morphology varies; (2) their geography, 
seasonal prevalence and malignancy vary; and (3) on inoculation, the 
type is maintained. 

(A) The Plasmodium in Man. — Special forms of the parasite: 

1 . The quartan parasite (Plasmodium malarise) has a life-cycle of three 
days. In the first twelve hours the young form is a small, amorphous, 
hyaline spot in the red cell ; there is some ameboid movement upon warm- 
ing the slide. Pigment or melanin appears as coarse, dark rods and 
granules with little movement. Melanin is hemoglobin digested by the 
parasite; it is dark or black and resembles the melanin of malignant 
growths. Movement of the parasite ceases as pigment increases. The 
parasite occupies one-half to two-thirds of the red cell after forty-eight 
hours, and almost the entire cell after sixty hours. Flagella and vacuoles 
(v. i.) are not frequent. The red cell on which the plasmodium feeds 
undergoes no change in size or becomes smaller and darker peripherally. 
As sporulation occurs, the pigment gathers centrally and the spores, 
usually numbering not more than ten, develop into the " daisy" form. 
After sixty-nine hours, segmentation occurs in the peripheral blood three 
hours before the paroxysm, which corresponds with their rupture from 
the red corpuscle into the plasma. Sporulation of the adult parasite 
means its "death in childbed," as Mannaberg describes it; the spores 
rupture through the red cell and escape into the plasma, whence they 
enter other red cells, to repeat their life-cycle. The pigment and frag- 



PLATE VIII 








8 






.?*■■, 



10 



3 



\| 








■v--; v 



10 



- 



B 











Malarial Parasites. 






A. Tertian parasite. 1, young form; 2-4, stages of growth and pigmen- 
tation ; S-7, segmentation ; 8, rupture of spores fronn. corpuscle ; 9, extra- 
cellular form ; lO, flagellate form. 

B. Quartan parasite. 1-6, development and pigmentation ; 7, 8, central 
grouping of pigment and spore formation; 9, rosette of spores with nuclei; 
lO, extracellular form; 11, flagellate form. 

C. /Estivo-autumnal parasite. 1, ring-like body; 2, 8, ameboid forms; 
4, parasite in brassy degenerated red cell; 5, pigmentation; 6, segmentation ; 
7, 8, half-moon bodies ; 9, flagellate forms. 



MALARIA 231 

ments of red cells are carried by the leukocytes to the liver and spleen. 
Some forms (gametocytes) do not mature nor sporulate, but are taken 
up by the mosquito, to complete in it another cycle. (Plate VIII.) 

2. The tertian organism (Plasmodium vivax) has a forty-eight-hour 
cycle. In its first day it is a small (lju or 2fj), bright, unpigmented 
disk in the red cell, thrusting out pseudopodia, with active ameboid 
movement, and possessing a large nucleus — partly clear chromatin, and 
partly deeply stained chromatin. It fills one-third of the cell. In its 
second day, pigment accumulates as fine granules or rods, which are 
peripherally located, and have a swarming movement, like that of boiling 
water, due to currents in its protoplasm. The ameboid movement de- 
creases in thirty hours, as the parasite grows and the pigment increases, 
but some movement remains for a long time. Vacuoles are frequent. 
The parasite occupies two-thirds to three-fourths of the red cell, which 
becomes distended and chlorotic. The most common form of sporula- 
tion is the concentric accumulation of pigment and the development 
of fifteen to twenty small, round, rough, refractile spores, which form 
in two concentric circles ("sunflower" arrangement), or are more fre- 
quently irregular, like a bunch of grapes. Sporulation occurs three hours 
before the chill and rise of temperature, and is completed in forty-eight 
hours, when the toxins secreted produce the rigor and fever. Few spores 
are seen at the time of the chill, because sporulation occurs to a greater 
extent in the internal organs than in the peripheral blood stream. When 
spores are seen between paroxysms they represent the sporulation of 
another generation of parasites, too few to induce a paroxysm. The 
generations are never absolute, as they are in the quartan type, and the 
parasites of the same generation vary six or eight hours in their cycle. 
This explains the clinical variations in periodicity. A few minutes after 
withdrawal of the blood, nodulated and clubbed flagella lash about and 
indent the red cells. They may break off and swim about. They occur 
in parasites which never sporulate in human blood, but remain as large 
bodies with vibrating pigment, representing gametocytes or "sexual 
forms," which develop later in the mosquito (MacCallum). 

3. The estivo-autumnal parasite has a life-cycle of from twenty-four 
to forty-eight hours. There are two subtypes — the tertian (Plasmodium 
falciparum) and quotidian (Plasmodium falciparum quotidianum) . It 
has a very small, unpigmented body, and possesses most active ameboid 
movement, thus attracting early attention, though it possesses almost the 
same refraction as the red cell. It becomes quiet after drawing the blood 
from the body, when it appears characteristically ring-like, often with a 
central vacuole. The shape may be successively ameboid, diskoid, 
annular, cruciform, or with a slight knob — the seal-ring form. Mature 
forms contain particles of hemoglobin. The pigment is extremely fine, 
powder-like, dark, peripherally located, and somewhat motile. When 
the parasite reaches one-third the size of the corpuscle, it is usually 
motionless, the pigment concentrating centrally. Motion in the parasite 
has been seen in the cadaver. The spores number six to sixteen, are very 
small, round, and without movement or vacuoles. Fever, pigment 
concentration and sporulation coincide (Golgi). Large parasites in the 



232 PROTOZOAN INFECTIONS 

peripheral blood with much pigment denote the onset of a paroxysm, 
and after the paroxysm, ring-forms without pigment may be observed. 
Young forms circulate in the blood stream, though sporulation occurs 
in the viscera. The half-moon bodies or crescents are delicate, highly 
refractile bodies, measuring eight to ten by two or three microns, develop 
in the bone-marrow or spleen, and possess pigment, which is usually 
mesially located and has little motion. They have no ameboid movement 
but may slowly change shape; they are spindle, oval or spherical. They 
occur singly in the red cell and do not multiply in the human blood. The 
adult forms are seen in the peripheral blood, which offers the best op- 
portunity for leaving the body — through the bites of mosquitoes. The 
male form of the crescent has flagella (microgametes) which penetrate 
the sexual elements of the female crescents (macrogametes), outside of 
the body, either on the slide or in the body of the mosquito (Ross). 
Fever rarely occurs when crescents alone are found in the blood; in fever, 
ameboid bodies, also, are nearly always found. The red blood cell 
becomes copper-colored or brassy. 

The parasite may be stained with the Nocht-Romanowsky fluid, 
methylene blue or hematoxylin, and counter-stained with eosin. For the 
beginner, study of the fresh blood under an oil-immersion is the best 
method. 

(B) The Life of the Organism without the Human Body. — 
King (1883) first suggested that the mosquito was the intermediate 
host and sole source of infection. It takes the plasmodium from man 
and reinoculates him with it after the life-cycle within its body. Other 
analogous infections are known, such as the hemosporidia of birds, 
frogs, bats, dogs, sheep, monkeys, Texas cattle-fever inoculated by the 
tick, and the African trypanosoma in animals and man, inoculated 
by the tsetse fly. Manson (1894), especially, then Ross, Grassi, Bas- 
tianelli, Bignami and others, have developed this interesting subject. 
The Plasmodium malarias is found only in man and the mosquito. The 
mosquito is the primary and higher host, since the sexual reproduction 
in its stomach is biologically higher than the simple sporulation in man. 
Of its two chief genera, the culex does not contain or convey the parasite. 
Its palpi are very short and its wings have no mottling. When sitting, 
its hindlegs are carried above the body and its body lies parallel with the 
wall, or may sag from the blood it has sucked. Its eggs are laid in tanks 
or puddles. It is the ordinary house mosquito and is found chiefly in 
cities. The anopheles conveys malaria. Its palpi are almost as long as the 
proboscis; the wings are mottled; the hindlegs usually depend, or 
touch the wall. Its body makes an angle of 45° with the wall. The 
eggs are laid in pools or sluggish streams with alga? growth, and the 
open country is its preferred habitat. Species: (1) The most important, 
the Anopheles maculipennis; (2) A. crucians; (3) A. punctipennis; (4) 
A. argyritarsis. After the female anopheles bites persons whose blood 
contains sexually mature forms of the plasmodium (gametocytes) , 
and the blood reaches the insect's stomach, flagellation in the male 
form occurs and the flagella enter the female cells. After fecundation 
the impregnated cell enters the muscular walls of the intestine, and, 



MALARIA 233 

after two days, small, round, refractile, pigmented bodies appear, which, 
after a week, grow to 60 to 70/x in diameter. They develop into myriads 
of sporoblasts which reach the salivary glands of the insect, whence they 
are again inoculated into man by biting. The sporozoids thus resulting 
from sexual conjugation in the mosquito, are equivalent to spores formed 
by asexual sporulation in the human blood. Entering the red cells in man, 
they follow the cycle of their type as above described, and produce 
either sporulating forms or sterile forms. The sterile forms in the human 
blood — i. e., the forms which do not sporulate — linger in the peripheral 
blood with the teleological purpose of preserving and continuing their life 
in the mosquito, and, on reaching its body, develop again the agents of 
reinfection. This knowledge concerning the mosquito explains many 
interesting and formerly incomprehensible details. We now know why 
those living in the first story of houses are more likely to be infected 
than those living in the upper floors and why those who slept in houses 
facing inland were infected while those in houses exposed to the sea air 
escaped, etc. Tn Rome, the fever prevailed just outside the Porta del 
Populo, while the Corso, three hundred feet distant in the city, escaped. 
During the winter, man, not the mosquito perpetuates the disease. 
Bass and Johns successfully cultivated all types of malarial parasites. 

Symptomatology. — 1. Fevek. — Fever is, next to the melanin and Plas- 
modium, the most constant symptom. It develops after an incubation of 
one and a half to fifteen days.- Fever bears a close relation to sporulation 
(Golgi, 1885). The fever-curve is irregular in some types or almost 
mathematically regular in others. It is usually irregular at first even 
in regular types. It may be remittent (subcontinuous), intermittent 
(tertian, quartan, quotidian), or continuous for a few days, when it ends 
by crisis or becomes remittent or intermittent before recovery. The 
paroxysm may be delayed beyond the time when it is due (postponens) , 
or may anticipate this time (anteponens) . In the algid variety there may 
be hyperpyrexia, or normal or subnormal temperature. Wade Brown's 
experiments suggest that the paroxysm is caused by the pigment. 

The classical components of the paroxysm are chill, fever and sweating, 
whose respective duration is in the proportion of 3-2-7, but any compo- 
nent may be absent, especially in virulent varieties and in persons partly 
immunized. The paroxysm lasts ten (four to forty-eight) hours, and in 
91 per cent, occurs between 10 a.m. and 3 p.m. (a) The chill is sudden in 
onset, often severe, with headache, emesis, coldness and lividity of the 
skin (cutis anserina) ; the temperature by rectum is elevated, the pulse 
rapid, small and hard; the respiration is rapid or even dyspneic, and the 
urine is increased. The parasites pervade the peripheral blood in the 
tertian and quartan types but largely the internal organs in the estivo- 
autumnal type, (b) The fever is high, perhaps not higher by rectum 
than during the chill, but is more evidenced by the red skin, thirst, 
delirium, headache, soft, full or dicrotic pulse, and other fever symptoms. 
In this stage the young parasites are free in the blood and begin to attack 
new red cells. After their entrance into these cells the fever ceases. 
(c) In the sweating stage the young parasites are found in the red cells 
and phagocytes take up the detritus and pigment. The sweat is usually 



234 



PROTOZOAN INFECTIONS 



profuse, giving off an odor like that of semen. Postfebrile euphoria is 
usual. 

Special Febrile Types of Malaria. — The quartan and tertian forms 
are regular and intermittent, and the estivo-autumnal forms are more 
irregular and remittent. 



Day 




1 




£ 




b 




4 






G 




TEMP. 

104 


























102 




















\ 






100 
9&6\ 


















V 


/ 

























Fig. 15. — Quartan malaria. (Silvestrini.) 

1. The quartan fever is the rarest of all types (0.8 per cent.), is 
found in the temperate zones, and occupies a position geographically 
intermediate between the tertian and estivo-autumnal varieties. It is 
caused by the quartan parasite, is the most regular of all types, and is 
called quartan because the simple form causes paroxysms every fourth 




Fig. 16. — Tertian malaria. 



day. The parasitic cycle is readily followed in the circulating blood, and 
the organisms do not accumulate in the internal organs. The fever is 
obstinate and recurrence is frequent, but quinine quickly exerts its 
specific action. The type may be single, from one generation of parasites; 
double, from two generations; or triple, from three generations producing, 



MALARIA 



235 



respectively, temperature, every fourth, every first and second, or every 
day of the cycle. 

2. Tertian fever, most frequent in the temperate zone, is found in all 
malarial countries and constitutes 50 to 65 per cent, of all malaria. 
The organisms accumulate in the internal organs. It is rarely per- 
nicious. The type may be single, or more frequently, double from two 
generations of parasites, causing almost continuous fever. It responds 
readily to quinine and may recover spontaneously. 

3. Estivo-autumnal fever, caused by the estivo-autumnal parasite, is 
often irregular, remittent, intermittent or continuous (subcontinuous) . 
It is characterized clinically by severe recurrent fever, marked anemia, 
frequently by absence of paroxysms (chills occurring in 71 per cent, only) 
and sometimes by pernicious symptoms. It was called estivo-autumnal 
by Marchiafava. and Bignami, in contradistinction to the milder or 
vernal forms. Subtypes: (a) Regular intermittent estivo-autumnal 
fever: (i) The estivo-autumnal tertian, in which the fever is apt to be 



Day 


1 


•2 


6 


4 


5 


6 


7 


8 


TEMP. 

106 
















i 


105 


















104 


















103 


















102 


















101 


















100 


















99 










¥ 


























93 





































Fig. 17. — Estivo-autumnal malaria. 



high, and the paroxysm doubly long. The typical curve may be modified 
by an exaggerated pseudocrisis, a briefer or longer duration of the 
attack, by anticipation or procrastination, and by double attacks, (ii) 
The estivo-autumnal quotidian, with a short attack, but an abrupt 
elevation of fever. This often irregular form has fewer symptoms than 
the other variety, and may recover spontaneously. It is readily confused 
with typhoid, (b) The irregular form presents marked irregular inter- 
mittency or remittency, or subcontinuous fever, because the attacks are 
duplicated, anticipated or prolonged. The paroxysm may last twenty 
hours. The symptoms may be mild or very severe. 

2. Blood Findings. — The blood findings are pathognomonic, viz., para- 
sites, melanemia, anemia, and absence of leukocytosis. 

(a) Red Cells. — Anemia results from deglobulization by the parasite. 
Acute anemia is more marked and rapid than in any other infection. 
The loss is greatest in the first attack, sometimes reaching half a million 
cells. Reduction to 500,000 red cells may give the picture of pernicious 
anemia. 



236 PROTOZOAN INFECTIONS 

(b) While Cells. — The absolute and relative leukopenia is due to the 
collection of the white cells in the liver and spleen, to destruction 
of the phagocytes, and to lesions of the blood-making organs. As in 
other anemias caused by disease of the bone-marrow and spleen, an 
increase of lymphocytes or large, mononuclear cells (20 per cent.), with 
decrease of the polymorphonuclear cells, may be observed. An absolute 
increase is sometimes observed in the "black-water fever," but the 
increase is in the lymphocytes. (Thomson describes a leukopenia (when 
many parasites sporulate) and a leukocytosis, even up to 50,000 or 
125,000, when few parasites sporulate.) 

(c) Melanemia. — Melanemia (Virchow and Heschl, 1847-50) is, next 
to the presence of the plasmodium, the most constant change in malaria. 
It is present during fresh infection and may occur shortly after the fever 
has disappeared, as in the half -moon forms. After infection it usually 
disappears within forty-eight hours. It is practically pathognomonic of 
malaria, though said to occur in recurrent fever, melanotic new growths 
and Addison's disease. It is found chiefly in the polymorphonuclears. 
It is seen in the smaller capillary walls where their diameter suddenly 
decreases (lung alveoli, intestinal villi, renal glomeruli, cerebral con- 
volutions, spleen, liver and bone-marrow) ; the capillaries may be occluded 
by pigment. Besides this pigment copper-colored hemosiderin may be 
found in the vessels and hepatic parenchyma. 

3. Spleen. — Enlargement of the spleen (Andouard, 1803) is the 
third important finding. It is palpable in 88 per cent, of cases and ana- 
tomically is rarely absent. Its size, hardness and plumpness are pro- 
portionate to the duration of the fever, increase with its rise, remit 
between attacks and disappear with recovery. In acute infections the 
spleen is increased three- to fivefold; it is soft and friable: the paren- 
chyma is flooded with infected red and macrophagic cells; and there 
are areas of focal necrosis. The Malpighian bodies contrast strongly 
with the congested pulp. A sticking pain over the organ is due to 
perisplenitis, and is often associated with pain and tenderness in the 
bones. In chronic infections the spleen is permanently enlarged (fever- 
cake), reaching even into the pelvis. It may weigh ten pounds, the cap- 
sule is thickened, even calcified, perisplenic adhesions occur and friction 
is frequent. Sometimes a systolic murmur is heard. The redundant 
pigment gradually decreases. The acute hyperemia and focal necrosis 
lead to increase of the connective tissue; ultimately little remains of 
the pulp, follicles and splenic function. Rare complications are pressure 
on the intestines, nerves and ureters, torsion of the pedicle of a wander- 
ing spleen, abscess or rupture (of which Choux collated 147 cases). 

4. Skin. — The vasomotor constriction during the chill gives way, 
during the febrile rise, to hyperalgesia and vasodilatation. Miliaria 
appear in the sweating stage. Herpes is very frequent, mostly nasal 
or labial. Edema and a cachectic hue occur in chronic cases. Slight 
urobilin icterus is not infrequent; icterus is sometimes intense. In- 
frequent complications are urticaria, erythema, roseola?, petechia?, etc. 

5. Circulatory Symptoms. — The heart is little involved. The pulse 
rises parallel with the fever, small at first from vasoconstriction, later 



MALARIA 237 

full from vasodilatation. Endocarditis, myocardial degeneration with 
dilatation, and phlebitis are rare developments. 

6. Respiratory Symptoms. — The rare dyspnea and pulmonary 
congestion during a paroxysm are due to parasites and phagocytes 
accumulating in or even occluding the capillaries of the lung. Plasmodia 
have been seen in the sputum. Chronic bronchitis, emphysema and 
" proliferating" interstitial pneumonia occur as complications. Broncho- 
pneumonia is frequent in malarial cachexia. Lobar pneumonia occurs 
only as a mixed infection. It is atypical and, in malarial cachexia, is 
especially fatal. 

7. Digestive Symptoms. — The oral mucous membrane is dry, the 
tongue heavily coated and the breath foul. The stomach may be the 
seat of hyperemia or infarction with plasmodia. Anorexia, vomiting 
and gastralgia are common symptoms. Ulceration from amyloid de- 
generation is observed only in a few chronic cases. Hematemesis from 
chronic splenic tumor has proved fatal. 

The Intestines. — Swelling of the lymphatic structures, hyperemia, 
thrombosis from parasite aggregation, meteorism and rarely diarrhea 
are observed. Acute abdominal pain is not uncommon; it may simulate 
peritonitis. Rarely the disease may resemble dysentery, with ulcers in 
the large and small gut. 

The Liver. — In acute infections the liver is enlarged, hyperemic, and 
its macrophagic endothelial cells are swollen, though few parasites are 
present. Icterus may develop from red-cell destruction; it is usually 
polycholic. Pigmentation from degenerated red cells is more common 
than actual melanosis. In chronic infections the liver may weigh eight 
or ten pounds, is hard and smooth, and has a thick capsule. The changes, 
seriatim, are focal necrosis, atrophy or partial regeneration, and pig- 
mentation with hyperemia; angioma, lymph cysts or abnormal lobules; 
and hyperplasia of the perilobular connective tissue, with ultimate 
cirrhosis. Cirrhosis may follow chronic malaria without necessarily 
being of malarial origin. Amyloid degeneration and simple atrophy 
from pylethrombosis are uncommon sequels. Acute ascites may result 
from pylethrombosis, by plugging of the capillaries by melaniferous cells. 

8. Genito-urinary Symptoms. — Polyuria is often observed during 
the paroxysm. The urine is decreased in the estivo-autumnal type. 
The postmalarial polyuria of convalescence is frequent. In one instance 
the author observed a veritable diabetes insipidus. 

The urea, chlorides and specific gravity of the urine are increased. 
Albuminuria is present in 30 per cent, of cases, and usually disappears 
with the paroxysm. Ehrlich's diazo reaction is obtained in 5 per cent, 
of the cases. Nephritis occurs in 4.5 per cent, but is seldom fatal. Plas- 
modia frequently abound in the intertubular capillaries but rarely in the 
glomeruli. Glomerular desquamation and epithelial exfoliation, endo- 
capsular exudation, necrosis and cast formation in the convoluted tubules 
occur. Chronic parenchymatous and interstitial nephritis may result 
from malaria. Hemoglobinuria, anuria and uremia occur in black- water 
fever. Gangrene of the genitalia is an uncommon sequel. Metrorrhagia 
and abortions occur frequently. 



238 PROTOZOAN INFECTIONS 

9. Nervous Symptoms. — The parasite especially affects the nervous 
system, whence Van Swieten called malaria a neurosis. There is scarcely 
a nervous symptom which is not observed occasionally in malaria. 
The sensorium, involved slightly in mild cases, is seriously affected in 
pernicious types (q. v.). Headache is usual, and neuralgias are frequent, 
especially of the fifth nerve. In pernicious types it is not easy to determine 
whether nervous symptoms are due to toxemia or cerebral thrombosis. 
The endothelial cells of the vessels are fatty, swollen and pigmented. 
Thrombosis in grave cases may result from swelling of the endothelium, 
though it is usually caused by the rough infected red cells. The infected 
erythrocytes never leave the vessels. 

Paralysis (hemiplegia, paraplegia and monoplegia), or motor irritation 
(tremor, chorea, contractures, epileptic attacks or reflex spasms), may 
occur in urgent types. Neuritis, psychoses, ascending spinal paralysis, 
bulbar symptoms, symptoms resembling multiple sclerosis, tabes or acute 
ataxia are rare sequences. 

10. Muscles and Bones.— /The muscles and bones are often painful. 
The bone-marrow at first shows fat and pigment which then disappear 
with marked vascularization, and ultimately, proliferation of the marrow 
cells and connective-tissue thickening. 

Latency. — Craig analyzed the latent malarial infections in which the 
Plasmodia may be demonstrated in the blood, without conspicuous 
symptoms. The latent type amounted to 24 per cent, of the cases 
examined, which were discovered only in the routine examination; they 
might have been sources of infection to others for weeks or months. 

Relapses. — Relapses are almost invariable in all forms, but are most 
obstinate in the estivo-autumnal type. Craig believes that the chief 
cause of maintenance of malarial infection is intracorpuscular conjuga- 
tion, thus producing within the body a resting or zygote stage of the 
Plasmodium which resists quinine. 

Chronic Malaria. — Untreated infection, or reinfection, persists for 
months, notably in the estivo-autumnal variety. It is accompanied 
by irregular fever, marked anemia, the parasite in the blood, and splenic 
and hepatic swelling. In severe chronic cases, the malarial cachexia 
develops, usually after years of infection. It is most marked in intensely 
malarial regions, in estivo-autumnal infection, and in reduced subjects. 
The fever is slight, irregular or absent. The features of malarial cachexia 
are (1) anemia from defective blood regeneration, with its general symp- 
toms, such as edema, rapid pulse, venous thrombosis and hemorrhages 
in the skin, retinae, etc. ; (2) vascular changes, possibly due to pigment 
occlusion; (3) enlarged spleen and liver; and (4) gangrene, nervous 
symptoms, alimentary and respiratory catarrh, amyloid disease, liver 
hypertrophy, and extreme malnutrition. 

Relation to the Other Diseases. — Malaria and typhoid rarely coexist; 
Craig saw but 8 instances in 5000 personal cases. (The plasmodia, 
and typhoid bacillemia or the Widal test are necessary for diagnosis.) 
Surgical operations may arouse a latent malaria. Erysipelas, septicemia, 
dysentery, cholera , smallpox, tuberculosis, etc., very infrequently coexist 
with malaria. 



MALARIA 239 

Pernicious Malaria. — Pernicious malaria constitutes but a small propor- 
tion of cases of estivo-autumnal malaria, and very seldom follows infection 
with the ordinary tertian parasite. It is characterized by severe obsti- 
nately recurring fever, intractable anemia, pernicious visceral symptoms, 
abortive paroxysms without chills and by depression. The pathogenesis 
of perniciousness lies in the inelastic, irregular, infected red cells which 
cannot pass the visceral capillaries, and therefore slow the blood current. 
Melanosis, phagocyte aggregations and endothelial swelling are of second- 
ary importance. In cases of capillary hemorrhages, only the normal, 
not the parasite-laden red corpuscles, escape from the vessels. Regressive 
organic changes may occur in the cerebrum, gastro-intestinal mucosa, 
spleen, liver and kidney. Accessory factors are (a) arteriosclerosis, 
renal disease, cardiac dilatation, alcoholism, sunstroke, overwork, mal- 
nutrition and lack of acclimatization; (6) the number of parasites and 
their abundance in internal- organs. Estivo-autumnal parasites, with 
large blocks of central pigment, indicate many plasmodia in the viscera. 
The parasites are often few in the peripheral blood though abundant 
in the brain at autopsy; (c) great activity in multiplication may be 
observed in the peripheral blood even during the sporulating stage; 
and (d) necroses in the viscera and the great morphological alteration 
of the "brassy" red cells suggest an increased toxicity. 

1. The pernicious typhoid form (perniciosa typhosa) is inappropriately 
called typhomalaria. Its clinical picture is variable; chills are often 
absent. Years ago the differential diagnosis was made ex juvantibus 
by quinine. Without blood examination malaria and typhoid may be 
confused; benign or malign malaria may resemble typhoid closely, 
with slow dicrotic pulse, splenic tumor, headache, fever-curve, cerebral 
and abdominal symptoms, and even roseolse and intestinal hemorrhage; 
on the other hand, erratic typhoid with remittent temperature, chills 
and sweats, or typhoid in the latter part of its normal course, may 
simulate malaria. 

The following differentiation is modified from Baccelli: 

Malaria vs. Typhoid. 

Begins intermittently. Progressively remittent. 

Remissions very irregular. Regular in the morning; step-like. 

Temperature may be high at first. High fever only after several days. 

Headache in beginning is rare, variable in Early, permanent, frontal, oppressive, char- 
site and intensity, pulsating and neuralgic. acteristic. 

Eyes dull, subicteric from beginning. Glistening eyes; no icterus. 

Stupor, dry tongue and sordes, less. Marked. 

Breath nauseating. Mouse-like. 

Delirium from beginning; recurrent. In advanced stage; constant. 

Lung congestion begins suddenly; foci Slow development, hypostatic; dyspnea 
change recurrently; dyspnea from de- rare (from tympany), 

ranged circulation. 

Nervous restlessness, jactitation. Stupor, prostration. 

Meteorism not characteristic; stools darker. Meteorism and diarrhea begin gradually; 

pronounced; ochre stools. 

Liver congestion frequent; subicterus. Less congestion; rarely icterus. 

Herpes frequent. Rare. Roseola?. 

Cycle, none. Typical. 

Blood: plasmodia and melanemia. Widal reaction and typhoid bacillemia. 

Recurrence. Relapses less frequent. 

Convalescence more rapid and easier. Tardy. 

In adynamic type, icterus, hemoglobinuria, Does not respond to quinine, which is a 
leukocytosis, great anemia, 25 per cent, specific in malaria, 

mortality, 



240 PROTOZOAN INFECTIONS 

2. Of cerebral forms, the comatose (perniciosa comatosa) is the most 
frequent. Mental depression is followed by contracted pupils, involuntary 
evacuations or paralysis. The pulse at first is slow; death is usually 
cardiac. The respiration may be noisy, hurried or Cheyne-Stokes's. If 
fever is present it is irregular. The author has seen four such cases in 
Chicago. Apoplexy, uremia and sunstroke must be considered. The 
splenic tumor per se suggests a blood examination. The "meningeal 
type" occurs especially in children; the slow pulse, headache, rigid, 
tender neck, stupor, convulsions, hyperesthesia and ultimate coma can 
be correctly interpreted only after a blood examination. Delirium may 
be the main symptom, and may appear as a mania, as fixed ideas, hallu- 
cinations or as melancholia. The rare convulsive type may be generalized, 
simulating hysteria, uremia or epilepsy, or localized, with contractures, 
trismus or opisthotonos. The paralytic is the least frequent type; hemi- 
plegia with aphasia is more common than monoplegia, the bulbar form, etc. 

3. The algid pernicious type occurs with cyanosis, collapse, Hippo- 
cratic expression, alimentary symptoms, and usually, early death. 

4. After the cerebral type the pernicious g astro-intestinal variety is 
most frequent, with vomiting, epigastric distress, icterus and dysentery. 
In soldiers from Cuba, the author observed profuse hemorrhages from 
the bowel, promptly responding to quinine. 

5. The pernicious biliary fever ("jungle fever") occurs with vomiting, 
polycholia, icterus, nervous symptoms, hemorrhages, adynamia, edema 
and dark albuminous urine; even after the administration of quinine 
this type may be lethal. 

6. The hemorrhagic types resemble Werlhoff's disease, and scurvy. 

7. The febris biliaris hemoglobinurica ("black-water fever") occurs in 
South America, in Africa and in our Southern States. The suspected 
causal factors are repeated malarial attacks, undue exertion, cold, and 
the use of quinine. Some maintain that it is a separate disease. The 
cardinal symptoms are (a) hemoglobinuria ; the urine is always albumin- 
ous, neutral or alkaline in reaction; hemoglobin is detected only after 
the destruction of at least one-sixth of the red corpuscles; (b) icterus, 
invariable except in the mildest cases; (c) irregular fever; (d) the Plas- 
modia, found in 96 per cent, before the attack and in 62 per cent, at the 
onset. The mortality of 50 per cent, is due to syncope, anuria and coma. 

Diagnosis. — 1. From Symptoms. — A probable diagnosis can often be 
made, for instance, by typically intermittent fever which occurs early 
in the day and is distinct from the vesperal hectic or septic fever. The 
three elements of the paroxysm are most marked in the benign malaria. 
In estivo-autumnal forms the chills may be absent. Splenic enlargement 
and herpes are suggestive, but also occur in ephemeral fevers, pneumonia, 
etc. Much emphasis was once placed on intermittent neuralgia, vertigo, 
herpes zoster, etc., but intermittence is not synonymous with malaria. 

2. The Diagnosis ex Juvantibus. — Laveran excluded malaria, 
when the fever resisted 30 grains of quinine for more than four days; in 
tropical forms more quinine may be necessary. 

3. The Plasmodium may be mistaken for vacuoles resulting from 
mechanical injury to the red cells; retraction of the hemoglobin; swarm- 



MALARIA 241 

ing particles from the red blood cells; blood plates, sometimes mistaken 
for spores, in unstained specimens; and poikilocytosis. Fewest mistakes 
are made when the inexperienced observer examines the fresh blood. 
Leukocytes containing pigment are distinguished by their large nucleus, 
and by their ameboid movement which is lacking in plasmodia sufficiently 
large to cause confusion. 

Positive findings are obtained in 98 per cent. The malarial parasite 
is found in the blood of malarial patients only. It is usually stated 
that they occur in largest numbers before or at the time of the paroxysm, 
though it must be admitted that the early examinations are often negative. 
Quinine may obscure the findings. Melanemia is practically pathog- 
nomonic. (Pigment lying free in the plasma is most often contamination.) 

Negative findings are of relative value only, and depend upon the 
skill of the observer and the time of examination. The findings were 
negative in only 2 per cent, of Baccelli's series. 

Differential Diagnosis. — 1. From typhoid (v. pages 46 and 239). 

2. Sepsis, pyemia (page 46), ulcerative endocarditis, liver abscess 
or pulmonary phthisis may be confounded with malaria. We find in 
malaria the plasmodium, melanemia, response to quinine and absence 
of leukocytosis; whereas in sepsis, leukocytosis, positive blood cultures 
and septic localizations are distinctive. 

3. Irregular grippe, recurrent fever, miliary tuberculosis, fever in 
malignancy, especially sarcomatosis, pernicious anemia, pseudoleukemia, 
Weil's disease and yellow fever may be confused with malaria, without 
careful blood examinations. Pernicious malaria may superficially simu- 
late apoplexy, sunstroke, meningitis, cholera or purpura. Among 1267 
malaria patients, 25 per cent, were " masked," simulating tuberculosis, 
pneumonia, dysentery, appendicitis, etc. (Craig). 

Prognosis. — The type of parasite, reinfection, habits of the individual, 
and antecedent renal or cardiac disease, are most important considera- 
tions. The prognosis must be conservative in pernicious and cachectic 
forms. In Italy the yearly death-rate was 16,000, and the French lost 
6000 soldiers in Madagascar in three months. On the other hand, fully 
20 per cent, recover with rest in bed and a full diet, as is shown in cases 
treated with placebos and saved for clinical demonstrations; in spon- 
taneous recovery the factors are the phagocytes in the spleen, bone- 
marrow and to a less degree, the endothelium of the hepatic and cerebral 
vessels, Kupffer's cells in the liver, and possibly the leukocytes. 

Treatment. — 1. Prophylaxis embraces more than personal prevention. 
In Italy and elsewhere it is a national economical problem. Drainage, 
the filling-in of stagnant pools and swamps and the planting of pines, 
eucalyptus trees and sugar-cane, have proved successful; the drainage 
of the great Bordeaux swamp in 1805 cost 3000 lives. In digging canals 
or building roads, immunes should be employed, but whites may work 
successfully if they avoid alcohol and nocturnal infection by mosquitos, 
minimized by nettings on all doors and windows. The pools where the 
insects breed should be filled in, or covered with crude petroleum to 
kill the larvae. The stocking of semistagnant streams with fish is of 
value. The prophylactic use of quinine in daily doses of 10 to 40 grains 
16 



242 PROTOZOAN INFECTIONS 

is effective. Sick malarial patients and those with malaria but without 
symptoms, should be protected from the bites of mosquitos, which 
carry infection to others. In the Isthmian Canal Zone, Gorgas reduced 
the mortality to one-seventeenth of the French death-rate. The Italian 
death-rate has been reduced from 16,000 to 3500 annually. 

2. Specific Treatment. — Quinine is one of our few specifics. Cin- 
chona has been used for ages in Peru and was known as the "tree of 
health" to Pizzarro in the conquest of Peru. Introduced over one hundred 
years later into Europe by del Vego (1640), its alkaloid was discovered 
by Pelletier and Caventou in 1820. It acts on the malarial organism 
while it is developing (Marchiafava and Bignami); when the parasite 
has transformed all the hemoglobin into melanin, and segmentation 
begins, quinine is ineffectual. All malarial manifestations as fever, 
splenic tumor and anemia are cured by quinine except in pernicious forms. 
It acts as a direct protozoan poison. Malarial subjects escape many or 
all of the symptoms of cinchonism, such as tinnitus aurium, cephalic 
distention and slight deafness resulting from therapeutic doses (gr. x). 
(Deafness, disordered vision, flushed face, cerebral congestion, vomiting, 
staggering, tremor and twitchings result from larger doses ; and delirium, 
complete deafness and amaurosis, dilated pupils, convulsions, paralysis, 
hemoglobinuria, dyspnea, coma, weak heart, or hemorrhages result from 
toxic doses.) 

Administration. — Its antiperiodic action is enhanced by combining 
it with opium gr. ss. Laxatives are unnecessary. Pills are insoluble, 
and the drug is best given in powders involved in starch wafers, or with 
one drop of sulphuric acid to each grain of the sulphate. Coffee, cognac 
and extract of glycyrrhiza but poorly disguise its bitterness. If the 
stomach rebels, a warm-water enema with equal parts of quinine and 
tinct. opii deodorat. may be used. In severe cases the hydrochloride 
(gr. vij) in 15 minims of water may be used hypodermically, but, 
though every care be taken, abscesses develop often. In pernicious 
types, Baccelli injects quinine intravenously (sterilized solution of 
sodium chloride, quinine muriate and water, in the proportion of 1, 10, 
and 100 parts, respectively). 

Time of Exhibition. — If the fever recurs regularly, gr. xx-xxx 
should be given as the fever falls, to act on the young growing forms 
in the red cells, to be repeated before the next paroxysm, in order to 
have the drug in the circulation when the spores are scattered (Torti 
and Golgi). If the fever is continuous or subcontinuous, or if the type 
is severe, gr. v should be given every four hours. Large doses are more 
effectual; small doses only aggravate malaria and develop quiescent 
forms. In the treatment of black-water fever, one view maintains that 
quinine is its cause; it should be given only when plasmodia are found, 
and given, as in Italy, a daily dose of six grains, for three months. 

3. Treatment of the Paroxysm. — During the vasoconstriction 
of the chill, morphine gr. J and nitroglycerin gr. ^, hypodermically, 
and spirits of chloroform 5 j, in hot whisky and water afford great relief. 
The fever is short-lived and requires little beyond cool sponging. The 
sweating requires no treatment. 



RECURRENT FEVER 243 

In chronic malaria, iron and full, increasing doses of arsenic should 
be combined with quinine. Arsenic is said to act on the gametocytes. 
Salvarsan is recommended for obstinate types. 



RECURRENT FEVER. 

Synonyms. — Relapsing fever; febrisrecurrens; typhus recurrens; seven- 
day fever; famine or prison fever; bilious typhoid. 

Definition. — A specific infectious disease caused by Obermeier's spiril- 
lum; endemic in Ireland, Russian Poland and India; characterized 
clinically by cyclic febrile attacks lasting six or seven days, followed by 
an equally long apyretic interval and recurrence of the fever. 

Etiology. — Recurrent fever was first described by Rutty, of Dublin, 
in 1739. It appeared in America in 1844, and was last seen in 1869. 
Obermeier in 1873 described a specific spirillum or spirochete {Spirillum 
Obermeieri) . S. T. Darling concludes that the Panama spirochete is of a 
strain differing from the European; the African tick fever is caused by 
the S. duttoni, the relapsing fever of India by the S. carteri and the 
American form by the S. novyi. The secretions are apparently not in- 
fectious. The disease has been inoculated in monkeys and in man, from 
postmortem cuts. Bed-bugs and lice also convey it. Infection is carried 
chiefly by vagabonds and emigrants. Males are especially affected 
(90 per cent.). Most cases occur between the twentieth and the fortieth 
years. 

Symptoms. — After an incubation of five to seven days, usually without 
prodromes, the invasion begins with a chill, high temperature (reaching 
possibly 104° on the first day), throbbing headache, and, in the young, 
convulsions and vomiting. The vertigo and cerebral confusion may 
resemble acute alcoholism. Because of the severe neuralgic pain in the 
back and legs, the patient lies motionless. There are great depres- 
sion, conjunctival suffusion, subicteric sclera?, facial pallor, epigastric 
oppression, with or without vomiting, and tenderness over the liver 
and spleen. 

Specific Findings. — 1. The blood is dark and reveals the pathog- 
nomonic, motile, cork-screw-shaped spirillum. It appears with the 
fever, disappears before it falls, and reappears with the next attack. 
The spirilla are found in the blood only. Without the immersion lens 
they may be located by the lashing about of the red cells. They always 
lie between and never in them, appear as fine threads, sixteen to forty 
microns in length, with five to ten waves in each, and move by undulation 
along their long axes. They stain best with fuchsin, after extraction of the 
hemoglobin. Their life in the blood is usually thirty-seven days. The 
white blood cells are increased. 

2. The spleen is enlarged, painful and palpable. In no other infection 
is the spleen so large, being increased five- or sixfold and weighing even 
twenty pounds. The capsule is tense, the pulp is a fluid red, the Mal- 
pighian bodies are increased, and necrotic areas and infarcts are common. 
Microscopically there are hyperemia, hyperplasia, spirilla and fatty, 



244 



PROTOZOAN INFECTIONS 



desquamated endothelium from the veins, thus explaining the spindle cells 
found in the blood stream. Suppuration and rupture may occur. 

3. The bone-marrow resembles the splenic follicles and contains granular 
cells, and aggregations of white blood cells. 

Other Symptoms. — 1. Nervous System. — Headache is frequent. The 
sensorium is usually free, delirium and insomnia being rare. 

2. Temperature. — The temperature rises abruptly to 103° or 104°, 
and remains continuously high (105° to 107°) from five to seven days, 
when the crisis occurs. In no other disease is the defervescence so pre- 
cipitate (5° to even 16°). In five to seven days the patient is well, when 
in 99 per cent, of cases the cycle is repeated, with usually two or three 
relapses (as many as seven are recorded). The temperature-curve 



Day 


4 


5 


c 


7 


8 


9 


10 


11 


12 


13 


14 


15 


10 


17 


18 


19 


•20 


21 


22 


'23 


•24 


•25 


•20 


27 


TEMP. 

105 






i 












































104 




V 














































103 


/ 


V 


\ 


1 


















k 


A 


Jl 


1 


















102 
























A 


J 


i 


V 














h 






101 
























/ 


\ 
















H 


\l 


1 




100 








' 














/ 


















/ 


V 


1/ 




A 


99 










\ 




































V 


ft 












\ 












/ 


















/ 










98 














/ 


\ 


































97 














J 


\ 


A 


v/ 


















M 












96 












/ 






















\ 


[/ 














95 










1 


i 
























V 














94 












V 







































Fig. 18.— Fever chart in recurrent fever. 



is diagnostic. Lysis occurs in 1 per cent. The crisis is followed by 
sweats, shrinkage of the spleen, disappearance of the spirillum' and 
rapid convalescence. 

3. Circulatory System. — The pulse is rapid (120 to 140), hard, 
sometimes irregular and slow after the crisis. 

4. Respiratory Tract. — Bronchitis and increased respirations and 
in fatal cases hypostasis, pneumonia, glottis edema and pleurisy have 
been observed. 

5. G astro-intestinal Tract. — The tongue is white and later, 
yellowish-brown. Hematemesis, a tender, swollen liver, icterus, gall- 
bladder distention, bloody effusions in the alimentary mucosa, and 
hyperplasia of the lymphatics may be observed. 



KALA-AZAR 245 

6. Genitourinary Tract. — The urinary findings resemble those of 
typhoid. Nephritis is infrequent and abortion occurs in 66 per cent. 

7. Skin. — The skin is usually subicteric, yet the stools remain colored. 
Herpes, erythema, petechia?, desquamation and even roseola? have been 
noted. The skin becomes drenched at the crisis. 

Diagnosis. — The specific points are: A prevailing epidemic; onset 
with chill and fever; swelling and tenderness of the liver and spleen; 
muscular pains; abrupt crisis; apyretic interval with recurrence of the 
cycle, and spirilla found by blood examination. 

In bilious typhoid or septic recurrent fever, there is severe icterus, 
hemolysis, and liver findings suggestive of acute yellow atrophy. Hemor- 
rhages and death from collapse in the first attack are common. The 
colored stools and enlarged spleen are significant. Malaria, typhoid, 
typhus, yellow fever, acute yellow atrophy and Weil's disease, are 
excluded by examination of the blood. 

Convalescence. — Convalescence is rapid, after four or five weeks, 
Death results from toxemia, heart collapse or complications. The 
prognosis is good, the mortality averaging 4 per cent, or 60 per cent, 
in the bilious type. One attack is not certain to confer immunity. 

Treatment. — The treatment is that of typhoid. Pain often necessitates 
the use of opiates. Salvarsan has been used successfully. 

KALA-AZAR. 

The Leischmaniases, diseases caused by Leischman's organism, include 
two visceral and one cutaneous disease. Indian kala-azar (Assam or 
Dumdum fever) and infantile kala-azar (splenomegaly) are caused by 
the Leischmania donovani (Leischman and Donovan, 1903), and the 
oriental sore by the L. tropica. 

Indian kala-azar is characterized by splenomegaly, progressive 
anemia and remittent fever. The protozoon is found in the spleen, 
liver, bone-marrow and sometimes in the blood. It can be cultivated 
and may be transmitted by the bed-bug. The disease begins with fever, 
which is oftenest remittent, rising two or three times daily; it recurs. 
Marked emaciation develops with abdominal tenderness, nervous toxemia, 
neuritic or arthralgic pains and various hemorrhages. The skin is dark, 
even icteric and pigmented. The spleen is greatly enlarged, tender and 
is crowded with parasites. The liver becomes swollen and tender from 
perihepatitis, is packed with parasites and frequently becomes cirrhotic. 
There is secondary anemia; there is relative lymphocytosis, usually with 
leukopenia. The course averages 6 to 9 months and the mortality is 
96 per cent. The parasites are found constantly and in all stages by 
splenic puncture (which, however, may entail hemorrhage or rupture). 
Quinine hypodermically is of some benefit. 

Infantile kala-azar or splenomegaly is identical with the Indian type 
and is found on the Mediterranean littoral and islands. It is probably 
transmitted by dog fleas. 

Oriental sore is also known as Delhi boil, Bagdad sore, etc. It occurs 
on the face and exposed parts of the body as a small node, which becomes 



246 PROTOZOAN INFECTIONS 

covered with a crust. Beneath it is granulating tissue, which often ulcer- 
ates, invades the lymphatics, or perhaps the nasal mucosa — simulating 
lues, tuberculosis or leprosy. 

TRYPANOSOMIASIS. 

The trypanosoma is a protozoon found by Gruby (1843) in frogs, 
Doflein (1845) in rats, and later in many other animals and in man 
(Neprue, 1890-98). There are many species. The T. gambiense is 
leech-shaped; its body is granular, measures 13 to 25, by 2 to 4/* and 
contains a nucleus and micronucleus (centrosome) ; on one side and 
attached to an "undulating membrane" is a solitary flagellum by which 
the parasite moves. In cool and moist hanging-drop preparations they 
may live for a month and a half. Novy and McNeal cultivated the T. 
Lewis and Brucei. Infection is carried by the tsetse fly, flea, louse, 
mosquito and ticks. In man trypanosomiasis is conveyed by the tsetse 
fly (Glossina palpalis) or possibly by bites from infected rats; apparently 
the fly is the true host. Animals may be infected during coitus, by 
subcutaneous inoculation or by the stomach. 

Trypanosoma fever was first described by Nepreu. It prevails in 
central and western Africa. The atrium may be present as an inflamed 
bite or the history of a bite may be obtained. Parasites in the blood 
may cause no symptoms, even for a year ("carriers"); parasites occur 
in the plasma, not in the corpuscles; some anemia is present and the 
large lymphocytes are increased up to 20 per cent., but the eosinophiles 
show no increase. Most parasites are found in the lymph glands which 
are constantly enlarged, especially the posterior cervical. Fever is irregular, 
subcontinuous or remittent, and lasts from three days to three weeks. 
An erythematous eruption is almost constant. Edema, particularly 
of the lower lids, weak and rapid pulse, prostration and splenic tumor 
usually occur. In treatment, arsenic (atoxyl and salvarsan), antimony 
(gr. 1.5, intravenously) and trypan red are apparently helpful, while 
quinine is without effect. Careful feeding and cardiac stimulation are 
indicated. The patient, as in yellow fever, should be so screened that 
flies can neither convey fresh infection to him nor bite him and thus 
infect others. 

Sleeping sickness or African lethargy, endemic in Central Africa, is 
due to localization of the trypanosomes in the nervous system, causing 
a diffuse meningo-encephalomyelitis (Mott). Negroes are chiefly affected 
and slaves imported to America developed the disease; Caucasians may 
contract the disease. 

The incubation is long, possibly years. Incipient symptoms are those 
of the trypanosoma fever or less often there are preliminary psychical 
phenomena, as epileptiform convulsions, melancholia or mania. There 
is a fine tremor and shuffling gait. Somnolence develops, from which at 
first the patient can be aroused, but which later develops into profound 
lethargy. The parasite is found in the blood in 92 per cent. (Bruce) 
and in 100 per cent, of cases in the cerebrospinal fluid, withdrawn by 
lumbar puncture (Castellani). Malnutrition, decubitus and sometimes 



SMALLPOX— VACCINATION 247 

secondary infections develop, and after the convulsions deepen into 
coma the patient dies. The course lasts from months to several years. 
Treatment is usually unavailing; some 10 cures are reported. More 
than a quarter of a million people died in Uganda in the last few years 
from this affection. 

OTHER PROTOZOA. 

Amebiasis has been described with bacillary dysentery. 
Yaws, or frambesia is a highly contagious disease, found in Africa, 
Asia, Central and South America and various islands. In the days of 
slavery it was common iu the South, where cases are still found. It is 
due to the Treponema pertenue (Castellani, 1905) ; the parasite resembles 
the T. pallidum and the clinical course resembles syphilis. At the site 
of inoculation, usually on the legs or face, a papule forms, which in one 
week becomes an ulcer ; this heals in another week ; the fungoid tubercle 
resembles a raspberry (frambesia) and is called the initial lesion. In 
six weeks to three months, fever, malaise, headache and joint pains 
reappear — the secondary stage — in which the lesions resemble the primary 
or condylomata. In some instances destructive tertiary lesions develop. 
In differentiation from lues, the primary and secondary lesions are identi- 
cal, extragenital and lack the endothelial proliferation and perivascular 
exudation of syphilis ; the lesions are not pleomorphic, involve the mucosa 
only at its junction with the skin and never the viscera, brain, etc. The 
death-rate ranges under 1 per cent, and salvarsan is absolutely specific. 

The trichomonas (cercomonas) is found in acid vaginal mucus and the 
intestines. It may initiate enteritis or cystitis. The Lamblia intestinalis, 
a pear-shaped flagellated monad, may occasion diarrhea; it has been 
found in pleurisy, pulmonary gangrene and bronchiectasis. The Balan- 
tidium coli, common in hogs, may cause dysentery (q. v.) in apes and man; 
it is found in the stool and submucosa and sometimes in the bloodvessels 
and lymph glands. 

Coccidia may rarely be found in the liver, kidneys, bladder, spleen, 
intestine, peritoneum, etc. Tumors, like tubercles or mucous cysts 
may develop. A typhoid-like course is described. 



INFECTIONS OF DOUBTFUL ETIOLOGY. 

SMALLPOX (VARIOLA). VACCINATION. 

Definition. — Smallpox is an acute, highly infectious disease. It begins 
suddenly with a chill, headache, vomiting and intense epigastric and 
lumbar pain, and is characterized by a typical fever-curve and by an 
eruption on the skin and mucosae of papules, vesicles, pustules and crusts 
successively. 

History. — Smallpox prevailed in China and India 1000 years before 
the Christian era. Galen's pesta magna of the second century was 



248 



INFECTIONS OF DOUBTFUL ETIOLOGY 



probably variola. Epidemics occurred in the sixth century and during 
the crusades. Rhazes (Arabia, ninth century) gave us the first clinical 
description of the disease. Smallpox was introduced into Mexico in 1520 
by the Spaniards, and three and a half million persons contracted the 
disease. Sydenham's classic of the seventeenth century is most accurate 
and reliable. In 1718, Lady Montague introduced into England preven- 
tive inoculation, which had been practised for centuries in Asia, and 
though the mortality fell to 1 per cent, the disease was disseminated 
in a mitigated form. Jenner's discovery of vaccination, in 1796, greatly 
lessened the terrors of variola, which in Europe alone carried off nearly 
half a million persons yearly. 

Etiology. — The virus is unknown. Weigert and others found pyogenic 
organisms in the skin and elsewhere, but suppuration is due to a later 
mixed infection. The cytorrhyctes variolas of Guarnieri (1892) is an 
ameba found in the blood in the incipient stage; and in the lower epithelial 
layers, in vacuoles in the cells ; these small structureless bodies measure 
one to four microns and become granular and segmented. 



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INCUBATION PRODROMAL STAGE ERUPTION OF MACULES ERUPTION OF SUPPURATION EXSICCATION 4 
12 DAYS 3 .DAYS AND PAPULES 3 DAYS VESICLES 3 DAYS CECRUSTATION 

2 DAYS 7 OAYS 

Fig. 19. — Temperature chart and stages of smallpox. (Pfeiffer.) 



That the blood is infectious at an early stage was demonstrated by 
the infection of an individual on whom skin had been transplanted from 
a person in the early stages of smallpox. As variola without eruption 
is contagious, it seems that the secretions and excretions convey the virus. 
The greatest infectiousness is noted in dried pustules in which the virus 
localizes. Infection is direct from person to person, or indirect by a 
third party or by fomites. Cadavers of variola victims are dangerous. 
The virus is very penetrative, even beyond the room, building or area of 
the isolated case. The disease persists in infected communities for 
years. 

Susceptibility to smallpox is almost universal; only 1 per cent, of 
people are immune. Temporary immunity is more frequent than con- 
genital. Practically, immunity is only acquired by vaccination or a 
previous attack. Either sex and all ages may be affected. Mothers 
with the disease may deliver babes with the florid eruption or with scars. 
The virulence of the virus is great in aboriginal and colored races (Indians 
and Mexicans). Severe cases may follow mild infection, as shown in 
Osier's description of the Montreal epidemic, in which 3164 persons, 



SMALLPOX— VACCINATION 249 

infected by a mild case in a Pullman-car conductor, died among the 
French Canadians, who oppose vaccination. Variola occurs sporadically, 
epidemically, or pandemically. 

Atrium. — Infection occurs through the respiratory, and perhaps also 
the digestive tract. 
Symptoms. — Forms : 

I. Variola vera — 1. Discreta, discrete. 

— 2. Confluens, confluent. 
II. Variola — 3. Purpura variolosa (black smallpox), 

hemorrhagica — 4. Variola hemorrhagica pustulosa. 
III. Varioloid — 5. Smallpox modified by vaccination. 

1. Variola Vera Discreta. — (A) The incubation is symptomless and 
averages twelve days (five to twenty). 

(B) The prodromal stage, dating from the first symptom to the 
eruption, is the same in all types, and averages three days. It is shorter 
in children and in confluent smallpox; the longer it is, the more severe 
is the infection. Its intensity bears no invariable relation to prognosis, 
for mild smallpox may begin severely; however, if the onset is mild, 
the disease will not be confluent or hemorrhagic. 

The invasion begins acutely with chill, fever, rapid pulse and respiration, 
nervous toxemia, intense headache, backache and vomiting, (a) The 
chill is severe, and frequently is repeated. In children it is often absent. 

(b) The initial fever rises suddenly to 103° or 104°, and reaches its maxi- 
mum on the second or third day. The pulse is rapid (120) and full. 
The more frequent respirations (30 to 36) constitute the so-called toxemic, 
"cerebral respiration." The skin is red, hot {color mordax) and dry; 
there may be sweating in the discrete variety and in favorable cases. 

(c) Nervous toxemia is evidenced by the benumbed sensorium, depression, 
restlessness, insomnia, delirium especially in alcoholics, or convulsions 
and meningeal symptoms in children. Headache appears with the chill 
and is frequently frontal or temporal. When severe, it may suggest 
meningitis, especially when accompanied by vomiting and neckache. 

(d) Backache appears with the chill, and lasts one or two days. It occurs 
in nearly all cases, though less frequent than headache and vomiting. It 
is severe, like lumbago, or actually agonizing. The " veritable paraplegia" 
described by Trousseau is only immobility due to toxemic pain. It is 
rare in other fevers likely to be confused with variola. Pain is sometimes 
observed in the intercostal nerves, sciatics, muscles, joints, pharynx, 
larynx or heart, (e) Vomiting and early epigastric pain are constant in 
children. The spleen is not often enlarged in the initial period. It is 
often tender, as are the liver and epigastrium. (/) The initial or prodromal 
eruptions, present in 10 per cent., have considerable diagnostic value. 
They are commonly limited to the lower abdomen, inside of the thighs, 
axillae and sometimes to the extensor surfaces of the knees and elbows. 
There are two varieties: 

1. The morbilliform variety (roseola variolosa) appears during the 
second day on the face and body as small, sometimes crescentic maculae 
and usually lasts one day; it is hyperemic but may be purpuric. Most 
often seen in varioloid, it is a favorable prognostic. 



250 INFECTIONS OF DOUBTFUL ETIOLOGY 

2. The more rare scarlatinal form (erythema variolosum) occurs on 
the first day. It is less punctate, extensive and bright than the scarlet 
fever rash. If it is purple and purpuric, it is almost always variolous. 
It occurs on the lower abdomen, thighs and knees, forming a triangle 
with base upward when the legs are together. Sometimes it is found 
over the axilla or shoulders, and is seen in women more frequently than 
in men. These areas are rarely invaded by the pustular eruption. Some 
writers speak of an erysipelas-like and urticarial, prodromal rash. 

(C) The eruptive stage comprises several serial substages. 

1. Macules and papules (stadium maculosum et papulosum) occur on 
the fourth day, and advance for three days, beginning on the forehead 
near the hair and on the cheeks, with itching and burning macules, re- 
sembling flea-bites, which soon become papules. The papules are reddish, 
discrete, circular, elevated, and hard or "shotty." A day later they 
appear on the body, and on the next day, on the extensor aspects of the 
extremities; i. e., the papular eruption advances for three days, and is 
descending. The papules are thickest on the face and trunk. The eyelids 
show collateral edema. If the eruption appears on the second day, the 
confluent type may be expected; if on the third day of the disease, the 
discrete type. 

Weigert holds that the first changes are necrobiotic or diphtheroid 
in the rete Malpighii followed by inflammation in the necrotic areas. 
Other authorities consider inflammation the primary, and necrosis the 
secondary process. 

Unlike measles and scarlatina, the fever remits when the eruption appears, 
and the backache and headache improve. In three days the fever reaches 
normal by irregular steps. The lower the fever falls in this remission, the 
lighter is the type of smallpox. 

2. In the stage of vesiculation (stadium vesiculosum) , lymph gathers 
in many but not in all of the papules. This occurs on the seventh day 
of the disease and lasts about two days. The vesicles are multilocular, 
since they occur in the cells of the rete Malpighii. Umbilication occurs 
in the centres of many vesicles, caused by elevation of their edges by 
infiltration and by the follicles in their centres; it corresponds to the 
area of primary necrosis and is suggestive but not pathognomonic 
of smallpox. On the soles and palms the fluid is situated deep in the 
resistant tissues. 

3. The stage of suppuration (stadium pustulosum) or maturation 
begins on the ninth day with clouding of the vesicles and inflammatory 
congestion about them (areola) ; it advances for three days. The pustules 
become opaque, then yellow, and the thick pus obliterates the umbilica- 
tion and renders the eruption globular. The areola or halo becomes more 
vivid and inflammatory edema may result from fusion of the areolae. 
This causes increased tension, deformity especially in the face and parts 
where the skin is most loose, closure of the eyes, occlusion of the nose, 
and great tenderness and pain. Pustulation follows the descending 
direction of the initial eruption and the pustules are thickest on the 
extremities and head. On the volar and plantar surfaces they are less 
prominent and there is less edema. The pustules evacuate spontaneously , 



SMALLPOX— VACCINATION 25l 

especially on the face, but may dry without rupture. Various stages of 
the eruption may be observed in different parts of the body at the same 
time; not all vesicles become pustules. The skin exhales a peculiar, 
penetrating, offensive odor, and bed-sores may develop. 

Anomalies are variola siliquosa — air in the pustules, and very large 
eruptions three-quarters of an inch in diameter. The pus originates from 
the vessels of the papillae which undergo pressure-atrophy, or even necrosis. 

Mucous membranes: The pock eruption occurs mostly in the mouth 
and nasopharynx; the successive stages of papulation, vesiculation, 
pustulation, etc., may develop, but less typically than in the skin; 
erosions, stomatitis, glossitis, phlegmonous angina, etc., may result. 
The eruption is found in very rare instances in the Eustachian tube, 
eye, respiratory, alimentary and genito-urinary tracts. 

With pustulation there is a gradually rising secondary fever, due to the 
smallpox virus and mixed pyogenic infection, and proportionate to the 
degree of pustulation. In variola discreta the temperature does not 
remain high more than twenty-four to thirty-six hours, with morning 
remissions. A marked leukocytosis, of 10,000 to 34,000 attends the 
secondary fever and parallels the degree of infection. The lymphocytes 
are increased (to 66 or 50 per cent.), the polymorphonuclears decreased 
(to 50 or 33 per cent.), and the myelocytes may reach 12 per cent. 

Delirium with suicidal tendencies, albuminuria, acute exhaustion and 
heart paralysis may develop. 

( D) The Stage of Involution. — Exsiccation, decrustation begins on the 
twelfth day. It occurs in the same descending order as the florition 
and suppuration, with decrease in the edema, redness and pain, but 
with an intolerable itching. Crusts form, and remain longest on the 
soles and palms where they may form complete casts of the parts. Mucous 
erosions heal more readily. The hair falls out, and by the end of the 
second week the fever reaches normal. Fever at this stage indicates 
some complication. The higher the granulating surface, the deeper is 
the cicatrix. Scars occur when the true skin has been involved, and are 
seen chiefly on the face, scalp, palms and soles. Sydenham held that 
discrete smallpox rarely leaves its mark but others maintain that sup- 
puration and cicatrices are necessary stigmata of variola vera. Scar 
formation lasts three or four weeks. Complete convalescence follows the 
disappearance of the last crust. 

2. Variola Vera Confluens. — This malignant type was more 
frequent in prevaccination days, and is now seen largely in persons 
unvaccinated or vaccinated but once. The initial stage is violent. The 
headache and backache are agonizing. The status typhosus and gastric 
symptoms are marked, the fever remission is slight or absent, or if the 
fever remits there is little or no improvement in the symptoms. The 
exanthem is precipitate both in its development (on the second or third 
day), and in its extension. The earlier the exanthem in variola, the 
greater is the probability of confluent smallpox. The eruption becomes 
confluent especially on the face and head, and sometimes on the hands 
and feet; on the body and limbs it is largely discrete. With fusion of the 
eruption, great inflammatory edema appears, swelling and erosion of the 



252 INFECTIONS OF DOUBTFUL ETIOLOGY 

mucous membranes, closure of the eyes, keratitis and obstruction of the 
nose develop. The general aspect is desperate. High fever, high pulse, 
rapid, even irregular or stertorous breathing, delirium, albuminuria, 
persistent nausea and vomiting, great thirst, salivation in adults and 
diarrhea in children, husky voice, enlarged cervical glands and often 
parotitis, are present. As to prognosis, Sydenham says that " if upon the 
face the pustules are as thick as sand, it is no advantage to have them 
few and far between upon the body." Death occurs from acute toxemia 
(variola typhosa), with hyperpyrexia and cardiac asthenia usually within 
a week; or, if the patient lives longer, from septicopyemia, phlegmon, 
gangrene, pneumonia and nephritis. The patient usually dies if the 
eruption does not appear. Recovery from variola confluens is infrequent. 

3. Purpura Variolosa. — This is the black smallpox — smallpox 
with primary hemorrhage in the initial stages. It is the worst type, 
results almost uniformly in early death and is important because of the 
difficulty in its diagnosis. It is seen most frequently in the unvaccinated. 
The incubation is short (six to eight days), the invasion is stormy, with 
agonizing lumbar pain, great prostration, a rapid, small and soft pulse, 
and disproportionately increased respiration. The initial epigastric 
pain and vomiting may last until death. 

On the second day (or even on the first) , there appears a plum-colored 
eruption, with brick-red, purple or inky ecchymoses, especially about 
the eyes. The aspect of the discolored and swollen face, and ecchymotic, 
sunken and alert eyes, is desperate. Hematuria is the most common 
of visceral hemorrhages. Other forms are hematemesis, enterorrhagia, 
epistaxis, metrorrhagia and hemorrhage from the gums, ears and bronchi, 
sometimes accompanied by gangrene of the pharynx. Tympanites and 
albuminuria may be noted. Miscarriage is frequent. The disease does 
not usually reach the real eruption of variola, or, at the most, only the 
papules are observed, because it is fatal in four or five days. The mind 
often remains lucid to the end. In most cases the fever is not high, but 
in the most fulminant type it reaches 105° or 106°, with collapse, coma and 
death in a few hours, even before cutaneous hemorrhage is seen, although 
internal hemorrhages are found at autopsy. The "blood dissolution" 
of the older writers is a mycotic coagulation thrombosis. 

4. Variola Pustulosa Hemorrhagica. — Hemorrhage after the 
eruption appears (secondary hemorrhage) is more common than primary 
hemorrhage. This form occurs in weakly or alcoholic subjects. The 
initial stage is severe, and secondary hemorrhages occur into the vesicles 
or pustules, or into the lower parts of the body or there may be "blood 
dissolution," epistaxis, hematuria and metrorrhagia. Adynamic mani- 
festations are usual, and the outcome is almost always fatal, though 
hemorrhage at the vesicular stage may be followed by rapid abortion 
of the rash and recovery. 

5. Varioloid. — Varioloid (variola modificata s. mitigata, variolois) is 
variola mitigated by vaccination. The more marked the initial eruption, 
which is often morbilliform, the less the number of pustules. Varioloid 
begins suddenly. The fever is atypical; it may reach 103° and usually 
falls with the specific eruption, reaching normal on the fourth day; 



SMALLPOX—VACCINATION 253 

secondary suppuration is rare or absent. The eruption varies in amount, 
being present on the trunk only, or being typical chiefly on the hands and 
feet. It may be absent entirely. It may not be umbilicated and may 
desiccate rapidly without rupture; scars are rare. The mucous surfaces 
are little involved. The entire course is shorter, more irregular and 
rudimentary, and more benign than in variola vera. 

Complications and Sequelae. — The many complications and sequelae of 
variola embrace severe early toxemia and later, secondary infections. 

1. The Nervous System. — Delirium is caused by cerebral toxemia, 
alcoholism or hyperpyrexia. Convulsions are frequent in children. 
The unusual psychoses are generally asthenic. Meningitis, encephalitis, 
embolism, cerebral softening, and abscess are occasional complications. 
Myelitis and neuritis are exceptional sequels. 

2. The Vascular System. — Circulatory changes are more rare. The 
heart muscle may soften and dilate, microscopically revealing segmenta- 
tion, cloudy and fatty conditions, coronary endarteritis and myocarditis; 
a systolic bruit may be heard at the apex, with weak first tone and tachy- 
cardia, as in typhoid. Aortitis, pericarditis, ulcerative endocarditis and 
phlebitis are infrequent. 

3. The Respiratory Tract. — Edema of the larynx and perichondritis 
are usually fatal, for laryngeal anesthesia promotes inhalation pneumonia. 
Bronchitis is invariable in severe cases. Pneumonia, usually lobular, 
occurs in 60 per cent, of fatal cases; lobar pneumonia, lung abscess, 
embolism and gangrene are uncommon. 

4. The Digestive System. — Glossitis, retropharyngeal abscess, paro- 
titis, noma, phlegmonous esophagitis, and hemorrhage in the throat 
are ominous though uncommon complications. The early vomiting 
rarely persists. Diarrhea is not common, but a simple form is seen in 
children and a dysenteric form occasionally in adults. Peritonitis, retro- 
peritoneal cellulitis, mediastinitis and perineal abscess are infrequent. 
The alimentary tract, with the exception of the rectum, is commonly 
exempt from the eruption. The liver may suffer cloudy or fatty change, 
focal necrosis or diffuse hepatitis. The spleen is usually swollen and 
soft. 

5. The Genito-urinary Tract. — Albuminuria occurs early in 25 
per cent, of cases, during the eruption, suppuration or convalescence. 
Nephritis now and then develops during the fever or in convalescence; 
it is often glomerular. Pyelitis, ovaritis and vulvar gangrene have been 
observed. Menorrhagia is common in the early stages of onset or in 
hemorrhagic forms, and abortion from hemorrhagic endometritis is the 
rule in pregnant women. Orchitis variolosa is very frequent; the 
multiple inflammatory foci lie mostly in the connective tissue, but are 
rarely suppurative. 

6.- The Special Senses. — The eye is involved in 1 per cent. Pox 
in the conjunctivas are rare, as are conjunctivitis, keratitis, irido- 
choroiditis, metastatic panophthalmitis, etc. Otitis and suppurative 
thrombophlebitis may occur. 

7. Locomotor System. — Muscular abscess and arthritis may occur 
during desiccation. Arthritis is more often suppurative than serous, 



254 INFECTIONS OF DOUBTFUL ETIOLOGY 

and is but one feature of the secondary sepsis. In the bones there 
are almost invariably hemorrhage into the marrow, hyperplasia of the 
marrow cells, and multiple foci of necrosis or non-suppurative osteo- 
myelitis (in 72 per cent., Chiari). 

8. Skin. — Decubitus, erysipelas, local or pyemic abscesses, desqua- 
mation, acute gangrene, hemorrhages into existing exudates, and less 
often into the viscera, also occur. 

Diagnosis. — The diagnosis of smallpox is usually easy when chill, 
fever, headache and vomiting occur after exposure to infection. Vac- 
cination and revaccination scars must be searched for. Mistakes in 
the diagnosis of the first cases of an epidemic or in abortive or purpuric 
cases, are often inevitable. Hemorrhagic scarlatina or measles sometimes 
causes confusion; in the former the mucous membrane hemorrhages are 
less frequent than in smallpox. The initial suggestive scarlatiniform erup- 
tion has been unduly emphasized; the prodromal eruptions plus purpura 
are highly suggestive. An acute onset and high temperature are signi- 
ficant, although acute onset and high fever may occur in typhus, pneu- 
monia, scarlatina and influenza; lumbar and sacral pain is more common 
in smallpox. Intense frontal headache, severe backache, vomiting, 
chill and fever are sufficient grounds for a tentative diagnosis and isolation 
but the diagnosis is uncertain until the eruption is seen. In the variola 
sine exanthemate (febris variolosa, variola sine variolois, varioles frustes) 
the diagnosis must be made from the history of exposure, the presence 
of an epidemic, fever, pain, delirium, possibly the initial rash, and the 
absence of secondary fever because there is no suppuration. An erup- 
tion which appears on the third day of the affection, accompanied by a 
fall of the fever and euphoria, is most important. Jenner described an 
early cutaneous inflammation in the vaccination site, in those who are 
immune to smallpox; this diagnostic phenomenon was later described 
by v. Pirquet as allergistic (see diphtheria therapy, allergy). 

Varicella vs. Variola. 

Vaccination and smallpox do not protect. Smallpox may closely resemble chicken-pox; 

mild cases especially misleading. 

Age: usually before puberty; it may occur Usually after puberty (numerous excep- 

in adults. tions). 

An initial stage is practically absent. It is severe, even in mild cases. 

Temperature: no remission with onset of Typical remission and a secondary fever 

rash. White cells normal or decreased. (except in varioloid). Leukocytosis (mono- 
nucleosis) . 

Prodromal rash: very exceptional. Frequent (10 to 16 per cent.). 

Vesicles and roseolas simultaneously and in Never in crops; first macules, then hard, 

crops; very rarely shotty. shotty papules, vesicles, etc. 

Rash evolution: much more rapid; vesicles Much slower; vesiculation on the seventh 

on the first or second day. day (see Pfeiffer's table). 

Eruption is universal; successive crops; Development progresses downward — face 

most abundant and characteristic on first, then hands and feet; less on trunk. 

back; begins on body; less on face, 

scalp, mucosa?, hands and feet. 

The vesicle is superficial, and the fluid trans- The fluid is pearl-colored, not transparent, 

parent. (Wyss observed confluent erup- and has a thicker covering. 

lion and umbilication). 

Areola (halo) is usually absent, Marked. 

Involution is rapid. Tardy. 



SMALLPOX— VACCINA TION 255 

Mistakes may be made even by smallpox experts, but attention to 
the history, somatic findings and course, rather than to the eruption, 
prevents many disastrous results. 

Measles vs. Variola. 

Both present the same prodromal duration; in each the eruption begins on the face; 
according to some observers, simultaneously on face and trunk. 

Age: eminently a childhood affection. Chiefly in adults. 

Catarrhal stage characteristic. Catarrh, if any, rudimentary. 

Fever: present in catarrhal stage, but low High before eruption and falls with the 

before exanthem, and rises with its ap- exanthem even in severe cases. 

pearance. 
Koplik's spots on buccal mucosa; bluish- Absent. Early papular eruption on palate, 

white surrounded by red. etc. 

Eruption later with rise of fever. Possibly an initial morbilliform eruption 

with the primary fever. 
Papules "grouped," crescentic. Never so. 

Papules remain relatively flat, smooth, Change into vesicles, pustules, crusts, scars; 

velvety. hard and shotty. 

Grisolle's sign absent and the eruption dis- Grisolle's sign present; i. e., persistence of 

appears under pressure. the smallpox papule on stretching the 

skin, distinguishing it from scarlatina, 
varicella, etc. 
Areola (halo) absent. "Halo" present. 

Scarlatina vs. Variola. 

Rash on the second day, angina, straw- Rash later; slow evolution of different 

berry tongue, desquamation, glands, phases. No * angina; no strawberry 

nephritis, etc. (See cardinal symptoms tongue; the initial scarlatinal eruption 

of scarlet fever.) is not punctate and less bright. 

No double elevation of fever curve. Double summit to curve. 

In drug rashes (copaiba, etc.), the pustules occur largely on the face, 
head, arms and forearms. In syphilis the chancre, glands, polymorphic 
rash, and the moderate fever, are easily distinctive. 

The lumbago form of acute nephritis, acute myelitis or erythema, 
septicemic rashes and acne only superficially resemble variola. 

Glanders may cause more hesitation in diagnosis. Its features are 
pyrexia, pains, papules, pustules, nasal discharge, the bacteriological 
findings, and general symptoms severer than the skin eruption. 

Prognosis. — The prognosis depends on (a) previous vaccination, the 
disease being fatal in 50 per cent, of those unprotected by vaccination. 
Smallpox is rarely fatal in persons vaccinated within five or six years; 
only 8 per cent, of those vaccinated once die, and only 4 per cent, of those 
vaccinated twice, (b) On the genus epidemicus: In the last American 
epidemic the death-rate was but 1.6 per cent, (c) On the type, being 
practically 100 per cent, in purpura variolosa; nearly 100 per cent, 
in variola pustulosa hemorrhagica; 60 per cent, in variola confluens — 
especially fatal in the first decade of life; 25 per cent, in variola 
discreta — particularly dangerous in those over fifty or under ten 
years, in pregnancy, the puerperium, in weakly and alcoholic subjects; 
1 per cent, in varioloid; recovery usual in variola sine exanthemate. 
(d) On individual symptoms: (i) Incubation is short in unfavorable 
forms, especially in purpura variolosa, (ii) Initial symptoms are mild, 
chiefly in varioloid; but maybe severe in both the benignant and malignant 



256 INFECTIONS OF DOUBTFUL ETIOLOGY 

forms, (iii) The initial rash is usually a partial erythema in mild forms 
of smallpox; in general, morbilliform eruptions occur in varioloid. 
Scarlatiniform eruptions occur in rather severe forms and a universal 
scarlatinal hemorrhagic eruption, especially in the groins, occurs par- 
ticularly in purpuric types, (iv) The danger is proportionate to the 
amount of the eruption on the face and hands. A slow, typical exanthem 
indicates variola discreta, and a precipitate atypical eruption presages 
variola confluens. (v) A prompt fall in temperature after the eruption 
is favorable. A slow, complete fall occurs chiefly in the severe forms. 
Accession of fever after pustulation is ominous. Hyperpyrexia or tem- 
perature collapse during suppuration is a sign of imminent death, (vi) In 
the stage of suppuration the danger parallels the height of the fever and 
the amount of efflorescence. Enlargement of the spleen is ominous. 

Treatment. — 1 . Prophylactic Vaccination. — Vaccinia. — Protection 
by cow-pox vaccination was discovered by Jenner, who published his 
results in 1796, although certain of his evidence twenty years earlier; the 
idea had been long prevalent among farmers that cow-pox afforded 
immunity to smallpox. Professor Waterhouse, of Harvard, in 1800, 
introduced vaccination into this country. 

The nature of cow-pox or vaccinia is still disputed. It is probable that 
cow-pox and horse-pox are human smallpox modified by transmission 
through animals. Variola inoculated in the cow produces typical vaccinia. 
The other view is based upon Chauveau's experiments, which conclude 
that the two affections are distinct. The bacteriology of vaccinia is 
also uncertain; micrococci, bacilli and amebse (Guarnieri's cytorrhyctes 
vaccinia?) have been found. 

Usual Symptoms. — During the incubation period of three days, there 
may be slight local traumatic reaction. On the third day a hard papule 
develops, surrounded by a delicate halo. The papule enlarges, and on the 
fifth (or sixth) day shows Jenner's vesicle filled with clear serum and umbili- 
cated in its centre. In the indurated and painful skin around it the magni- 
fying lens shows many minute vesicles by the eighth day. By the tenth day 
the vesicle becomes purulent and the surrounding tissues hard and painful. 
By the eleventh day a small central crust appears, which, by the end of 
the second week, covers the entire vesicle, when the adjacent cellulitis 
regresses. In one or two weeks the ulceration, decrustation and granula- 
tion are usually complete, and a scar or pit remains, which pales with 
time. Constitutional reaction is greatest in children. The fever in most 
cases appears on the fifth day, and lasts a few days, with leukocytosis, 
restlessness, headache or backache. Swelling, depending on the site of 
inoculation, occurs in the axillary or inguinal glands. School physicians 
should not accept certificates of recent vaccination but should watch 
the evolution of the vaccination. 

Unusual Symptoms. — The vesicles may run a course shorter by half 
than the usual one, or the eruption may be tardy and atypical. In both 
instances revaccination is indicated. 

Complications. — (1) Erythema, urticaria, roseola? or erysipelas (third 
to eighth day); in Germany, in 1895, two deaths (from erysipelas) 
occurred in two and a half million vaccinations. To offset this theo- 



SMALLPOX— VACCINATION 257 

retical risk there is the almost universal susceptibility to smallpox in 
all unvaccinated individuals. (2) Accessory vaccinia near the original 
inoculation; or generalized vaccinia, on the trunk and extremities; vesicles 
sometimes continue to develop for over a month, and in weakly subjects 
are very exceptionally fatal. (3) Secondary infection in the first week 
or two, either local (deep ulceration, gangrene, lymphangitis or lym- 
phadenitis), or systemic (sepsis, pericarditis, meningitis and parotitis). 
In 95 reports, McFarland (1903) collected 68 certain cases of tetanus. 
Albuminuria is infrequent. (4) Later infections: Tuberculosis is prob- 
ably never inoculated; it can be prevented by the Belgian method of not 
using the lymph until the animal has been killed and found healthy. 
In some cases a latent tuberculosis in the patient may be awakened by 
vaccination, which seems to act like tuberculin. There was danger 
of inoculating syphilis when human virus was used; in fifteen days a 
chancre, and in eight weeks more the secondaries appeared. Syphilis may 
be inoculated accidentally and also intentionally, as in the oft-cited 
case of Dr. Cory. In exceptional cases, latent syphilis may be aroused 
by vaccination. There are no clear cases of inoculation of leprosy. 
Howard found the ray fungus 24 times. 

Age. — Children should be vaccinated in the third or fourth month, 
but never later than the first year. 

Technique. — The arm or leg should be washed, but no antiseptics 
should be employed, lest they neutralize the virus. A fold of skin is 
raised and rubbed with sterile gauze or scraped with a knife held almost 
parallel to the skin, until the epidermis is removed and slight oozing 
of lymph appears. The virus must reach the lymph stream, and therefore 
blood should not be drawn, as coagulation somewhat inhibits "taking." 
The vaccine should be slowly rubbed over and into the abraded skin. 
Only after the virus has thoroughly dried should the spot be covered with 
a sterile dressing or cloth held in place by adhesive plaster. Boric, 
carbolic or bichloride gauze must not be used. 

Lymph. — Vaccinia virus is harmless if it is collected in the vesicular 
and not in the pustular stage, and preserved in sealed sterile tubes with 
three parts of glycerin. This obviates pyogenic infection, preserves the 
virus four months, and is more economical. Human virus must be 
taken from a perfectly sound child, carefully examined for tuberculosis 
and syphilis, and taken on the seventh day from the clear, unbroken 
vaccinia vesicle, which must be free from pus ; no blood should be with- 
drawn. 

Results. — The successful vaccination, accompanied by typical papula- 
tion, vesiculation, pustulation, crustation, cicatrization, and by local 
and often general reaction, confers immunity in almost all cases. Vac- 
cination is the greatest triumph of prophylaxis. The nature of the 
immunity conferred is still disputed, but, unlike the immunity of diph- 
theria, it is probably due to actual tissue change. Vaccination imme- 
diately after exposure is thought to prevent or modify an impending 
attack. Partial immunity is evidenced by varioloid (smallpox mitigated 
by vaccination). Immunity is not life-long, as Jenner thought, nor is it 
absolute. In some few cases, the individual is permanently protected by 
17 



258 INFECTIONS OF DOUBTFUL ETIOLOGY 

one vaccination, but protection lasts on an average ten years, after which 
60 (to 90) per cent, can be successfully revaccinated once or twice. Con- 
versely, the child should be revaccinated in his tenth to twelfth year, and if 
the vaccination does not "take," it should be repeated. The reaction, fever, 
induration, and size of the vesicle and scar, are less in re vaccination. As 
immunity is more enduring when more than one inoculation has been 
made, the Germans vaccinate two areas or even four or six. The general 
beneficence of vaccination needs no multiplied statistics. There has been 
no epidemic of smallpox in Germany since 1875. Epidemics prevail in 
communities which are least protected, and conversely, they disappear 
with systematic compulsory vaccination. 

2. Other Methods of Prophylaxis. — Isolation hospitals and 
stations are indispensable. Isolation is necessary from the invasion 
until disappearance of the last crust. The dead body is dangerous and 
the funeral must not be public. The clothes used by the patient must 
be steamed, and other articles must be washed with bichloride of mercury 
and fumigated with formaldehyde vapor; Schoch's method has the 
advantages of requiring no special form of apparatus, of cheapness, and 
freedom from danger of fire. 1 Disinfection of the face, hands, beard and 
hair of attendants by bichloride solution is imperative. The family 
should be isolated for sixteen to twenty days. 

3. Actual Treatment. — There is no specific treatment. The hygiene 
and dietary are the same as in typhoid. For headache, the ice-bag, 
opium and hydrotherapy are employed. Pain is relieved by opiates. 
The initial vomiting is difficult to overcome, but its duration is fortunately 
short. Ice-pills, lime-water, iodine, chloroform, morphine, carbolic acid 
and bismuth may be used as in typhoid (q. v.); mustard plasters may 
necrose the skin. 

Early hydrotherapy is important in fever. It lessens the derma- 
titis; when the rash develops, baths are contra-indicated. 

Delirium may be relieved by hydrotherapy, by chloral, bromides 
and hyoscine. Morphine, in half-grain doses, is invaluable to lessen 
itching and pain and conserve metabolism. The patient, if delirious, 
may escape or injure himself. A classmate of the author killed himself 
by jumping through a window. Patients should never be confined by 
straps, lest serious skin necrosis ensue. 

The eruption may be pricked and cauterized with silver nitrate, treated 
with bichloride or boric compresses or covered with mercurial plaster; 
1 per cent, carbolic vaseline is the best, because it counteracts the 
particularly offensive odor, but should be used on the face only, since 
general use may cause carbolic poisoning. These measures do not prevent 
cicatrix formation, but relieve dermatitis and itching. Protecting the 

1 The following are required: Good quicklime in lumps, commercial sulphuric acid and 
ordinary 40 per cent, formaldehyde solution. For every 1000 cubic feet of space, the size 
of the average room, one pound of commercial formaldehyde (40 per cent.), one-half pound 
of sulphuric acid and three pounds of quicklime are required. The acid and the formalde- 
hyde are first mixed in an earthenware vessel by pouring the acid into the formaldehyde. 
Then the lime is placed in a shallow vessel in the centre of the room. All openings to the 
room arc carefully closed, the mixture is poured on the quicklime, and the operator leaves 
the room. The rooms should remain closed for from five to eight hours. 



CHICKEN-POX 259 

face from the light with wet compresses seems to lessen the pitting. 
The crusts should be kept soft with olive oil. The hair should be cut 
short and the eyes douched frequently with boric acid solution. The 
mouth, larynx, circulation, skin and diarrhea should be treated as in 
typhoid fever. 

For sepsis, quinine (v. sepsis) and alcohol (v. typhoid) are given by 
the rectum, since dysphagia is always present. Egg-nog properly prepared 
will not irritate the throat. During convalescence the crusts should be 
carefully washed, and the patient may be considered safe only when the 
skin is clear of the last scab. 

CHICKEN-POX (VARICELLA). 

Definition. — An acute specific febrile contagious disease, chiefly of 
childhood, characterized by an exanthem of vesicles. 

History. — Varicella was recognized by Ingrassias in 1553, Heberden 
in 1767, and by Trousseau, as a disease distinct from smallpox. 

Etiology. — It is transferable by direct inoculation, personal contact, 
by the air or by a third person. It is infective while crusts remain. 
Epidemics of varicella may coincide with, precede, or follow, smallpox. 
Smallpox does not prevent an attack of varicella nor is the converse 
true. The disease occurs chiefly in epidemics. It occurs chiefly in the 
first year of life, or, according to others, 66 per cent, of cases occur under 
the sixth year. The actual cause is not determined. Guttmann described 
a staphylococcus; and Pfeiffer and Guinon, a protozoon. 

Symptomatology. — 1. Incubation. — This stage, like that of measles, 
lasts thirteen or fourteen days. 

2. Stage of Prodromes. — Prodromal symptoms are rare, or they 
last but twenty-four hours. Severe intoxication is rare, but the follow- 
ing have been observed: delirium, convulsions, vomiting, hyperthermia, 
angina, conjunctivitis, dysphagia, muscle pains, bloody vomiting and 
stools, and an initial erythema (usually scarlatiniform, rarely morbilli- 
form, in the fifteen cases recorded). 

3. Stage of Eruption. — The exanthem appears usually in one day, 
as red macules or papules, comparable to the typhoid roseolas, slightly 
elevated, disappearing on pressure, lenticular and becoming vesicular. 
The vesicles mature within a day, are very superficial, and do not occupy 
the whole roseola, but leave a slight areola about them, which is not 
inflammatory as in smallpox. In some cases the areola may be absent, 
the eruption appearing like drops of water sprinkled on the skin. Though 
usually discrete, confluent eruptions are described. The vesicles may 
be few or numerous; Thomas counted 800 in one case. The eruption 
is mostly elliptical or circular. The vesicles may be very large, and, 
in exceptional cases, resemble pemphigus. 

There is no point of predilection for the eruption, and no part is exempt, 
though most vesicles appear on the trunk, fewer on the face, arms and 
legs, and the least number upon the hands and feet. 

The vesicle, clear at first, becomes turbid within two days. Pustula- 
tion and hemorrhage into the vesicle rarely occur. The vesicle may con- 



260 INFECTIONS OF DOUBTFUL ETIOLOGY 

tain air. Umbilication is rare; crusts may simulate umbilication. The 
vesicles of varicella are not always unilocular. 

Occurrence in crops is frequent, when the skin shows simultaneously 
macules, vesicles and crusts. Yellowish-brown crusts form on the 
third and fourth days and gradually disappear. Distinct scars may 
result from scratching or infection, and a few cicatrices are usual in 
every case of varicella, but they are smooth, white and some disappear 
with time. 

Enanthems are not frequent; vesicles may easily be overlooked on 
the palate; breaking down, they resemble aphthae. On rare occasions 
they are seen on the tongue, larynx, prepuce or labia. 

Fever. — The fever is slight, atypical and not parallel to the eruption. 
Fever as high as 106.8° is recorded. It is very rare in the prodromal 
stage, but may occur with profuse eruptions, or with successive crops; 
its persistence suggests complications. 

General Symptoms. — These sometimes include dysphagia, cervical and 
submaxillary swellings, tracheitis, bronchitis or albuminuria. 

The entire course of an uncomplicated case lasts one or two weeks. 

Complications and Sequels. — These are usually dismissed with a few 
words. Nephritis is generally tubular, and occurs within two weeks 
after the rash declines. Though usually mild, fatal cases have been 
reported, as well as some eventuating in chronic nephritis, cardiac hyper- 
trophy and^ uremia. Gangrene of the extremities, scrotum or eyelids 
has been noted in delicate or tuberculous children. Infrequent complica- 
tions are pleurisy, pneumonia, miliary tuberculosis, erysipelas, glandular 
swelling, pemphigus, hemiplegia, polyarthritis, otitis, neuritis, etc. 

Diagnosis. — The diagnosis is very easy if the case is seen early. Dif- 
ferentiation from smallpox (page 254). In pemphigus the vesicles are 
larger and run a slower course of weeks or months. Miliaria rubra are 
preceded by sweats, occur chiefly on the covered parts, have acid con- 
tents, are smaller than the varicellous eruption and disappear more 
rapidly. Sometimes consideration must be given to molluscum con- 
tagiosum (soft, umbilicated tumors with white, granular contents); 
prurigo varicelliformis (with crop-like eruptions at longer intervals); 
eczema vesiculosum, which always occurs with great itching; herpes, 
always appearing in groups and often along nerve trunks; varicellas 
syphilitica^, and medicinal rashes from cantharides, bromide, arsenic 
and iodide. 

Treatment. — Active treatment is rarely indicated. Kling reports success 
from vaccination. 

SCARLET FEVER (SCARLATINA). 

Definition. — A specific infective disease of unknown bacteriology, 
characterized by sudden onset, fever, diffuse exanthem and angina. 

History. — It was recognized by Ingrassias and Coyttar in the sixteenth 
century, but first fully described and differentiated from measles by 
Sydenham (1660). It was introduced into America in 1735. 

Etiology. — The etiology is unknown. The virus of scarlet fever pro- 
duces severe necrosis, but no suppuration. Mallory describes a proto- 



SCARLET FEVER 261 

zoon, the Syclaster scarlatinalis. The streptococcus is the most important 
factor in the production of complications and in their mortality. Schleiss- 
ner found it in the blood in 55 per cent. It is found in about 70 per 
cent, of the fatalities, i. e., it is the cause of the malignancy of the 
disease, but not of the disease itself. 

Susceptibility is not universal — and only 38 per cent, of children and 
5 per cent, of adults exposed to infection acquire the disease; 90 per 
cent, of cases occur under ten years of age. It is rare in the first year 
of life. 

So-called "surgical and puerperal scarlatina," noted in 1864 by Paget, 
is in the vast majority of cases, sepsis, erythema or a drug rash. Alice 
Hamilton (1905) collected 174 cases from the literature, and concluded 
that these forms are mostly septic, or that the scarlatina is merely 
accidental. 

The virus circulates in the blood, whence the possibility of fetal 
infection. It was once held that the virus was disseminated during 
desquamation, but oral, nasal or otitic discharges probably perpetuate 
infection, perhaps months after scaling is complete. In no other disease 
is the virus so tenacious; it may persist ten years on clothes, furniture, 
etc. Light are as contagious as severe forms. Inoculations from the 
living subject have occurred and Leube acquired the disease by an 
autopsy cut. The atrium is probably the throat. Monkeys have been 
inoculated. 

As to the degree of infectiousness, smallpox ranks first, measles second 
and scarlatina third. Infection may be spread by servants, physicians, 
any third person, and by means of toys, books, clothes, milk and schools ; 
the mode of infection is often obscure. One attack usually confers 
immunity, but second, and even third, attacks are known. Some indivi- 
duals temporarily or permanently resist infection. Scarlet fever occurs 
more often in the autumn and winter. Scarlatina is observed more in 
the cities, and measles prevails more diffusely through the country. 
Scarlatina is more permanent than measles. When it becomes epidemic 
it spreads widely and with increased mortality. 

Scarlatina sometimes occurs with other infections, such as diphtheria 
or measles, and less often with varicella, pertussis, etc. 

General Symptomatology. — 1. Incubation. — The incubation, with no 
noticeable symptoms, lasts from two to four days (ten to fourteen days, 
McCollom). 

2. Invasion. — The invasion lasts one day. Symptoms begin suddenly, 
perhaps with a chill, followed by (a) vomiting, early and characteristic, 
which occurs in scarlatina more often (75 per cent.) than in other diseases 
of childhood except pneumonia ; (6) headache, convulsions and delirium ; 
(c) sudden elevation of temperature, with disproportionate pulse-rate, 
120 to 150, dry, burning skin and febrile urine; (d) burning and pain 
in the throat, dysphagia and intumescence of the cervical glands. 

3. Exanthem. — The eruption appears on the second day, first over 
the clavicles, upper trunk and neck and then on the extremities. The 
skin about the mouth is pale. The exanthem pales on pressure. It first 
consists of small red spots which fuse as the skin swells, and result in 



262 . INFECTIONS OF DOUBTFUL ETIOLOGY 

an intense diffuse lobster-colored erythema; it lasts four to six days. 
The tongue shows swollen red papillae — "strawberry tongue." On the 
tonsils and palate a grayish-yellow coating and confluent spots appear. 
The nostrils slightly swell, and the conjunctivae redden. Some rales 
over the larger bronchi, a slight cough, swelling of the cervical and other 
glands, and sometimes albuminuria, may be noted. 

4. Desquamation. — Scaling begins first on the face, from the sixth 
to ninth day and lasts several weeks. The glandular swelling disappears, 
the fever falls by lysis, and convalescence is established unless com- 
plications intervene. 

Special Symptoms, Complications and Sequels. — 1. Fever. — The fever 
is less typical than in smallpox and measles. There is an initial rapid 
rise to 104° or 105°, with slight remissions and gradual subsidence when 
the rash is mature. 

In the most severe types there may be low fever or no fever at all, or 
it may rise to 107°. A close parallelism is generally noted between 
the abundance of the exanthem and the height of the fever. The tem- 
perature should be taken for one month after the rash disappears, lest 
such complications as sloughing of the throat, pleuritis, endocarditis, 
pericarditis, synovitis or adenitis be overlooked. 

2. Eruption. — Typically, it begins as light red, pin-head-like points, 
especially in the axilla and groin; second, there are red spots in a 
diffuse erythema; and lastly, there are red spots alone. This minute 
papulation is a very important aid to diagnosis in the second week. There 
may be minimal white lines in the eruption, but rarely spaces, as there 
are in measles. The eruption appears first on the neck, below the mastoid 
and clavicles, then upon the trunk, arms and hands, and lastly legs and 
feet. It is most intense over the extensor surface of the joints and on 
the trunk, and is least developed on the face and scalp. The palms and 
soles are usually free. The pallor around the mouth is triangular, bounded 
by the nasolabial folds above and the chin below, and contrasts vividly 
with the scarlet cheeks and minutely papulated forehead. Though not 
pathognomonic, it is valuable in differentiation, and is due to vascular 
spasm. Herpes near the angles of the mouth is very common; The 
eruption is occasionally roseolous about the ankles and wrists. The 
skin is always swollen. The hyperemic eruption pales on pressure and 
disappears after death, unless there are punctate hemorrhages, 1 which 
are not uncommon in severe types of the disease. After twentj^-four 
hours the tension disappears, and the bright red color becomes a yellow- 
ish-red. After complete florition desquamation begins from a slight 
exudation of serum between the layers of the skin; it is usually bran- 
like, as in measles, on the head, face, neck and trunk, but is more scale- 
like and lamellar on the hands and feet, complete casts of which are 
sometimes shed. In severe cases even the hair and nails are shed, or 
the nails become furrowed. It begins on the cheek with the "rouge- 

1 The Rumpel-Leede phenomenon, consisting of the production of hemorrhages above 
the elbow after constriction as by a blood-pressure arm band, is not specific; nor is Pastia's 
sign, the occurrence of two to four small, dark red o reven hemorrhagic lines on the anterior 
surface of the elbows. 



SCARLET FEVER 263 

and-powder" appearance, and the skin may present a "pin-hole" or 
"worm-eaten" aspect before desquamation begins. Its duration is 
usually from one-half to three weeks. Scarlatina levigata is the typical 
rash described above. Anomalies of eruption are scarlatina levis (rudi- 
mentary eruption); scarlatina sine exanthemate (the rash being absent); 
scarlatina papulosa (marked papulation) ; scarlatina miliaris (from sweat- 
ing, and exudation between the rete Malpighii and epidermis); scarla- 
tina variegata (like measles, though not equally elevated); scarlatina 
hemorrhagica (usually ominous, and at times part of a general hemor- 
rhagic diathesis). In general, irregular forms are dangerous. 

3. Throat. — The throat changes are the most constant lesions in scarlet 
fever, and constitute the internal eruption (enanthem). The disease 
begins in the throat with uniform redness and early swelling. The 
throat becomes speckled with fine red points like the skin papulation. 
(a) In mild cases, a simple catarrh with little swelling, a thick mucous 
coating, and reddening of the palate and tonsils, develop, (b) In mod- 
erate cases there is more swelling of the palate, and tonsillitis, (c) In 
severe cases, membrane, small abscesses, gangrene, minute hemorrhages, 
sloughing, edema, adenitis or cellulitis develop. Severe inflammation 
in the throat occurs in 65 per cent, of cases. 

Clinical and anatomical diphtheria are often confused. "Necrotic 
inflammation" in scarlatina is that caused by the virus of scarlatina 
alone. Genuine diphtheria may accompany or follow scarlatina. 

Diphtheritic Membrane vs. Scarlatinal Membrane. 

Firm, adherent. Softer, loosened in fragments. 

Yellowish-gray. Brownish tint. 

Deep ulceration rarer, in more severe cases More frequent and earlier (even in twenty- 
only, and later. four hours). 

Phlegmon rare. Not infrequent. 

Laryngeal membrane (croup) frequent and Rare, membrane thinner; lung complica- 

deeper. tions rare. 

Bacteriologically, the Klebs-Loeffler bacil- Streptococcus (Klebs-Loeffler bacillus only 

lus. as a complication) . 

Paralysis frequent. Rare, except local paralysis due to local 

swelling of pharynx. 

Recurrence frequent. Infrequent. 

4. Respiratory Tract. — Though often unaffected, the respiratory 
tract may become involved secondarily by a descending process. The 
nose is involved in direct ratio to the severity of the throat developments, 
such as necrosis or diphtheria. Acute edema of the glottis is infrequent. 
Bronchopneumonia, acute lobar pneumonia (usually in the upper lobe 
and coexisting with nephritis), gangrene, infarcts and hypostasis are 
not uncommon. Pleurisy occurs in 5 per cent, of cases. It is likely 
to be severe and is frequently purulent. 

5. Circulation. — The heart is greatly damaged by the scarlatinal 
virus in 35 per cent, of cases, not including the cases of sepsis and neph- 
ritis. Endocarditis is frequently mural, whence its frequent latency, 
but it may result in chronic disease, especially of the mitral valves. 
After rheumatism, scarlatina is the most frequent cause of endocarditis. 
Pericarditis is usually septic. Disquieting cardiac dilatation may be 



264 INFECTIONS OF DOUBTFUL ETIOLOGY 

seen in severe cases, accompanied by the usual evidences of acute cardiac 
insufficiency; the causal myocarditis may occur during the fever or in 
convalescence. The blood-pressure is reduced 25 per cent. Tachy- 
cardia may result from toxemia or acute infective myocarditis. The 
pulse is irregular in 90 per cent, of cases and is both weak and fast. 
Dilatation and hypertrophy are much more frequent in children than in 
adults, and often complicate renal lesions. Blood: Leukocytosis develops 
early and may become extreme in fatal cases. The average count in 
adults is 10,000 and in children 23,000. The polymorphonuclears are 
increased two or three days after the eruption. The eosinophiles are 
increased. In the polynuclears, Dohle's so-called " inclusion bodies" 
are found, oval, rod-like or sickle-shaped inclusions, and present up to the 
fourth day; they also occur in other infections. The hemoglobin suffers 
an early and increasing reduction. A hemorrhagic diathesis is generally 
septic. 

6. Digestive System. — The tongue is swollen, indented, broad and 
thick. Its coating is first grayish, but on the third to fifth day disappears, 
leaving the tongue red, dry and glistening, on which the enlarged papilla? 
appear granular and warty — the "strawberry" or " cat's tongue." It 
is quite pathognomonic and McCollom found it the only constant sign 
in 1000 cases of scarlatina. Diphtheritic ulcers and secondary necrosis 
in the stomach, esophagus and intestines; vomiting from nephritis or 
toxemia; moderate swelling of the liver and spleen or abdominal pain 
may be noted. Constipation is usual. Diarrhea may result from (a) 
catarrhal enteritis; (6) dysentery, with tenesmus and blood; or (c) the 
so-called "scarlet typhoid," accompanied by tympany, hemorrhage, rapid 
pulse, lethal outcome, and autopsy findings of splenic intumescence, and 
hyperplasia and ulceration of Peyer's patches. 

7. Kidneys. — The urine is febrile. It often responds to Gerhardt's 
reaction and the diazo test; urobilinuria is ascribable to hepatitis. Albu- 
minuria occurs in 75 per cent, of cases. The initial "catarrhal nephritis" 
is marked by Jiyperemia, parenchymatous changes, little interstitial 
involvement, some fluid in the glomeruli and a few cylinders in the 
tubules. 

Nephritis usually develops in the third week. Its frequency varies 
with the epidemic, between 5 or even 90 per cent. No relation exists 
between its frequency and the severity of the infection. Glomerulo- 
nephritis is the most frequent anatomical form, characterized anatomi- 
cally by hyperemia, increased consistence, and such glomerular changes 
as gray color, diffuse fatty granular degeneration, increase of nuclei, 
and increase in the size of the tufts, which become sausage-like, solid 
masses. We also note exudation of leukocytes about the afferent vessels, 
multiplication of capsular epithelium with occlusion of the lumen, hyaline 
alteration of the vessels, and early interstitial changes, and later, con- 
nective-tissue growth. 

Clinically (a) the urine is decreased or suppressed, heavy with sediment 
and albumin (averaging 0.5 per cent.), poor in urea, turbid (specific 
gravity 1.030), and full of casts of all types — especially, long, flat, band- 
like, twisted and frayed casts. Much oxalic and uric acid is found and, 



SCARLET FEVER 265 

in many cases, blood. Pollakiuria occurs in 10 per cent. (b) Hydrops 
shows the characters of renal dropsy; it appears first under the skin, 
the bloodvessels of which are altered by the virus. It shifts its location 
without cause, and may also produce hydrothorax, ascites, edema of the 
larynx, lungs or genitalia. Rarely hydrops occurs without nephritis, and 
kidney inflammation without urinary alterations. There may be lumbar 
pain, vesical tenesmus and (c) uremic symptoms, such as headache, 
twitchings, convulsions, wide pupils, amaurosis, coma, vomiting, diarrhea, 
cardialgia, rapid pulse and breathing, and pale skin tinged with cyanosis. 
Many convulsions usually imply a lethal termination in coma. The 
prognosis is more favorable if the pupils are not immobile. Uremia, 
hydrops and intercurrent inflammation are always dangerous. Recovery 
is possible after one or even three weeks of anuria. Convalescence is 
the rule after four to six weeks and the nephritis rarely becomes chronic. 

8. Special Senses. — Middle-ear inflammation (22 per cent.) usually 
begins before desquamation, and is accompanied by fever alone or with 
pain, glandular swelling, difficult hearing, tinnitus, a reddened, glisten- 
ing, sunken membrane, and, in children, by some brain manifestations. 
It is quite frequent in early life and rare after the fifteenth year; at 
least 10 per cent, of cases of acquired deafness result from scarlatina. 
Catarrhal conjunctivitis, diphtheritic inflammation, herpes or necrosis 
of the cornea; panophthalmitis, muscular paralysis and disturbance in 
accommodation, are possible complications. Uremic amaurosis, septic 
or nephritic neuroretinitis and retinal hemorrhage, are rare. 

9. Lymphatic System. — The glands, spleen, follicles and in severe 
cases, all lymphatic structures, are affected by the sepsis. McCollom 
found enlargement of the cervical glands in 50 per cent., and suppuration 
in 8 per cent. The " collar of brawn" results from cervical adenitis and 
periadenitis. Gangrene, retrosternal abscess and jugular phlebitis with 
sepsis, occur in desperate cases. 

10. Bones and Joints. — Scarlatinal arthritis (in 6 per cent.) usually 
occurs in the second or third week, with desquamation and subsidence 
of the fever, and lasts three or four days. It attacks the smaller rather 
than the larger joints, the wrists and ankles rather than the elbows, 
shoulders and knees. It is not so migratory as ordinary rheumatism. 
Swelling of the joints does not always occur. It occurs in old rather 
than in young subjects. The prognosis is usually good. 

Scarlatinal sequels are anemia, retarded development, decreased phy- 
siological resistance and rarely tuberculosis. Latent sepsis with brain 
"foci, valvular disease, chronic nephritis, chronic adenitis, otitis, mastoid- 
itis, arthritis, meningitis, hemiplegia, facial paralysis, etc., are fortu- 
nately rare complications and sequels. 

Diagnosis. — Typical cases are determined easily when an epidemic 
prevails, and when the eruption is subordinated to other criteria: 

1. Suclden onset and rapid development, with fever and vomiting. 

2. Angina, punctate spots in the throat, swelling and dysphagia are 
practically always present. Severe throat symptoms are always sus- 
picious. 

3. Strawberry tongue, which is constant. 



266 INFECTIONS OF DOUBTFUL ETIOLOGY 

4. Exanthem, first about the clavicles, with the face less involved; 
the mouth free and intense on the body; papules, then erythema develop; 
there are no free spaces; it results in desquamation. 

5. Lymphadenitis. In this the cervical are less important than the 
inguinal or other glands. 

6. Fever, hydrops, albuminuria and nephritis in atypical cases. 

7. Scaling, tender joints and albuminuria help in making a retrospec- 
tive diagnosis if the initial symptoms were not clear. 

Diagnosis of Atypical Scarlatina. — 1. Severe scarlatina, (a) 
The anginose form resembles septic diphtheria, with marked toxemia, 
necrosis and adenitis. (b) Atactic form; violent intoxication, high 
fever and death before the eruption appears; blood dissolution, vomit- 
ing, diarrhea, convulsions, coma and a rapid, weak heart, are the chief 
symptoms, (c) Hemorrhagic scarlatina, characterized by severe fever 
and brain symptoms at the onset; incomplete exanthem, necrosing 
angina, marked glandular and splenic swelling; subcutaneous, serous 
and mucous membrane hemorrhages with exulceration. It is usually 
lethal after ten to twenty hours from hyperpyrexia, vomiting, diarrhea, 
delirium, convulsions and dyspnea, especially in reduced subjects under 
two years of age. 

2. Very light cases may present (a) all the usual signs, though but 
mildly developed; or (b) some symptoms may be absent (scarlatina 
fragmentaria) , as in cases with no temperature (scarlatina sine febre), no 
rash (s. sine exanthemate) , or no angina (s. sine enanthemate) . In some 
atypical cases a definite diagnosis is impossible, as in acute nephritis 
with uremia, fever, sore throat and gastro-enteritis, without the character- 
istic rash. Recurrence is noted in 0.2 per cent.; many of these cases 
are septic complications. 

Differentiation.^The differentiation is as follows: 

Scarlet Fever vs. Sepsis. 

Bright red erythema, with small red A very deep purple-red rash, sometimes 
papules. spreading over entire body. 

The eruption is much the same in both diseases, the same places being exempt. 

Miliaria are rare. Frequent. 

Rather typical desquamation. Desquamation observed less frequently. 

Criteria: angina, tongue, onset, glands, etc. Etiology, chills, sweats, fever irregularity, 

polymorphous exanthems, etc. 

Diphtheria is often differentiated with difficulty. A simple erythema - 
is sometimes observed in diphtheria, which is darker, more on the trunk, 
and more transitory than in scarlatina (v. s.). 

Drug rashes, from belladonna, iodoform, quinine, iodide, chloral or 
copaiba may be easily differentiated, if the cardinal signs of scarlatina, 
rather than its rash alone, are considered. 

Measles and German measles (page 273). Acute exfoliating dermatitis 
also begins with fever, with a spreading erythema, and early desquama- 
tion, but the cardinal' criteria of scarlatina are lacking. Erythema is 
more transitory; the points are absent; it occurs with less fever and 



SCARLET FEVER 267 

without angina or adenitis. Erysipelas presents edematous swelling, a 
sharp border, marked pain and a slow advance. 

Prognosis. — The death-rate depends on the genius epidemicus (between 
2 and 40 per cent.), but averages 10 per cent. The prognosis is least 
favorable in hospital cases and most deaths occur under six years; in 
children under five years the mortality is 25 per cent., and still higher 
in the first year of life. . 

Uremia accounts for 50 per cent., and respiratory complications for 
20 per cent, of scarlatinal fatalities; 15 per cent, of nephritic cases die. 
The severity of the infection, hemorrhagic forms, severe toxemia, com- 
plicating sepsis, necrosis in the throat, otitis and heart complications 
are the other factors in prognosis. 

Treatment. — The disease runs its self-limited course. 

1. Prophylaxis. — Isolation is imperative in all cases; indeed, light or 
ambulatory forms more often convey infection. Susceptibility is not uni- 
versal and the virus is less penetrative than in measles, whence it is 
possible to circumscribe its diffusion. Care should be taken to prevent 
transmission through schools, fomites or third persons. The infected room 
should be kept empty and exposed to the wind and sun for one month 
afterward. The physician should wear an operating gown and carefully 
wash his face, beard and hands after leaving the sick-room. Quarantine 
should be maintained from eight to ten weeks, or longer if discharges 
from the nose, nasopharynx, or ears continue. All discharges should be 
disinfected. Formaldehyde fumigation has been discussed (page 258). 
Care in surgical and puerperal cases is important, but the danger has 
been overestimated. Bichloride wrappings should be placed about the 
dead body, and the funeral should be private. 

Schools must be closed during epidemics. In hospitals the cases of 
scarlatina with streptococcus infection are well separated from cases of 
simple scarlatina. Sound children should be sent away from the house 
and isolated lest they spread the disease. If they remain at home, 
one-quarter of them will contract scarlatina. 

II. General Treatment. 1. Decubitus. — The prone position is im- 
perative, during the disease and the first two weeks of apyrexia. 

2. Room. — The room should be light, well ventilated, dry and warm, 
especially in convalescence. A grate fire is advisable and the windows 
should be open at the top. 

3. Skin. — During the fever the skin should be covered with linen, 
and in convalescence with wool. The eruption may be brought out, 
when necessary, by mustard baths. During the fever, the patient is 
washed daily with warm water and soap, avoiding unnecessary exposure. 
The tension of the skin is thus lessened, the fever decreased and toxemic 
symptoms allayed. During desquamation, oil-rubs were once employed 
to decrease the dissemination of dry scales, but they decrease the func- 
tions of the skin, which are of great importance when the kidneys are 
involved; also, infection is carried by means of throat secretions. Soap 
and warm water serve equally well. The author is opposed to antiseptic 
soaps because of the chance of renal injury. 



268 INFECTIONS OF DOUBTFUL ETIOLOGY 

4. Fever. — The following fever formula is harmless : 

1$ — Liquoris ammonii acetatis oiss 

Tincturae aconiti TItxxiv 

Aquae q. s. ad. 5vj 

Fac misturam et signa. 

One to three teaspoonfuls every four or five hours, according to age. 

This mixture tranquilizes, promotes the rash and allays fever. Hydro- 
therapy is useful, such as the warm sponge or full warm bath, not the 
full cold bath. Special care is indicated in adynamic cases, because of 
danger of heart-failure, in pericarditis, stenosis of the air passages or 
dyspnea, in hemorrhagic forms and nephritis. 

5. Diet. — Water should be given freely. A fluid diet is indicated by 
the fever, the renal complications and the dysphagia. Concentrated 
foods, milk, soups and jellies, and in defervescence, milk-toast, custard, 
puddings, bread and butter may be given. Eggs and meats should be 
avoided. In severe throat complications, rectal feeding is indicated. (See 
Gastric Ulcer.) 

6. Arthritis. — The A-B-C liniment (aconite, belladonna and chloro- 
form), warm wool and flannel bandages are helpful. 

1$ — Tr. opii 3iij 

Phenolis 5j 

Tr. belladonnas 3hj 

01. olivae 5iv 

M. et S. — Apply on muslin covered by cotton. 

Salicylates are beneficial, but unless given carefully, may injure the 
kidneys. If the arthritis is obstinate or purulent, aspiration with all 
surgical care, and even drainage may be indicated. 

7. Angina. — Ice in the mouth and Dobell's solution as a nasal douche 
should be given. Care should be exercised in the use of antiseptics, 
lest children swallow them. A 10 per cent, hydrogen peroxide, 2 per 
cent, chlorate of potash, or 2 per cent, carbolic gargle may be used; 
formalin is too irritating. Caustics are contra-indicated. 

For the nose the following formula is excellent: 

R- — Phenolis 3ss 

Acidi borici 3ss 

Glycerini 5j 

Tr. myrrhae 5j 

Aquae q. s. ad. qv 

M. et S. — Locally, in such dilution that no irritation is felt. 

A 10 per cent, nitrate of silver solution is used with advantage in the 
early stages of the angina. Coincident diphtheria (q. v.) is treated by 
antitoxin, and antistreptococcus serum may be exhibited in streptococcic 
angina. 

8. Heart. — Cardiac stimulants may be exhibited according to Rotch's 
dosage table: 



SCARLET FEVER 



269 



Age. 


Tincture of 
digitalis. 


Strychnine. 


1 per cent, solution 
nitroglycerin. 


Atropine. 


3 months 


to- 2 minim 


2 000 1000 


grain 


yVsV minim 


3000 1500 grain 


6 


1 3 a 

10 4 


l -i 

15 5 00 


« 


1 1 « 


i l « 


2 5 15 


2500 1000 


9 


1_1 " 

4 J- 


1 1 

5 00 3 00 


a 


1 1 « 

2 5 10 


l l « 

1500 750 


12 


111 << 

4 J- 2 


] 1 

500 250 


a 


1 1 it 

2 5 5 


1 1 « 
10 5 


2 years 


§-2 minims 


1 1 
5 00 15 


a 


1 1 « 
15 3 


1 1 a 
T50 250 


3 


1 o " 

2 ° 


1 1 

3 00 100 


a 


1 1 u 
10 2 


• 1 1 u 
500 200 


4-10 


1-5 


1 1 
2 6 


it 


13 <( 
2 4 


1 1 a 
2 5 15 


10-12 


3-8 


1 1 
100 40 


a 


i_1 " 

2 ± 


1 1 u 
200 100 



9. Lymph Glands. — Secondary infection is decreased by prophylactic 
care of the mouth and throat. Ice is applied in the beginning only, and 
later, hot boric acid dressings when the blood and lymph streams stag- 
nate. Iodine or ichthyol salves and surgical intervention are indicated 
in the order named. 

10. Otitis is treated by copious boric irrigations, given quite hot and 
at low pressure, and followed by equal parts of glycerin and laudanum, 
or 5 per cent, carbolic acid. Leeches over the mastoid often relieve the 
pain. Examination of the drum is difficult in children with a small, 
sensitive meatus. Early puncture under cocaine is much safer than 
awaiting spontaneous rupture. After rupture a small amount of boric 
powder should be applied. 

11. Nephritis is treated (a) according to the old prophylactic rule, 
by which all cases, severe or light, are confined to bed for at least four 
weeks, and to the milk diet. Irritants, like cantharides, always are to 
be avoided. Tepid baths lasting a quarter of an hour should be given 
daily. Watch the temperature and the urine in convalescence. The 
results with urotropin as a prophylactic are at least suggestive, (b) 
Treatment of established nephritis. Hot baths increase the sweat and 
flow of urine. They are given twice daily, for half an hour, and the 
patient kept afterward between blankets. Alkaline diuretics, such as 
potas. acet. and p. citrat., may be given; pilocarpine for a child two 
years old, -J^ to 2V gr., and calomel as a laxative and diuretic must be 
used with great care, (See Treatment of Nephritis.) 

R^ — Infusi digitalis 3v 

Potassii acetatis 3ss 

Syrupi simplicis 3ij 

Aquae destillata3 q. s. ad. §ij 

M. et S. — One teaspoonful every two hours. 



High arterial tension indicates nitroglycerin. For convulsions, chloro- 
form, chloral and bromides are valuable. For vomiting, iodine is effi- 
cacious. Venesection and digitalis are necessary in pulmonary edema. 



270 INFECTIONS OF DOUBTFUL ETIOLOGY 

For uremia, two drops of croton oil placed undiluted on the tongue, 
should produce free cartharsis in two hours. If not successful by that 
time it should be repeated. Pulvis jalapse compositus (gr. xv to 3j) 
unloads the bowels in less urgent cases. Early evacuation is indicated 
in streptococcic pleurisy. 

12. Tonics. — Such tonics as iron, arsenic and cod-liver oil are indi- 
cated in convalescence. The heart must be watched for weeks, because 
the myocardium is often degenerated. Salvarsan is recommended. 

13. Serum. — Diphtheria antitoxin apparently benefits some scarla- 
tinal infections. Streptococcic sera have given no definite results. 
Immunization against one variety of streptococcus does not produce 
immunity against other varieties. In Vienna, Moser's serum has 
apparently been efficacious; the mortality was 8 per cent., as against 
14.5 per cent, without serotherapy. 

MEASLES (MORBILLI, RUBEOLA). 

Definition. — An acute, highly infectious disease, characterized by initial 
coryza, inflammation of the air passages, rapidly spreading eruption, a 
fever-curve with a double summit, and by toxemia. 

History. — Its first clear description dates from Rhazes (980-1037 a.d.). 
It was widely epidemic in the eighteenth century. 

Etiology. — (a) Susceptibility is almost universal and few individuals 
escape (14 per cent.). One attack generally confers immunity; Maiselis 
collected 106 cases with a second attack; third and fourth attacks are 
known, (b) Age: It is rare during the first five months of life, and 
occurs most frequently after the first year. It is more common in adults 
than is scarlet fever. In 16,981 cases, 50.4 per cent, occurred in the first 
five years; 42 per cent, between five and ten years; 5.2 per cent, between 
ten and twenty years, and 2.4 per cent, after twenty years of age. 
(c) Season: Measles occurs mostly in the winter and spring, (d) The 
unknown virus exists in the blood, tears, bronchial and nasal secretions, 
and in the skin or scales. Monkeys were successfully inoculated by 
Anderson and Goldberg, who proved that the virus was filterable and 
that infectivity was greatest during the catarrhal and eruptive stages. 
Propagation occurs by personal contact, and the healthy carrier is a 
most important mode of infection. In the home the disease usually 
runs through the family. The most frequent means of dissemination 
is the school-room. It is more often epidemic than scarlatina, especially 
in the country. After smallpox in the unvaccinated, measles is the 
most infectious disease. 

General Clinical Course. — -The stages are: (1) Incubation of nine 
or ten days; (2) initial or catarrhal stage of three or four days, with 
fever, catarrhal symptoms and an enanthem; (3) the eruptive stage, 
lasting four or five days, with renewed fever, intoxication, eruption and 
inflamed mucosae; and (4) the desquamative period. 

1 . Incubation. — The incubation lasts nine or ten to fourteen days. 

2. Catarrhal Symptoms. — Early catarrhal symptoms are more com- 
mon in measles than in any other acute infection of childhood. Chilly 






MEASLES 



271 



sensations, malaise and frontal headache precede redness of the eyes, 
lachrymation, photophobia, coryza and sneezing, pain in the nose, 
throat and bronchi, and cough, which develops after one day. Examina- 
tion of the mouth reveals Koplik's spots in 90 per cent, of cases, described 
by him in 1886 and Filatow in 1885 (Plate IX). They are found on 
the buccal mucosa near the molars, on the first day, as round, bluish- 
white spots, surrounded by a reddish areola. The initial fever reaches 
102° or 103°, and declines gradually during the third and fourth days. 

3. Eruption. — The eruption begins on the fourth day with papules 
on the temples, cheeks, forehead, then on the back, wrists, forearms, 
and on the anterior surface of the body and legs, in order of progression 
as named; with the appearance of the eruption, the fever again rises. 
The eruption disappears on pressure and is palpable and superficial. 
There are always islets of normal skin. The glands are usually enlarged. 



IDay 

TEMP. 


2 


3 


4 


5 


6 


101 










- 


103 A 












102 / \ 












io/^V 












100 












99 




































INITIAL 
RISE 


FALL 




RISE WITH 
RASH 


EXTENSION 
OF RASH 





Fig. 20. — Fever-curve in measles. 



All symptoms abate on the sixth day, by crisis. In severe cases, 
diarrhea, toxemia, bronchiolitis, pneumonia, cyanosis and asphyxia, 
may be observed, and death may result from lung involvement or mixed 
infection. 

4. Desquamation. — The skin pales, becomes slightly pigmented, and 
fine scales form, with convalescence in eight or ten days. 

Individual Symptoms in Detail. — 1. Eruption. — It is essentially the 
same on the skin and mucosae. In the mouth the mucosa is red on the 
first day of fever, and Koplik's spots are found; on the second day 
redness is noted on the tonsils and palate. The enanthem may reach 
the larynx, intestines and genitalia. The skin eruption (exanthem) is 
circumscribed, and hyperemic rather than exudative. It fades on press- 
ure; the roseolse may not fade on pressure in the nodular form of measles. 
The roseolce usually are discrete, slightly elevated, light to dark red in 



272 INFECTIONS OF DOUBTFUL ETIOLOGY 

color, round or crescentic in shape, and average 2 to 6 millimeters in 
diameter. They always leave islets of normal skin between the indepen- 
dent spots of eruption, even in the most diffuse types. The eruption 
follows a descending order and reaches the lower parts of the body last. 
When the eruption develops on the body first, the course is usually 
anomalous. Desquamation follows the same order as the eruption and 
is usually fine. Scars never result. The eruption is rudimentary in those 
who are debilitated by chronic diseases, and is exuberant in the healthy. 
The varieties are: (a) Morbilli Iceves, the usual form, with small 
elevations, (b) M. 'vesiculosi sen miliares. (c) M . papulosi, the nodular, 
slightly "shotty" induration is always superficial, (d) M. conflaentes 
sen conferti. (e) M. hemorrhagica?, benign or malignant (black, typhoid 
or septic type); early hemorrhage into the eruption is almost always 
fatal. (/) M. sine exanthemate; sine enanthemate. "Recession," "strik- 
ing in" of the eruption usually denotes heart-failure. 

2. The Fever. — The curve begins suddenly without a chill, and falls 
on the second day, perhaps to normal, usually rises again with the erup- 
tion, and reaches its maximum in thirty-six hours, thus giving a curve 
with a double summit. It usually falls by crisis before the eruption disap- 
pears. The temperature is normal during desquamation. Fever, after 
the eruption begins to fade, indicates complications. In rare cases 
fever is absent. 

3. The Respiratory Tract. — Nasal catarrh, if obstructive, is of 
special moment in sucklings; 50 per cent, of cases suffer from erosions 
of the larynx, 16 per cent, from pseudomembranous laryngitis, and 15 
per cent, from simple inflammation. Bronchial catarrh may reach the 
smaller tubules, usually late in the disease. It produces a clear, stringy, 
viscid sputum which later may become purulent and nummular. The 
bronchial glands are always swollen. Atelectasis may occasion indeter- 
minate breathing and dulness, which decrease with change of posture 
or deep breathing. Bronchopneumonia occurs in 6 to 12 per cent, of 
cases and is the most frequent fatal complication, patches of broncho- 
pneumonia occurring in every fatal case. It differs from other lobular 
pneumonias in its rapid development, and its greater tendency to pus 
formation, because the measles-catarrh favors mixed infection. Bron- 
chial breathing and other physical signs are not always detected clinically. 
The temperature is often no higher than in bronchitis. Toxemia and 
carbon dioxide narcosis accentuate the patient's distress. Broncho- 
pneumonia is rapid in development, but slow or sometimes incomplete 
in resolution. It may result in interstitial pneumonia, gangrene or 
tuberculosis, which dreaded sequel of measles occurs (a) as a miliary 
invasion, and in the brain more frequently than in the lungs, bacilli 
from old, caseated bronchial glands being released by solvent substances 
reaching them from the lungs by way of the lymph vessels, (b) It also 
occurs as a fresh tuberculosis developing upon a bronchopneumonia. 
Croupous pneumonia is as infrequent as pleurisy, which is in most cases 
secondary to lobular pneumonic foci. 

4. Cardiac Symptoms. — Accidental bruits may be heard. Toxemia 
exceptionally causes myocardial degeneration. 



PLATE IX 



FIG. 1 



FIG. 2 





FIG. 3 



FIG. 4 




The Pathognomonic Sign of Measles (Koplik's Spots). 

Fig. 1. — The discrete measles spots on the buccal or labial mucous membrane, showing 
the isolated rose-red spot, with the minute bluish-white centre, on the normally colored 
mucous membrane. 

Fig. 2. — Shows the partially diffuse eruption on the mucous membrane of the cheeks and 
lips; patches of pale pink interspersed among rose-red patches, the latter showing numerous 
pale bluish-white spots. 

Fig. 3. — The appearance of the buccal or labial mucous membrane when the measles 
spots completely coalesce and give a diffuse redness, with the myriads of bluish-white specks. 
The exanthem on the skin is at this time generally fully developed. 

Fig. 4. — Aphthous stomatitis apt to be mistaken for measles spots. Mucous membrane 
normal in hue. Minute yellow points are surrounded by a red area. Always discrete. 



MEASLES 



273 



5. Digestive Tract. — The tongue is coated. There is thirst, and 
aphthae and stomatitis may be observed. Diarrhea, mucus in the stools 
and, anatomically, swelling of Peyer's patches, have been described. 
The liver is seldom swollen. 

6. Nervous System. — Delirium, coma or convulsions in rare cases, 
result from severe toxemia, though even the delicate nervous system of 
children is seldom involved in measles. Nervous symptoms in protracted 
pneumonia, may arouse suspicion of miliary tuberculosis or tuberculous 
meningitis. 

7. Genitourinary JTract. — Acetonuria and albuminuria are fre- 
quent. Ehrlich's diazo reaction occurs in 75 to 100 per cent, of cases. 
Nephritis is very uncommon; gangrene of the genitalia has been observed. 

Differentiation from German Measles and Scarlatina. 



German measles. 



Incubation; 14 to 21 days. 
Prodromes; absent, short or 

light. 
Invasion; very mild. 



Exanthem ; the rash is the first 
symptom, usually appear- 
ing on the first or second 
day on the face; as small 
red dots, rosy and brighter 
than in measles; small, 
little elevated, and thick 
about the mouth. They 
do not fuse. Less crescentic 
than in measles. 

Enanthem; may be diffuse 
redness of throat and con- 
junctivae. 



Glands; usually enlarged, 
hard, tender, especially 
posterior cervical, also 
axillary and inguinal. 
Spleen somewhat enlarged. 

Constitutional symptoms; 

few; no depression; no 
leukocytosis; little pulse 
increase and fever. 



Complications; 
none. 



practically 



Convalescence; rapid; des- 
quamation rarely copious, 
and always fine. 

18 



Scarlatina. 



2 (1 to 7) days. 

Brief, a few hours to 1 or 1 J 
days. 

Sudden, stormy, vomiting, 
convulsions, angina, and 
adenitis. 

Appears on first or second 
day, reaching a maximum 
on second to fourth day, 
first below clavicles, in- 
volving face later; dusky 
red, diffuse, burning, leav- 
ing mouth and eyes free. 



Angina proportionate to 
skin eruption; dusky red; 
tonsillar plugs; conjunc- 
tivae, bronchi, intestines 
usually intact. 

Proportionate to angina, 
hence largely cervical. 
Enlarged spleen. 



Much depression with rash, 
coated tongue with peel- 
ing on the fourth day 
(strawberry tongue) ; fever 
105° to 106°; pulse in- 
creased more than fever; 
lysis on seventh day ; poly- 
nuclear leukocytosis; 
eosinophilia. 

Nephritis, arthritis, endo- 
carditis, sepsis, periaden- 
itis. Diazo in 10 per cent. 

Prolonged ; tardy ; desqua- 
mation copious and usually 
in shreds (hands and feet). 



Measles. 



9 to 10 days. 

3 to 4 days, generally mark- 
edly catarrhal. 
Catarrhal symptoms. 



Occurs on fourth day, great- 
est on fifth or sixth day 
on the face, forehead, and 
about the mouth; biick- 
red, elevated papules or 
crescentic islets of erup- 
tion, always with areas of 
healthy skin between. 



Koplik's spots; patchy red- 
ness of throat; photo- 
phobia; conjunctivitis, 
marked bronchitis, very 
often bronchopneumonia ; 
diarrhea in some cases. 

Mostly at angle of jaw; 
rarely systematic enlarge- 
ment. No enlargement 
of spleen. 

Depression, coated tongue, 
anorexia; fever-curve with 
two elevations; crisis on 
seventh day; no leuko- 
cytosis. No eosinophilia. 



Catarrhal pneumonia, pleu- 
risy, tuberculosis. Diazo 
in 75 per cent. 

Often prolonged ; desqua- 
mation rarely copious and 
always fine. 



274 INFECTIONS OF DOUBTFUL ETIOLOGY 

8. Other Symptoms. —The spleen and lymph nodes are but slightly 
swollen; bone and joint complications and keratitis are infrequent; 
otitis media occurs in a small percentage of cases. There is a relative 
lymphocytosis, with an absolute leukopenia. 

Diagnosis. — The diagnosis depends upon the consideration of all the 
symptoms (coryza, cough, fever, enanthem) rather than of the eruption 
alone. Differentiation from typhus is made by the greater general dis- 
turbance in typhus, its more violent onset and the roseolous eruption 
becoming petechial. 

Sepsis with a morbilliform exanthem, influenza, syphilis and variola 
(q. v.) sometimes delay the early diagnosis. In the drug eruptions of 
turpentine, iodide, quinine, chloral, cubebs, copaiba and antipyrin, the 
fever, Koplik's spots, catarrh, and central elevations in the eruption 
are indicative of measles (see page 273). 

Prognosis. — The mortality is very great among aboriginal races; in 
the Fiji Islands 140,000 died out of a population of 160,000. The usual 
prognostics are: (a) The genus epidemicus: The mortality may be 30 
to 37 per cent, in certain epidemics; or as in a German epidemic of 
2881 cases, only 1 per cent. (b) Individual resistance: It is higher in 
institutional practice and is 16 per cent, in the children's hospitals, as 
against 3 per cent, in private practice. Measles ranks third among the 
exanthemata in mortality, (c) Age: 55 per cent, of fatal cases occur 
in the first two years of life, (d) Complications are more important 
than the disease itself, e. g., tuberculosis and bronchopneumonia, which 
is the worst complication, with a mortality of 33 per cent. 

Treatment. — 1. Prophylaxis is important, especially in weakly chil- 
dren under two years, in severe epidemics with pneumonia and in cases 
of pertussis. It is of no advantage for the young to contract measles, 
and the prevalent practise of allowing the disease to run through the 
family must be condemned. The secretions from the nose, throat and 
bronchi must be disinfected, and general sanitary care should be exercised 
as in smallpox (q. v.) and scarlatina; quarantine is maintained for ten 
days after the onset. 

2. Hygiene. — The patient should have fresh air, warm quarters, rest 
in bed until after desquamation, and a liquid diet. 

3. Catarrhal Symptoms. — Photophobia does not necessitate a dark 
room; a boric acid solution should be dropped frequently into the eyes 
and vaseline applied to the lids. To relieve pain in the ears, belladonna, 
opium and a 1 per cent, cocaine solution may be used; paracentesis is 
indicated for gathering. The nose should be douched with Dobell's 
solution. Tr. belladonnse, Nlj-iij, may be given every two hours for 
coryza until flushing of the face, increase of pulse-rate, or a dry red 
throat develops. 

4. Antipyresis. — In high fever with cerebral toxemia and diffuse 
bronchitis or pneumonia, baths are most efficacious with cold affusions 
to the head and neck; wine, mustard plasters and laxatives may also be 
indicated. 

5. The Circulation. — The heart rarely requires support except in 
pneumonia (q. v.), when camphor, aromatic spirits of ammonia, strych- 
nine, or coffee is indicated. (See dosage table, page 269.) 



RUBELLA 275 

6. Respiratory Symptoms. — Care of the mouth, a soft or liquid diet, 
inhalations of steam, hot fomentations over the larynx, warm baths 
and possibly intubation or tracheotomy, are indicated for laryngeal 
complications. Bronchitis should be treated with ipecac, codeine, 
inhalations of steam, massive hot packs to the chest, and cold affusions 
over the nape of the neck. (See Acute Bronchitis.) 

7. Alimentary Tract. — Enemata relieve constipation. When diarrhea 
is excessive, opium, hot wine or cognac, demulcents, hot applications, and 
physiological salt solution by rectum, are indicated. 

8. The Skin. — The skin should be rubbed with olive oil; a 2 per cent, 
menthol salve, or 1 per cent, carbolic solution, relieves itching. 

RUBELLA. 

Synonyms. — Rubeola notha, German measles, Rotheln. By the 
Germans it is called rubeola, though we employ rubeola as synonymous 
with measles. 

History. — Rubella was first described by Bergen (1752) and its existence 
as an independent infection was established by Maton (1815). It is more 
often confused with atypical scarlatina than with atypical measles. 

Etiology. — Its etiology is not known. Most cases occur during the 
first half of the year. The disease most frequently attacks children. 

Symptoms. — 1. Incubation. — The incubation lasts from ten to twelve 
(perhaps fourteen to twenty-one) days. 

2. Prodromes. — Prodromes are usually lacking; for a period of two 
hours to a day, there may be cough, photophobia, sneezing, slight tem- 
perature, chilliness or headache. 

3. Eruption. — The eruption appears, as the first symptom of the 
disease, on the first day, usually in the palate and throat, and consists 
of hyperemic punctate red spots (Forchheimer's spots). The skin is red, 
and the spots, which are more rosy than in measles, disappear at first 
under pressure, then become darker and more circumscribed; later, the 
eruption does not entirely disappear under pressure. The eruption does 
not fuse as in measles, and erythema is not present about the points of 
eruption as in scarlatina. It advances in " jumps," and fades in one 
place while it blossoms in another. It appears first on the scalp and 
face, and progresses downward to the neck, body (where the eruption is 
greatest), arms and lastly to the legs and feet. Unlike scarlatina, spots 
are aggregated about the mouth. Its average duration is from two to 
four days. The papilla? of the tongue show slightly through the fur. 
Desquamation is minimal and fine. Almost characteristic is the swelling 
of the posterior cervical and postauricular glands. There may be some 
angina, dysphagia, anorexia, tracheitis or, rarely, bronchitis. 

4. Constitutional Symptoms. — The fever is usually slight, runs 
three days, and falls when the eruption matures. Except in a few 
American epidemics, urgent nervous and other complications, such as 
icterus, albuminuria, nephritis or colitis, have rarely been observed. 

Diagnosis. — The diagnosis is often difficult and the unity of the disease 
is sometimes questioned. The "fourth disease" of Dukes cannot be 



276 INFECTIONS OF DOUBTFUL ETIOLOGY 

admitted to our nosology. Erythema infectiosum, emphasized by Esche- 
rich, is a weakly contagious, maculopapular erythema, prevalent in 
the spring and fall, and occurring chiefly on the extremities, and rarely 
on the trunk (v. page 273). 

Prognosis. — The prognosis is good, and therapy is symptomatic. Isola- 
tion is theoretically advisable. 

TYPHUS FEVER. 

Synonyms. — Typhus fever; exanthematous typhus; war, prison, ship 
or famine fever. 

Definition. — An acute, highly contagious, specific infection, with a 
sudden onset and a high cyclic temperature, falling by crisis, a character- 
istic eruption, and severe nervous symptoms. 

Etiology. — All stages of the disease are highly contagious. Infection 
is usually direct from person to person. The danger to attending nurses 
and physicians is great. The more intimate the contact the greater is 
the danger of direct infection. It is communicable indirectly by a third 
person, fomites and fleas. 

Nicolle, Ricketts, Anderson and Goldberger inoculated monkeys and 
noted that infection from animal to animal occurred by the body louse. 
The bacteriology of typhus is undetermined. 

Geogeaphy. — Ireland, Russia, Galatia, Hungary, Italy, Asia Minor 
and Mexico are its most frequent homes. It is endemic in Berlin among 
the lower classes and vagabonds. Typhus was one of the greatest 
scourges of the middle ages, with its wars and famines, but it has decreased 
in the past century, the epidemics in Ireland (1817 and 1846), in the 
Turko-Russian war (1877-78) and the present European war being the 
last general outbreaks. Its most recent occurrence in this country was in 
New York (1881-82 and 1893), in Philadelphia (1883), and in Baltimore 
in 1901. 

Age. — Most cases occur between the fifteenth and twenty-fifth 
years. 

General Clinical Picture. — 1. The incubation lasts twelve days or less, 
usually without symptoms. 

2. The invasion is sudden, exhibiting chills and high temperature on 
the first day. Thirst follows, with vomiting, epigastric oppression, 
suffusion of the face, conjunctivas, nose and pharynx, delirium, backache, 
severe pains in the extremities, rapid pulse, and splenic intumescence. 

3. On the third or fifth day a pale red and purely hyperemic roseolous 
eruption develops, first on the abdomen and chest, extending rapidly to 
the back and extremities. The eruption then becomes petechial, with 
some serous infiltration in the flecks, which become dirty and copper- 
colored. It lasts seven to ten days. Pain is succeeded by apathy, 
prostration, delirium or mania. The tongue and mouth are dry and dark. 
Catarrhal inflammations of the pharynx, larynx and bronchi develop, 
with hoarseness and cough. The fever is continuous. Coma-vigil, 
rapid respiration and pulse, and hypostatic pneumonia may end the 
course. 



TYPHUS FEVER 277 

4. A crisis occurs on the tenth day. The pulse becomes slower; the 
skin often desquamates in dusky scales; profuse sweats are common; and 
convalescence is established in two weeks. 

Special Symptomatology. — 1. Fevek. — After a rigor, the temperature 
rapidly rises to 103°, 105° or even 107°, being highest on the fifth day. 
No other acute exanthematous disease produces an equally high, early 
temperature. On the tenth day it remits, except in severe cases, usually 
with a crisis in two or three days. Death occurs with a preagonal rise 
or with collapse temperature. 

2. The Skin. — The eruption consists of two elements: Roseola? 
changing to petechia?, and a dusky red mottling under the skin. The 
roseola are seen on the third or the fifth day, increase rapidly though 
never in recurrent crops, are located chiefly on the lower abdomen, chest, 
back or shoulders, are least abundant on the thighs, and do not appear 
on the face except in women and children whose skin is delicate. The 
palms and soles are exempt. The hyperemic roseola? are pale red, washed 
in outline, round or oval, the size of a pin-head or a lentil, and disappear 
on pressure. They are easily overlooked at night. They last one to 
three days, later becoming livid, copper-colored petechia persisting on 
pressure and after death, because hemorrhagic. The petechia? occur 
mostly on the back or in the groins. The hemorrhage may extend more 
widely into the skin or subcutaneous tissue. Many petechia? are ominous, 
especially in cachectic and alcoholic subjects. A morbilliform eruption 
on the arms and legs is occasionally observed before the usual typhus 
rash, especially in thin-skinned individuals. The skin is usually dry, 
but miliaria appear in 10 per cent, of cases, notably in the young. Icterus 
without decolorization of the stools is a frequent and unfavorable sign. 
Desquamation is sometimes profuse; herpes occurs in 12 and bed-sores 
in 3 per cent, of cases. The skin has a peculiarly pungent, offensive 
odor. 

3. The Nervous System. — Toxemia is profound. Headache is con- 
stant until the exanthem appears; it is usually frontal and temporal 
and radiates into the neck or shoulders. It is associated with vertigo, 
backache and hyperesthesia of the fingers and toes. The sensorium first 
shows depression, apathy, insomnia, incoherent speech or disturbing 
dreams, which increase as the pains disappear. In the second week coma- 
vigil, low delirium, mania and hallucinations, involuntary evacuations 
and noisy cerebral respiration often develop. Tremor of the forearms 
and hands is almost constant. Convulsions are rare, but ominous, 
chiefly in alcoholic subjects and children. Paraplegia and aphasia are 
recorded. 

Special Senses. — There is conjunctival catarrh and the " pin-head 
pupil" of Graves. The ears are involved in 32 per cent, of cases. 

4. Circulation. — The heart and vasomotor system suffer greatly. 
The pulse is small and reaches 100 to 120, or more. It is slow only in 
light cases. Acute myocarditis may occur with acute dilatation 
(v. Typhoid). In fatal cases the heart muscle is granular and deep red. 
The blood is dark and fluid; the red cells and hemoglobin are decreased, 
and the white cells are increased. 



278 INFECTIONS OF DOUBTFUL ETIOLOGY 

5. Respiration. — Bronchitis and tracheitis are present at the onset, 
increase with the fever and are evidenced by cough and slight expec- 
toration; and with weak heart result in hypostasis and lobular pneu- 
monia. Pneumonia occurs in 15 per cent, of typhus cases, usually in 
the second week and is frequently atypical. 

6. Gastrointestinal Tract. — The tongue, at first moist and white, 
becomes dry and dark — the "parrot tongue." Nausea and vomiting 
are common, but meteorism is infrequent. The epigastrium only- is 
tender. The liver is swollen, soft and grayish. There is constipation 
in 90 per cent, of cases; diarrhea may appear at the crisis. Gastro- 
intestinal hemorrhage, a hemorrhagic diathesis, parotitis, ulceration of 
the esophagus and pharynx, and phlegmons are infrequent. 

7. Genitourinary Tract. — The urine is febrile. The urea is 
increased. Albumin frequently appears in the second week. Nephritis 
(in 6 per cent.) is dangerous. Uremia and hematuria are rare. The 
urine frequently shows the diazo reaction. 

8. Spleen and Glands. — An early splenic tumor is palpable in 50 
per cent, and disappears in the second week. The splenic pulp is fluid. 
Rupture has been described. Lymphadenitis was noted during the 
Crimean and Turko-Russian epidemics. 

Anomalous Courses. — Light forms run a course of six to ten days, 
with less fever, fewer nervous symptoms, and less rapid pulse, and 
include the abortive type without eruption, and the ambulatory type. 
Very severe forms are the hyperpyretic (fatal in two to three days), or 
the adynamic. 

" Brill's Disease." In 1910 W. E. Brill, of New York, described 
a febrile affection characterized by: (i) a short incubation of 4-5 days; 
(ii) brusque onset; (iii) chills, intense headache, and a facies expressing 
pain and apathy; (iv) fever, which rises suddenly, reaching 103-104° 
on the third or fourth day and continuing until the eleventh to fourteenth 
day when it falls by crisis ; (v) an eruption, developing on the sixth day, 
which is maculopapular, dark red, and does not disappear on pressure 
nor appear in crops; and (vi) by negative Widal reaction, blood cultures 
and at autopsy, by the absence of typhoid lesions. The pulse runs 
86-100 and the white cells average 11,000. Anderson's and Goldberger's 
immunity experiments identify the disease with European typhus and 
the Mexican type — Tabardillo, in investigating which Howard Ricketts 
lost his life. The Manchurian typhus is mild like Brill's disease, but 
Tabardillo is virulent. Brill's type has been found in most of our larger 
cities. 

Differentiation. — This is not difficult if the case is seen from beginning 
to end, or during an epidemic. There. are no absolute pathological or 
bacteriological criteria. Mistakes in the diagnosis of sporadic cases 
are often inevitable. In the initial stage only a probable diagnosis can 
be made. 

In smallpox the initial scarlatiniform eruption in the angles of the 
arms and groins is characteristic. Morbilliform eruptions occur in both. 
Smallpox invades the face more than does typhus, and the relation 
of the eruption to the temperature remission is not observed in typhus. 



EPIDEMIC PAROTITIS 279 

Even at postmortem examinations, differentiation between the hemor- 
rhagic form of typhus and purpura variolosa is frequently impossible. 

Typhus. Typhoid. 

Invasion: sudden; chill, coryza. Slower and more gradual; no coryza. 

Roseola: more numerous and earlier, second Usually less points of eruption (are excep- 

to fifth day. tions, e. g., measles-like) ; on extremities, 

as in Franco-German war. 

Never in crops. • In successive crops. 

Distribution on body and extremities. On body; rarely on extremities. 

Sparingly on face. Almost never on face. 

Flat, pale, washed, hyperemic, not disap- Papular, pink, sharply outlined, always 

pearing upon pressure when they become hyperemic, disappearing upon pressure. 

petechial. 

Course: more rapid. Slower. 

Face and eyes injected. Paler; conjunctivitis rare. 

Fever: abrupt rise, higher, less remission, Slow rise and regular stages. 

if any; shorter; crisis, or short lysis, on 

fourteenth day. 

Soon bed-ridden. Oftener ambulatory. 

Earlier and severer nervous symptoms. Second week or later, and less severe. 

Pulse: rapid and not dicrotic. Dicrotism and slowness. 

Spleen: early swelling, but less frequent. Later, but lasts longer; more frequent. 

Less meteorism. Meteorism. 

Stools: not characteristic. Ochre stools. 

Blood: leukocytosis. Leukopenia, Widal reaction; bacteria in 

blood, urine, roseolse. 
Diazo reaction in both. 

Prognosis. — The prognosis depends upon the intensity of the toxemia 
and the complications — especially pneumonia. Death from toxemia 
usually occurs in the second week; from pneumonia in the third week. 
The mortality varies between 6 and 20 per cent., but reaches 50 per 
cent, in virulent epidemics and in patients over fifty years of age. 

Treatment. — The treatment is that of typhoid, with the added indica- 
tion of strict isolation. Open-air treatment in tents is indicated, with 
thorough disinfection of everything coming in contact with the patient. 
Cardiac stimulants are often required. Tr. iodi, Tfl,iv, t. i. d., appears 
to be beneficial. 

EPIDEMIC PAROTITIS (MUMPS). 

Definition. — An acute specific infection, characterized by a primary 
inflammation of the parotid glands. 

History. — Hippocrates described every essential of mumps, but later 
it was confused with other parotitides. 

Etiology. — (a) Its cause is unknown, (b) Most cases occur between 
six and fifteen years of age; isolated cases are seen in adults, (c) Most 
cases occur in the cold, moist, spring months, (d) Contagion is more 
frequently direct — perhaps before parotitis sets in — from person to 
person, than indirect, (e) It prevails largely in epidemics. Immunity 
is usually conferred by one attack, yet Catrin observed recurrence in 
6 per cent. 

Symptoms. — After an incubation of two or three weeks, the disease 
begins with fever (101° or even 104°), and in two days parotid intumes- 
cence and pain. The severity of certain epidemics determines such severe 



280 INFECTIONS OF DOUBTFUL ETIOLOGY 

initial symptoms as vomiting or convulsions in children; or a typhoidal 
condition in adults. The characteristic parotitis is clearly inflammatory — 
swelling, pain, temperature and interference in function. It is bilateral; 
Bouchoud said "Mumps have no singular;" in rare epidemics the paro- 
titis is unilateral. In the early unilateral involvement, the face inclines 
to the affected side to relax the swollen tissues; in the later bilateral 
parotitis, the head is often bent forward to the same end. We know 
little of its pathology beyond what Virchow described — hyperemia of 
the parenchyma, interstitial swelling, catarrhal secretion in the ducts 
and contiguous lymphadenitis. The swelling about the gland may 
reach the eyelids, forehead, mastoid region or even the clavicle, effacing 
the features and even invading the pharynx and larynx; it is due less 
to periparotitis than to pressure on the facial and other veins. It is 
soft and does not pit. Compression of the masticatory muscles by the 
swollen glands makes opening the mouth difficult; chewing elicits pain 
because it excites salivary secretion which often cannot pass the turgid 
ducts. Compression of the Eustachian tube or external meatus may 
occasion tinnitus. The salivary secretion may be normal, increased or 
decreased. Suppuration is due to mixed infection. Wile maintains 
that a lymphocytosis of over 50 per cent, is pathognomonic. 

In severe cases the submaxillary and sublingual glands are swollen 
(in 50 per cent, of some epidemics); they may be the sole seat of the 
disease. The parotitic swelling reaches its acme within four days and 
an equal period is necessary for its subsidence. The fever is remittent 
or intermittent, and falls by lysis. 

Complications and Sequels. — 1. The most important are metastatic 
orchitis and epididymitis, described by Hippocrates. In about a week 
fever returns (102° to 105°). Swelling, redness and pain in the testicle 
develop, often accompanied by general symptoms. In some epidemics, 
orchitis precedes or even occurs without parotitis. Urethritis is some- 
times observed, analogous to the catarrh of the parotid duct. Testicular 
localization occurs in the sexually active testis, whence its rarity in 
children or the aged. Comby observed it in 30 per cent, of mumps 
among French soldiers. Orchitis or epididymitis is usually unilateral. 
Testicular atrophy occurs in 50 per cent, and if bilateral may occasion 
sterility. In women, ovaritis and vulvovaginitis are infrequent. Mastitis 
is rather more frequent, and may also be observed in men and bo\ T s. 

2. Other glandular organs. Of these the lachrymal glands are most 
often affected, then the thyroid, with acute Graves's disease, pancreas, 
thymus and spleen. 

3. Other complications are very rare. These are meningitis, otitis, 
polyneuritis, optic neuritis, endocarditis, nephritis, bronchopneumonia; 
suppuration or gangrene of the parotid or testis. 

Diagnosis. — Osteomyelitis of the jaw, periostitis, lymphadenitis, jugular 
thrombophlebitis and furuncle should, be excluded. Epidemic parotitis 
must not be confused with secondary parotitis, which results from trauma, 
or pus burrowing from the middle ear, or with mercurial, iodide or lead 
parotitis, and purulent metastasis in typhoid, pneumonia and erysipelas, 
iu which the pyogenic virus enters by the ducts or settles from the blood 



ACUTE ARTICULAR RHEUMATISM 281 

current. In postoperative parotitis, after laparotomy, trauma to the 
gland, from holding up the jaw, may promote infection. 

Prognosis. — The prognosis is good; but 7 deaths occurred in 58,331 
cases. The course is lighter in children than adults. 

Treatment. — The fever is controlled as in other fevers, and diet, isola- 
tion, hygiene and rest abed for ten days are the same. Pain often 
necessitates the use of opiates. The local parotid or testicular inflam- 
mation is self-limited, and resists all attempts at abortion or mitigation. 
Local heat is soothing and better tolerated than the ice-bag. Complica- 
tions are treated symptomatically . 

ACUTE ARTICULAR RHEUMATISM (RHEUMATIC FEVER). 

Definition. — An acute, febrile, non-contagious disease, with multiple 
articular involvement and with a tendency to heart complications. 

Etiology. — Rheumatism is an acute infection, as evidenced by its 
occasional epidemiology; its tendency to recur like pneumonia and 
erysipelas; the autopsy findings of exudation, hemorrhage, cloudy 
swelling and acute splenic tumor; the frequency with which an atrium 
may be observed, such as an angina, and its indubitable affiliation with 
endocarditis, whose mycotic origin is established. The virus is unknown; 
Schottmuller's Streptococcus viridans, Horder's saprophytic strepto- 
coccus and other streptococcoid organisms are under suspicion. 

Common symptoms occur in rheumatism and septicopyemia — tem- 
perature, anemia, articular metastases, endocarditis, leukocytosis and 
peptonuria. Some explain the presence of organisms by bacterial inva- 
sion during the death agony, since bacteria are seldom obtained by 
aspiration of the joints during life. 

Predisposing Factors. — 75 per cent, of cases occur in the first half 
of the year; heredity is conspicuous in 25 per cent.; 70 per cent, occur 
in males. The greatest susceptibility exists between ten and thirty 
years (50 per cent.); M. Miller collected 19 cases in nurslings. Trauma, 
overexertion, exposure and occupation account for its frequency in 
sailors, divers, bakers and laborers. Rheumatism constitutes 2 per 
cent, of American hospital admissions, as against 3 to 7 per cent, in 
London hospitals. 

Acute articular rheumatism was described by Boerhaave, who suffered 
from the disease, and elaborated by his pupil, Van Swieten. Sydenham 
gave an admirable account. 

General Clinical Picture and Course. — The onset is sudden, with mod- 
erate fever, prostration, drenching sweats and polyarthritis. The joints 
are involved in succession, the inflammation lasting a few days in one joint 
and then passing to many others. In adults and adolescents there is febrile 
urine, constipation, conjunctival injection, coated, moist tongue, irritability, 
restlessness, and fever which revives as fresh joints are involved. There 
is marked anemia and loss of weight. If endocarditis occurs, valvular 
disease is the usual sequence. The usual duration without therapy is 
three or four weeks. Recovery is usual, but death may result from 
hyperpyrexia and toxemia. Recurrence and a family tendency to rheu- 



282 INFECTIONS OF DOUBTFUL ETIOLOGY 

matism and valvular lesions are noted. The articular disease is directly 
influenced by the salicylates, cardiac localizations much less so. 

Symptoms in Detail. — 1. Prodromal Symptoms. — Regarding the 
angina or tonsillitis (12 per cent.), there are two conceptions: (a) that 
the angina is primary and rheumatic, and (b) that the arthritis following 
angina is pseudorheumatism (polyarthritis anginosa), characterized by 
exanthems, occurring chiefly in the arms and reacting poorly to salicy- 
lates. Other possible prodromes are laryngitis, chorea, erythema nodo- 
sum, albuminuria or gastro-enteritis. 

2. Polyarthritis. — (a) Localization. — The most frequently involved 
joints are those of the lower extremity, particularly the knee (70 per 
cent.); usually one side is affected after the other; the ankles, elbows 
and wrists are next most frequently affected. Rheumatism may early 
involve the smaller articulations, such as the carpus — thought by Trous- 
seau to promote endocarditis; it also may invade the spine, jaw, sterno- 
clavicular joints, synchondroses of the ribs, sacro-iliac or pubic articula- 
tions and the larynx. Rheumatism may be localized by the occupation, 
e. g., in the arms of washerwomen. If a joint of an upper extremity is 
first involved, the opposite arm is usually next inflamed, (b) In general 
the arthritis is ascending and invariably polyarticular; Van Swieten 
spoke of it as " migratory inflammation" or "fleeting gout." Persistency 
in one joint always suggests pseudorheumatism (symptomatic or sec- 
ondary forms), (c) Signs and symptoms: Polyarthritis is a better term 
than polysynov ( itis because the inflammation pervades all structures 
of the joint, the periarticular bursse, cellular tissue, muscular insertions 
and tendons — indeed, the external edema is usually greater than the 
synovial effusion. The joints are swollen, red, tender and painful. 
Pain is the most prominent and frequent articular finding. Lasegue 
attributes pain to inflammation in the associated muscles and tendons, 
affirming that if these be suitably supported the joint can be moved 
freely (Lasegue's phenomenon). The contiguous tendon reflexes are 
lessened or abolished, (d) Duration: The inflammation remains in 
one joint from one to eight days, seldom longer, and its involution is 
shorter than its evolution, (e) Sequels: The joints become normal, 
and ankylosis reflects doubt upon a previous diagnosis of rheumatism. 
Suppuration results only from a most infrequent mixed infection. 

3. Temperature. — The fever is directly related to the intensity of 
infection, the number of articulations involved, and to the development 
and progression of visceral complications. As Wunderlich noted, it is 
usually highest when the patient is first examined. The fever curve is 
in nowise cyclic and rarely exceeds 102° or 104°. The fever rises with 
each new localization, be it arthritic, endocarditic or pericarditic. The 
temperature drops when the sweats occur, and averages ten days. The 
fever is longer when treatment is commenced late. Kahler held that 
fever could occur independently of joint inflammation (febris rheu- 
matica). Simple fixation of the joints reduces the fever, tachycardia and 
tachypnea. Chills suggest septicopyemia rather than rheumatism. 
Hyperpyrexia is exceptional; with Dr. Lackner, the writer saw a patient 
with a fever of 112° who recovered. Severe nervous symptoms, coma, 



ACUTE ARTICULAR RHEUMATISM 283 

convulsions, rapid pulse, transitory paralysis, stertorous breathing and 
hyperpyrexia constitute "cerebral rheumatism;" it is less frequent since 
the introduction of the salicylates. The pulse exceeds 100. The respira- 
tion follows the fever. 

4. Heart Complications. — These are an integral part of rheuma- 
tism and constitute visceral as distinguished from articular rheumatism. 
Heredity seems to be a factor in certain cases. Heart lesions occur 
as frequently in light as in severe forms. They are most frequent and 
most dangerous at puberty and increase in frequency with repeated 
attacks of rheumatism. Lasegue says "Acute rheumatism licks the 
joints, pleura and even the meninges, but it bites the heart." 

1. Endocarditis. — This, the most vital complication, was first described 
by Pitcairn (1788). Bouillaud (1832) held that in every severe rheuma- 
tism, endocarditis was the rule. The frequency of endocarditis is about 
20 per cent. Mackenzie finds endocarditis in 58 per cent, of first attacks, 
63 per cent, of second attacks and 71 per cent, of third attacks. We 
might divide McCrae's series into thirds; in one third the heart is nor- 
mal; in another third, it is doubtful; and in the last third, it is diseased. 
Hospital statistics, however, represent the severest cases. Clinically, 
endocarditis often escapes recognition and is found more frequently at 
the autopsy table than at the bedside. It is usually verrucose, and 
rarely ulcerative even in the fatal cases. To be certain that an endo- 
carditis exists, two points are absolutely necessary: (a) Continued 
observation after convalescence; and (6) attention to signs of valvular 
disease other than the murmur, such as dilatation, hypertrophy, etc. 
Therapeutically we must protect the patient and ourselves by keeping 
him sufficiently long in bed. We may interpret the disappearance of a 
murmur in two ways: first, as the disappearance of a functional mur- 
mur; or, second, as the healing of a slight endocarditis, always the less 
probable issue. 

Valves Affected. — The mitral valve is involved in 95 per. cent, of the 
cases, the aortic in 23 per cent., and both valves in 18 per cent. The 
fever of fresh or recurrent endocarditis may be continuous with that of 
the arthritis but is often higher. A patient with an old valvular lesion 
and recent temperature more often has recurrent endocarditis than 
malaria, pyemia or tuberculosis, which are commonly confused with 
endocarditis. Endocarditis exceptionally antedates the polyarthritis. 

Masked or atypical rheumatism embraces rheumatism masquerading 
under the guise of an endocarditis or trifacial neuralgia and yielding to 
salicylate treatment. Rheumatic pericarditis or endocarditis rarely 
occurs without arthritis — polyarthritis rheumatica sine arthritide — the 
rheumatic equivalent. 

2. Pericarditis. — Rheumatism explains more cases of pericarditis 
than all other causes combined. Its frequency is given as 5 to 10 per 
cent. In children, especially, a subacute or latent course is most com- 
mon. Baginsky found that adhesive pericarditis was the most common 
autopsy finding in rheumatic children. 

3. Myocarditis. — Disturbance of the heart in the acute stage is myo- 
cardial and toxic or mycotic. Some dilatation occurs in everv case. 



284 INFECTIONS OF DOUBTFUL ETIOLOGY 

Acute interstitial myocarditis 1 (in 28 per cent.), coronary disease and 
myocardial invasion by contiguity from endocarditis in the later stages 
are possible causes. Recovery is more common than chronic fibrous 
myocarditis. Myocarditis may cause sudden heart pain with weakness 
— the " heart rheumatism" of the laity — or transient palpitation, cardiac 
oppression, tachycardia or bradycardia. 

The right heart may be dilated as in other fevers, but it disappears 
with convalescence. When accompanied by a murmur it may lead to 
an incorrect diagnosis of endocarditis. French writers describe an acute 
arteritis with severe pain over the artery and pain over its smaller 
branches in the extremities; pathologically only part of the vessel wall 
is affected and healing usually follows; gangrene may follow complete 
arterial occlusion. Endophlebitis is more common. 

5. Skin. — Sweating is most profuse, constant and characteristic; its 
odor is sour or mouse-like. The skin is frequently macerated and 
sudamina alba or rubra are common. Rheumatic nodes are subcutane- 
ous, as large as buckshot, on the fingers, hands, wrists, elbows and 
spine and are aggregations of round or spindle cells; their structure is 
identical with that of endocarditic vegetations. They may appear 
during or after an attack, or independently of acute seizures. They 
sometimes number even sixty and are symmetrical, hard and usually 
tender. Nodes occur most often in chronic cases or in 88 per cent., with 
severe endocarditis or pericarditis. If very numerous or large they 
indicate an unfavorable prognosis. Hillebrecht collected 80 cases in 
children under fifteen years and 37 cases in adults. In contradistinction 
to these fixed nodosities, Fereol has described more fugitive and less 
indurated nodes (nodosities cutanees ephemeres). Erythema polymor- 
phum is regarded as an independent affection but in rheumatism the 
nodose form may occur. Some eruptions are septic or anginose. Pur- 
puric eruptions are not uncommon. 

6. Muscles and Bones. — Myositis is infrequent, though myalgia is 
common. Muscular atrophy may follow inflammatory extension from 
the joints to the muscles. "Muscle scars" are much more often due to 
trauma or other infections than to rheumatism. Some cases of albuminous 
periostitis are clearly rheumatic. 

7. Respiratory Tract. — Laryngitis may be the atrium for rheu- 
matic invasion, or may occur later as diffuse catarrh or local nodes. 
The rare acute edema of the larynx is very dangerous. Pleurisy may 
result from rheumatic or secondary infection (in 2 per cent.). Pleurisy 
is found in 54 per cent, of cases of endopericarditis. The so-called rheu- 
matic pleurisy (q. v.) is almost always tuberculous. Pneumonia occurs 
in but 1 per cent, of cases of rheumatism not involving the heart, and in 
66 per cent, of cases with endopericarditis. Most so-called pneumonias 

1 Romberg, Bret, Aschoff and Tawara describe nodules in the heart as rheumatic myo- 
carditis; their specificity is disputed but all observers found them. They are perivascular, 
subendocardial nodules containing large cells and giant cells, and surrounded by a zone of 
lymphoid elements, plasma cells, and fibroblastic cells. The adjacent muscle bundles 
suffer from pressure, so that functional heart disturbance may result. They tend to cicatri- 
zation. The same heart nodes have been observed in streptococcic sore throat. 



ACUTE ARTICULAR RHEUMATISM 285 

are pulmonary infarction, stasis or compression from pleural or pericardial 
exudates. 

8. Digestive Tkact. — Angina or tonsillitis occurs chiefly as a pro- 
drome (v. s.). The tongue is coated, and moist except in the severest 
cases. Gastric symptoms are rare, though Damash considers them the 
most frequent prodrome. Constipation is the rule. Diarrhea occurs 
as prodromal enteritis or as a rare complication. 

9. Genitourinary Tract. — Albuminuria is transitory, late in the 
course, and mostly after thirty years of age. The percentage ranges 
up to 30. Albumosuria is frequent, especially during resorption. Cylin- 
druria may occur without albuminuria. Renal infarction usually occurs 
late in the course of cardiac cases. Acute nephritis is seldom seen (0.3 
to 1 per cent.) ; it occurs early, chieflv in endopericarditis, and is usually 
benign. But few of the author's cases in private practice show nephritis, 
though it is present in 50 per cent, of hospital patients; it is probably 
latent until awakened by the fresh toxemia and is probably due to 
exposure and alcoholism. Hematoporphyrin has been found and the 
characteristics of fever urine, and reduction of the chlorides. 

10. Blood. — The red disks are reduced 25 per cent. The fever, 
anemia and intensity of articular involvement run more or less parallel. 
The white cells, in moderate cases, range between 10,000 and 15,000, 
and higher figures (20,000) are only reached in extensive endocarditis, 
pericarditis, pleurisy or pneumonia. The increase is in the polymor- 
phonuclear neutrophils . The eosinophiles vanish, but reappear with 
articular improvement; if increased in a florid case, the course will be mild. 

11. Nervous System. — The relation of chorea to rheumatism is 
unsettled; chorea, rheumatism and endocarditis are associated in 50 
per cent, of cases. Cases of chorea with rheumatic or endocarditic asso- 
ciation usually run a slow and often a relapsing course. Cerebral rheuma- 
tism is very infrequent; developing acutely at the acme of the disease, 
with psychical alteration, hyperpyrexia, delirium, convulsions and 
coma, it frequently results in death. High fever may be a cerebral 
symptom, but cerebral symptoms may occur without high temperature. 
The author has seen three recoveries after mania, convulsions, meningeal 
symptoms and coma. Chronic psychoses, hallucinations, mania, melan- 
cholia or convulsions, may occur in convalescence; they are due to 
toxemic inanition and generally terminate in recovery. Brain embolism 
from endocarditis, hemorrhage and rheumatic meningitis are infrequent. 
Spinal rheumatism may be confused with myelitis, multiple neuritis, 
local myopathies adjacent to the joints involved, or cerebral embolism. 
In Kraus's clinic the author saw one fatal case characterized pathologically 
by meningomyelitis. Multiple neuritis may be rheumatic; usually 
following it, neuritis presents the usual characteristics, as pain and 
tenderness over the muscles and nerve trunks, paralysis, muscle atrophy, 
reaction of degeneration, anesthesia and abolished reflexes. The prognosis 
is good in multiple and mononeuritis. 

The Eye. — Rheumatism may result in benign episcleritis, iritis or 
iridocyclitis. Optic neuritis, with or without atrophy, and retinal 
embolism or thrombosis occur exceptionally. 



286 INFECTIONS OF DOUBTFUL ETIOLOGY 

Acute thyroiditis is uncommon. Lymphadenitis is rarely marked. It 
occurs with arthritis, erythemata, endocarditis or pericarditis. 

Prognosis. — The prognosis as to life is excellent and is generally propor- 
tionate to the severity and duration of the infection and the number of 
joints involved. The mortality is 2 per cent, but hospital figures are 
higher than in general practice. The causes of death are hyperpyrexia, 
the most important; cerebral rheumatism, chorea, peri-, endo- and 
myocarditis, pneumonia and lung infarcts. Recurrence: a second attack 
occurs in 25 per cent., a third in 12, a fourth in 4, and five to eight recur- 
rences in 1 per cent. The prognosis is less favorable in children. Salicy- 
late therapy influences the disease, its relapses, and, to some extent, 
the heart complications. At the onset it is impossible to declare the 
case light or severe. Involvement of the small joints of the hands and 
feet presages a severe course. 

Diagnosis. — 1. Rheumatism in Childhood. — In the very young the 
disease is most rare (3 cases in 85,000 nurslings) but becomes more 
common after the fifth year. Heredity is most potent in the young. 
Generally speaking, the joints are less susceptible and the arthritis less 
intense, while the skin, nervous system and heart are more often involved. 
The various phases of rheumatism occur separately — first arthritis, 
then endocarditis, later chorea, subcutaneous nodules, pericarditis and 
so on. The child rarely lies quietly, but tosses about; the tendons and 
fasciae are involved more often than the joints. The pain is less and 
the arthritis may entirely escape recognition. The lower temperature 
is remarkable at this epoch of Jife, when high fever is often excited by 
trivial lesions. There is much less sweating, the urine is more nearly 
normal, and the. anemia is especially marked. The differential possi- 
bilities are acute osteomyelitis (causing monarthritis), pyemia, gonorrheal 
arthritis, Barlow's disease, syphilis and hemophilic joints. Endocarditis 
may not directly follow the polyarthritis, but develops more slowly, 
insidiously, later and twice as frequently as in adults. Watson knew but 
three instances of acute rheumatism, before puberty, which escaped severe 
heart disease. This is due to the greater functional demands on the 
child's heart and to the aorta being narrow at the isthmus. Pericarditis 
occurs later in what Cheadle terms the " rheumatic progression," after 
the valvular lesion has developed, and is almost always found in necrop- 
sies on children with valvular disease. Rheumatic heart disease at this 
epoch leads to greater hypertrophy because of greater nutrition, to more 
marked dilatation because of greater tissue elasticity, and to more 
frequent recurrence. In the diagnosis, functional murmurs are not 
frequent in children. The pulse is often irregular; the precordium more 
readily bulges; and left-sided pleurisy is more frequent. Oppression 
over the heart, pain, cyanosis, dropsy, hepatic congestion, pulmonary 
infarction, dyspnea and fever are infrequent. Rheumatic children are 
more nervous. More marginate, papular and urticarial erythemata and 
more purpura develop in children. Large subcutaneous nodes (rheuma- 
tismus nodosus) are serious prognostically and suggest severe intercurrent 
valvulitis. Chorea is prone to develop with arthritis, heart disease, nodes 
or ervthemata. 






ACUTE ARTICULAR RHEUMATISM 287 

2. Rheumatoides. — Rheumatoides or pseudorheumatism are symp- 
tomatic arthritides resembling rheumatism. The nomenclature of 
Quincke, who speaks of polyarthritis gonorrhoica, scarlatinosa, etc., is 
the least objectionable, (a) Polyarthritis gonorrhoica (q. v.) resembles 
rheumatism very closely and most frequently, (b) Polyarthritis scarla- 
tinosa often most closely resembles rheumatism (v. page 265). With 
it have been observed endopericarditis, nodes, erythema and chorea. 
(c) Polyarthritis may complicate many other infections; e. g., measles, 
smallpox, erysipelas, typhoid, angina, appendicitis, diphtheria, syphilis, 
pneumonia, etc. 

3. Severe Types. — In grave types the visceral findings are least 
confusing when secondary in development to the arthritis. In the 
primary visceral type the findings (e. g., cardiac) antedate the arthritis, 
but diagnosis is uncertain, until the joints are involved. 

4. Gout (q. v.). 5. Arthritis Deformans (q. v.). 6. Tuberculous 
Polyarthritis (q. v.). 

The number of joints involved is highly suggestive, but not diagnostic. 
Rheumatism and gonorrheal rheumatism are often polyarticular; diag- 
nosis of the latter in women is often difficult for notable reasons. Puer- 
peral infections and an acute monarticular osteo-arthritis in pregnancy 
or lactation may cause difficulty. 

Treatment. — 1. Diet. — Biot's results, with a strict milk diet, were 
extremely good; arrow-root, gruels, etc., may be given. 

2. Clothing. — The patient should wear a flannel gown and blankets 
are more comfortable than sheets on account of the sweating. Macera- 
tion of the skin by the drenching sweats can be avoided by dusting 
talcum powder in the axillse, etc., and sponging with warm water and 
alcohol. 

3. Local Treatment. — Hot boric fomentations and salicylic salve 
are useful (]$ — Acidi salicylici 3j, adipis lanse hydrosi § j). Cantharides 
blisters are indicated for tardy involution. 

4. Rest. — Fixation in the most comfortable position lessens pain, 
fever, pulse and respiration-rate. The absolute dorsal decubitus for 
three weeks must be enforced because of the weak heart. Muscular 
atrophy may result from the use of piaster-of -Paris casts. 

5. Salicylates. — Buss (1875) remarked their antipyretic affects, 
and Strickler and Maclagan (1876) discovered their remarkable action 
in rheumatism. 

(a) Effect on the Arthritis. — The pain and swelling are usually relieved 
after three to five full doses — within twenty-four hours. Salicylates 
are the best analgesic in rheumatism, and morphine is rarely necessary 
after the first twelve hours. Salicylates are thought to cause articular 
hyperemia. 

(6) Effect on the Temperature. — The fever falls coincidently with relief 
of the articular symptoms, and in the great majority of cases the acute 
stage is over within three days. In hyperpyrexia less influence is noted. 

(c) Effect on the Endocarditis. — The weight of opinion is that endocar- 
ditis occurs as frequently with the use of salicylates, i. e., salicylates 
are only analgesic and antipyretic. The writer believes that the salicyl- 



288 INFECTIONS OF DOUBTFUL ETIOLOGY 

ates are practically specific and that heart complications are lessened 
by shortening of the acute stage. 

(d) Relapses. — Relapses are not more frequent with the administration 
of the salicylates than with the alkaline treatment. They are less fre- 
quent under the use of salicylates for two weeks after the initial symptoms. 

(e) Physiological Action. — The smallest doses produce cinchonism, 
as fulness of the head or roaring in the ears. After larger doses dulness, 
headache, giddiness, a dusky and moist skin, disturbed hearing, and 
tremor develop. Toxic doses also produce eye-muscle paralysis, pupil 
dilatation, amaurosis, deafness, increased reflexes, restlessness, delirium, 
dyspnea, disturbed circulation, skin eruptions and green urine (indican 
and pyocatechin) . Postmortem, visceral congestion and serous ecchy- 
moses are seen. 

(J) Administration. — Sodium salicylate is the most prompt, certain, 
soluble and least irritating preparation. Where it fails, other prepara- 
tions arc usually unsuccessful. All salicyl preparations are absorbed as 
sodium salicylate, produced by the alkaline intestinal juices. Grains xv 
of the natural or synthetic acid — as both are equally good — or grains xx 
of the sodium salt, are given every three hours until salicylism appears, 
i. e., until slight dulness, dyspnea and deafness develop; 3 ij— iiss are given 
the first day, when the interval between doses is lengthened to six hours. 
The effects are better in proportion as the disease is more acute, the 
inflammation greater, the number of involved joints larger, and the 
fever higher. It usually can be given by mouth in fluid, if the taste be 
disguised by wintergreen oil, syrup of ginger or syrup of orange; even 
then it is frequently nauseating. 

1$ — Sodii salicylates 5vj 

Sodii bicarbonatis 5iv 

Syrupi zingiberis 5J 

Syrupi aurantii 5j 

Aquae q. s. ad. 3 viij 

M. et S. — Shake. Two teaspoonfuls every three hours. 

Capsules may irritate the stomach, but powders are well tolerated, 
taken in starch wafers. In case the stomach is intolerant, salicylates 
may be administered by rectum in peptonized milk. 1 Inunctions are 
uncertain. Aspirin (acidum acetylsalicylicum) is much less irritating 
to the stomach than salicylate of soda, less antipyretic and less analgesic 
but more sudorific; it is given in doses of twenty grains at the same 
intervals. Aspirin rarely occasions an angioneurotic edema of the face, 
lids or oral mucosa and urticarial, scarlatiniform or pemphigus erup- 
tions. Salol (phenylis salicylas) is given in the same dose at the same 
interval, but the kidneys must be carefully watched, because of the 
phenol component; it is far less efficacious. 

The claim that the alkaline treatment decreases the heart complications 
and shortens the disease, is not proved, yet in the above prescription, the 
sod. bicarbonate lessens the gastric and renal irritation of the salicylates. 

1 Hypodermic injections of the salicylates in rheumatism are advocated (10 c.c. of a 20 
per cent, sterilized solution of sodium salicylate to 100 pounds of body weight, fifteen 
minutes after a cocaine injection, every twelve hours). 



DENGUE 289 

Baginisky thinks the administration of gr. xv-xl of potassium iodide 
daily produces better results in children than do the salicylates. 

(g) Unusual Results. — 1. Nervous. — Delirium has been observed in 
chlorotics, neurotics and alcoholics. It may be violent and protracted. 
Convulsions are infrequent. 

2. Cardiac. — Small doses stimulate the heart, and 3 ij per diem seldom 
affect the heart, even with old valvular lesions. If the heart becomes 
weak or irregular, acute myocarditis is probably developing and the 
heart muscle must be stimulated by coffee, strychnine or camphor. 
Slight irregularity without weakness is no contra-indication. Thorne 
has observed collapse from aspirin. 

3. Respiratory. — With antecedent or concomitant bronchitis or tuber- 
culosis, the lungs should be explored for possible congestion due to the 
remedy. Cardiac depression, sudden respiratory failure and violent 
expiratory dyspnea are observed in a few cases. 

4. Renal. — Caution is necessary in old nephritics, because the salicy- 
lates are excreted by the kidneys as salicylic or salicyluric acid; how- 
ever, albuminuria or nephritis directly due to the rheumatic virus, 
indicates, rather than contra-indicates, the salicylates. 

5. Alimentary. — Vomiting and diarrhea may result from salicylic 
irritation or inhibition of the digestive ferments. 

Diagnostic Therapy. — Senator claimed that salicylates are specific 
in true rheumatism and inert in pseud orheumatism; there are certain 
exceptions — some rheumatics resist salicylates, and salicylates are of 
some value in the arthritic type of grippe, but usually are useless in 
other arthritides. 

Convalescence. — Absolute rest must be enforced for three weeks to 
save the heart. Antecedent tonsillitis indicates tonsillectomy. 



DENGUE. 

Definition. — An acute specific infection, extremely contagious, and 
characterized by fever, prodromal eruption, violent articular and mus- 
cular pains, and a secondary polymorphous eruption. 

Etiology and Epidemiology. — The actual cause is uncertain. Graham 
found, in the blood cells, an organism resembling the Plasmodium 
malarise, but small and unpigmented. It is transmitted by the bite of 
the Culex fastigans. Contagion is disseminated by indirect infection, 
fomites, bites, etc. It is carried by pilgrims, sailors and emigrants. 
The disease spreads with remarkable rapidity. Its home is in the tropical 
and subtropical zones and it prevails chiefly in the hot months. It is 
remarkable that the coast ports are chiefly invaded, and closely con- 
tiguous inland towns and higher places are exempt. The first epidemic, 
in 1779, in Java, was described by Brylon, and Benjamin Rush wrote 
of the Philadelphia epidemic in 1780; it was called " Front Street Fever," 
on account of the squalid condition of the houses along the river front. 
It has invaded Europe, Asiatic Turkey, South America and the United 
States. It has reached Savannah, New Orleans, Ohio and Virginia. 
19 



290 INFECTIONS OF DOUBTFUL ETIOLOGY 

No immunity is conferred by one attack, and it may recur two or even 
four times. 

Symptoms. — Incubation lasts one or two days. 

1. Febrile Stage. — The fever rises quickly to 102°, 104° or even 107°, 
with a chill, severe frontal headache and intense pains in the back and 
limbs, especially the knees, which incapacitate the patient. The names 
" break-bone fever," of Rush's description, and " dandy fever," given 
because of the mincing gait which results, bring out this salient feature. 
The pulse averages 100. Many joints are swollen, one after another. 
The muscles are painful, the face is suffused and swollen, the conjunctivae 
are injected and the flow of tears is increased. Total anorexia, coated 
tongue, and great thirst develop; vomiting is occasional and constipa- 
tion the rule. The prodromal hyperemic rash lasts one to five hours, 
and is frequently absent. Prostration, delirium, convulsions and coma 
may develop. This stage lasts three days (" three-day fever") and ends 
with profuse sweating. Fever is absent in the lightest cases. 

2. Exanthematotjs Stage. — The polymorphous eruption on the 
fourth day on the face, hands, forearms and chest, is scarlatiniform, 
morbilliform, urticarial, erysipelatoid, vesicular or even pustular. It 
is present in 80 per cent, of cases, lasting three days, and followed by 
desquamation, itching, sometimes by falling of the hair. An inflamed 
throat, lymph-gland enlargement, parotitis and orchitis occasionally 
occur. The temperature varies from subnormal to high. The pain 
recurs often. Herpes, splenic tumor, otitis, albuminuria and leukocytosis 
are absent. 

3. Convalescence begins in seven days. There is prostration, 
emaciation and anemia. In no other disease of equal duration is such 
marked constitutional disturbance noted. 

Complications. — Gastric hemorrhage, endocarditis, nephritis, pneu- 
monia, pleurisy or ulcers very rarely develop. 

Prognosis. — Though the morbidity is enormous, the highest recorded 
death-rate is 0.5 per cent. (10 deaths in 100,000 cases in Smyrna). 
Relapse may occur in one or two weeks. 

Diagnosis. — The geography and the presence of an epidemic are 
significant. The exanthemata, rheumatism, yellow fever (q. v.) and 
epidemic erythema exudativum multiforme may be suggested. Influenza 
is differentiated by its occurrence in all climates, seasons and inland 
as well as on seaboard, its usual respiratory catarrh and complications, 
its more severe nervous, intestinal and cardiac symptoms, and the 
greater frequency of herpes, splenic tumor, otitis and albuminuria. In 
the rare acrodynia, observed in France, Belgium, Turkey, Persia and 
Mexico, Scheube gives the following differential points: Digestive dis- 
turbance; facial swelling; pains in the extremities, sometimes with 
anesthesia; spastic symptoms; afebrile course; and erythema multiforme. 

Treatment. — Isolation and quarantine are necessary. Pain is the 
prominent indication, for which acetphenetidinum and salicylates serve 
fairly well, though they are much inferior to opium. 



YELLOW FEVER 291 



YELLOW FEVER. 

Definition. — A specific infection, transmitted by the mosquito, endemic 
in the American tropics and subtropics, and characterized pathologically 
by degeneration of the liver and kidneys, and clinically by fever, icterus, 
albuminuria, adynamia, and hematemesis. 

Etiology. — Transmission by the mosquito (Stegomyia calopus) was sus- 
pected by Carlos Finlay, in 1881, but was demonstrated by the investi- 
gating board composed of Walter Reed, James Carroll, A. Agramonte 
and J. W. Lazear. Dr. Carroll recovered from a severe attack, but Dr. 
Lazear and Dr. Myers, of the English Commission, died from inocula- 
tion. The Stegomyia breeds not only in stagnant street pools, but also 
in cesspools and sewers, whence its special danger in unhygienic tropical 
towns. Voluntary inoculations by mosquitoes, which twelve days pre- 
viously had bitten yellow-fever patients, produced yellow fever in non- 
immunes; Finlay failed to prove his suspicion because he allowed the 
mosquitoes only three to six days in which to develop the germs which 
they had ingested, whereas they must live twelve days before they can 
convey infection. The mosquito carries infection only when it bites the 
patient in the first three days of the disease. Transfusion of blood of 
an infected person, taken in the first three days of the disease, also 
conveys infection. The virus is filterable. As in malaria, the tropical 
foci, the hot summer and autumn seasons, the invasion of low altitudes, 
river courses and coast towns, humidity, and exposure to night air, are 
merely conditions suitable to the mosquito. Frost stops infection be- 
cause it kills the mosquito. Direct contagion does not occur. Nurses 
and physicians are not infected from contact with yellow-fever patients. 
Persons going from the City of Mexico to Vera Cruz may acquire the 
disease, but on coming home with it they do not cause its dissemination, 
because the mosquito is not present. Reed's committee exploded the 
theory that fomites, clothing, etc., were infective. Volunteers remained 
in rooms occupied by vellow-fever patients and slept in their soiled 
linen without contracting the disease. During the American occupa- 
tion, Col. Gorgas stamped out the disease in Havana, but 405 cases 
developed in 1905-8, from the New Orleans epidemic. No cases devel- 
oped since December, 1908. 

Predisposition. — The lighter races are more prone to infection. Im- 
munes are merely those who have had light and unrecognized infections. 
Yellow fever is kept alive in endemic foci by mild cases, especially among 
the Creole children. 

Foci and Epidemiology. — The habitats of yellow fever are (1) Mexico, 
the Antilles, Mexican Gulf and Caribbean Sea; and (2) Africa, from 
Senegal, through Sierra Leone, to the Gold Coast. The first clear descrip- 
tion of yellow fever was in 1686, but yellow fever was known before 
the discovery of America. It reached this country in the sixteenth 
century and has extended as far north as Boston, St. Louis, Quebec and 
Chicago. In Philadelphia (1793, 1797-1798), 4041 died in a year; in 
New York, 2080; and in New Orleans, in 1853, 8000 died. In New 



292 INFECTIONS OF DOUBTFUL ETIOLOGY 

Orleans, in 1905, there were about 9000 cases and 1000 deaths. Europe 
is seldom, but South America is frequently invaded. 

General Clinical Description. — Incubation averages three days. Pro- 
dromal symptoms last less than a day; they are malaise, fatigue, head- 
ache, dyspepsia or colic. The disease is divided into the following stages : 

I. — The stage of congestion begins with frontal or retroocular head- 
ache, the earliest and most prominent symptom, sometimes a chill, and 
flushed face; the conjunctiva? are injected and sometimes icteric; the 
eyes are sensitive to light, the lids puffed and the expression denotes 
pain, restlessness and confusion, comparable to the alcoholic facies; 
backache radiating into the calves, fever rising to 104°, and a full, tense 
pulse of 100 to 110. The tongue is slightly coated dorsally. The febrile 
urine is very early albuminous. The skin is intensely red and dry. 
The epigastrium is tender early and there is marked gastric intolerance 
of food, water and medicine. This stage averages two days. 

II. — The remission stage, or deceptive stage, occurs in some cases 
and is so-called because of the subsequent severe symptoms. The 
fever, pulse and the pain remit. Slight jaundice may appear. 

III. — The Reaction Stage. — Slight temperature, the "black vomit" 
(vomito negro) of blood, hemorrhage into the nose, intestines, uterus 
or skin, hiccough, epigastric pain and tenderness, liver enlargement, and 
icterus mark this period. The urine becomes scant and laden with 
bile pigment, or its secretion is suppressed; the pulse becomes weaker, 
and insomnia, prostration and restlessness may appear. 

Various issues are possible: Gradual amelioration; fatal anuria; 
profuse hemorrhages, which end in collapse, and rarely in recovery; 
profound icterus, which results usually in death; or death from cardiac 
insufficiency. 

(^4) Variations in intensity include (1) abortive, ambulatory, atypi- 
cal forms, especially in children; (2) the usual severe forms; and (3) 
the foudroyant type, rapidly lethal in one to two days. 

(B) Visceral Forms: (1) The hepatic type, with two weeks of the 
status typhosus, often with normal temperature and sometimes, with 
hemorrhages; (2) the uremic type; (3) the hemorrhagic; (4) the cardiac; 
and (5) nervous or atactic type. 

Special Symptomatology. — 1. Fever. — Fever is highest in the first 
stage, and averages 104°. It may fall on the second or third day to 
nearly normal in benign cases or in the ominous uremic type. High 
fever after the second day is a poor prognostic. In the second stage 
fever is usually 99° to 100°. In the third stage a high antemortem rise 
is frequent. In convalescence it is subnormal. 

2. Nervous Symptoms. — Nervous symptoms are often absent in both 
benign and malignant cases. Headache is common in the congestive 
period. Delirium is infrequent, and in 80 per cent, of cases, is uremic. 
In children, alcoholics and in the debilitated the status typhosus or 
meningo-encephalitic symptoms (convulsions, unequal pupils, Cheyne- 
Stokes's breathing and coma) are possible. Pathologically, few changes 
are found except the slight degenerations common to the febrile state, 
punctate hemorrhage or bile tinging. 



YELLOW FEVER 293 

3. Circulatory Symptoms. — (a) The pulse in the congestive stage 
is 100 to 110 and tense; on the third day, 70 to 80; in the second stage 
it is still lower in benign and more rapid in severe cases (110 to 140) 
and is small; in convalescence it is slow (50 to 60, or even 30). Faget 
considers slowing of the pulse with maintenance of the fever almost 
pathognomonic, (b) In severe forms the first tone of the heart becomes 
weak and embryocardia is found. The heart is rarely irregular or inter- 
mittent. In the third stage, cardiac dilatation is common (in 70 per 
cent, of autopsies), due to myocardial degeneration. Cardiac action is 
exaggerated when uremia is present, (c) There is no anemia. The 
white cells are decreased; the polynuclears are relatively increased. 

4. Respiratory Symptoms. — Respiratory symptoms may be due to 
intercurrent, or more often to cardiac or renal, complications. 

5. Digestive Tract. — Hiccough, epigastric pain, tenderness and 
anxiety may be symptomatic of cardiac distress, premonitory of the 
black vomit, or indicative of disturbed circulation in the medulla. 

6. Icterus (Yellow Fever, Typhus Icteroides). — Jaundice 
usually develops on the third to fifth day; its pathogenesis is obscure. 
It is frequently absent in children, in early death from uremia and in 
50 per cent, of cases which recover. 

7. Liver. — The liver is slightly enlarged and tender. Pathologically, 
it has a light cooked, fatty and anemic appearance. 

8. Urine. — Albuminuria occurs in 88 per cent, of cases in the first 
three days. Leucin, casts and bile pigment are common. The kidneys, 
anatomically, are pale or yellowish, and, microscopically, show great 
fatty degeneration of the tubules, which in severe cases are choked by 
desquamated epithelium and casts. The glomeruli show few changes. 

Uremia causes 33 per cent, of fatalities; it is marked by delirium, ner- 
vousness, convulsions, decreased or suppressed urine (fatal in 97 per 
cent, of cases), rapid or Cheyne-Stokes's breathing, and a tense pulse. 
Death in coma may occur on the third day. Uremia is rare in children. 

9. Hemorrhages. — They result from fatty degeneration or actual 
rupture of the bloodvessels. Hemorrhages may occur from the mouth, 
stomach or intestine. The black vomit, gradually transuded blood altered 
by the gastric acid, occurs on the fourth to sixth day, the " coffee-grounds" 
vomit; the stomach at autopsy shows the black contents and dark 
discoloration, epithelial desquamation and fatty change in the muscu- 
laris. Hemorrhage from the small intestine is equally frequent. Epistaxis 
is often profuse. Uterine hemorrhages are severe and in pregnant women 
cause abortion. Less frequent are skin petechia? and muscular hemor- 
rhages. 

Complications and Sequels.- — These include secondary infections such 
as endocarditis, pericarditis, pneumonia, erysipelas, parotitis, arthritis, 
suppuration and gangrene; coincident typhoid, malaria, influenza and 
insolation; and postfebrile psychoses. 

Diagnosis. — The diagnosis is readily made from (1) the flushed, semi- 
intoxicated facies; (2) icterus; (3) the early albuminuria — the most 
valuable finding in doubtful cases; (4) black vomit, gastric intolerance 
and epigastric tenderness; (5) hemorrhages, and (6) the slow pulse, which 



294 INFECTIONS OF DOUBTFUL ETIOLOGY 

is absent in some severe, but therefore clear, cases. Pernicious malaria, 
with icterus, is distinguished by the blood (plasmodium and anemia), 
enlarged spleen (always absent in yellow fever), the infrequency of early 
icterus, albuminuria and hemorrhages (except hematuria). This form 
of malaria is rare in cities, whence the constant suggestion of yellow 
fever, when more than sporadic cases are reported. Weil's disease and 
acute yellow atrophy are readily distinguished. 

Prognosis. — The mortality of epidemics varies from 10 to 85 per cent. 
The death-rate averages 30 per cent. The mortality, according to age, 
is 33 per cent, (one to three years), 14 (four to eighteen years) and 37 
per cent, (nineteen to forty years). Unfavorable events are hepatic, 
renal or cardiac insufficiency, the typhoid state, high fever with hepatic 
symptoms and hemorrhages. 

Treatment. — 1. Prophylaxis. — No greater triumph of hygiene exists 
than the stamping out of yellow fever during the American occupation 
of Havana. It illustrates not only the efficiency of the investigating 
commission, but also the possibilities of medicine in administrative 
capacity with unlimited discretionary power. In Havana the death- 
rate was 500 yearly, until Gorgas cut it down to nil. The patient should 
be isolated, not to prevent direct personal contagion but to keep mos- 
quitoes from the infected person. Healthy individuals avert infection by 
the mosquito by the same measures employed in malaria, e. g., screens, 
and extermination of breeding foci. The Stegomyia is found outside the 
habitual yellow-fever foci, and after biting patients from abroad, may 
inoculate other persons. 

2. Symptomatic Treatment. — (a) In the first stage, fluidextractum 
aconiti, Tfl,iij, and sodium salicylat., gr. xx, may be given every two to 
four hours, until the congestion and pains are relieved. Coal-tar pro- 
ducts are depressant. Calomel, gr. J every hour for five doses is followed 
by castor oil. Overmedication is to be avoided because of the gastric 
irritability. Violent cerebral, uremic or pulmonary symptoms are some- 
times treated by phlebotomy, (b) In the last Mage, the black vomit 
contra-indicates any fluid, food or medication by mouth; warm pepton- 
ized milk and normal salt solution are given by rectum; morphine by 
mouth is dangerous, (c) Digitalis is especially good, and is beneficial 
even when cardiac failure is absent; saline solution, by rectum or sub- 
cutaneously, is better than intravenous transfusions. The patient must 
be kept absolutely quiet, (d) Uremic symptoms are treated in much the 
same way. Water is given freely by the bowel, (e) Nervous manifesta- 
tions necessitate cool spongings, bromides, morphine and hyoscine, as 
in typhoid. (/) Vomiting is relieved most efficaciously by chopped ice. 
(See Typhoid.) 

HYDROPHOBIA (LYSSA; RABIES). 

Definition. — An acute specific infection, peculiar to carnivora, the 
bites of which convey infection to other animals and man. The disease 
is characterized by tonic and clonic spasms of the esophagus, respiratory 
and other muscles and by a fatal evolution. It was described in ancient 
Jewish, Egyptian and Indian writings and by Democritus in the fourth 



HYDROPHOBIA 295 

and fifth centuries, B.C. The first adequate account was by Youatt 
(1828). 

Etiology. — In Germany, from 1887 to 1894, only 16 cases occurred 
because of the strict laws. In Russia, France and America it is far 
more common. The disease has been eradicated in England, Denmark, 
Norway, Sweden, Switzerland and Australia. Dogs are most frequently 
affected and the chief cause of dissemination (90 per cent.) ; next come 
wolves, cats and cattle; and finally skunks, horses, deer, pigs, rabbits 
and even fowl may be inoculated. The virus is found in the nervous 
tissues most abundantly, in the saliva and also in small quantities, in tears, 
sputum, semen, urine and milk, and in the adrenals. Its propagation 
is along the nerve trunks, thus reaching the salivary glands (not by 
way of the blood stream). Noguchi cultivated small granular pleo- 
morphic bodies which produce the disease on inoculation. Inoculation 
occurs from bites of infected animals, which transmit the disease even 
during incubation. Punctured or deep wounds and those in the nerves 
or muscles are most dangerous; 10 per cent, of those bitten by mad dogs 
and 62 per cent, of those bitten by rabid wolves and cats die. In excep- 
tional cases, rabies results from being licked by an infected dog, kissing 
an infected person or dissecting an infected body. The disease prevails 
chiefly in warm weather in the "dog days" and most laws are based on 
this assumption; but it is also common in cool weather. In Paris most 
cases occur in March and May. Sixty per cent, of cases occur in males 
and 40 per cent, under fifteen years of age. 

The incubation period varies, averaging 40 days: (a) It is shorter in 
children; (6) if the wound is on the face or head, incubation is very 
short and the symptoms very severe; (c) it is longer and the symptoms 
less intense when the point of infection is on the body, because the 
clothing tends to clean the virus off the teeth. 

Symptoms. — Three somewhat arbitrary stages are described: 

Fikst or Prodromal Stage. — The scar may become painful. Psychical 
alteration is expressed by depression, irritability or extreme anxiety. 
Headache, hyperesthesia, anorexia and some elevation of the temperature 
and pulse-rate are usual. Sometimes the voice is hoarse, the pupils are 
somewhat dilated and premonitions of dysphagia are experienced. This 
stage lasts one or two days. 

Second or Excitation Stage. — (a) The excitement is more motor 
than psychical. The cutaneous and deep reflexes are increased. There 
is such hyperesthesia that the least sound or light, the slightest breath of 
air, or food and water in the throat, induce violent reflex spasms, whence 
the patient's dread of these excitants (photophobia, aerophobia, hydro- 
phobia). Tonic spasms, following attempts at swallowing affect chiefly 
the muscles of the mouth, the hyoid elevators and the laryngeal and 
respiratory muscles. Even without laryngeal involvement the respira- 
tion is labored, with jerky, deep or sighing inspirations, during which 
the shoulders are lifted and the epigastrium protruded. The spasms 
may extend to the trunk and limbs, (b) The psychical excitement is 
marked at the time of the spasm by restlessness and later by horror or 
even mania. Delirium tremens may be simulated. The mind is usually 



296 INFECTIONS OF DOUBTFUL ETIOLOGY 

clear between the spasms. The patient rarely attempts to injure at- 
tendants, although such an impression may be made by the peculiar 
growling sounds occasioned by pharyngeal and laryngeal spasm and the 
"frothing at the mouth," due to inability to swallow the increased flow 
of saliva. Less constant symptoms are fever, salivation and lachryma- 
tion; tremor, erection and ejaculation; increased pulse-rate; scanty, 
albuminous urine (25 per cent.), often with casts. The excitation stage 
lasts one and a half to three days. 

Third or Paralytic Stage. — This stage, less common in human 
rabies, in animals may be marked from the beginning and the other 
stages may be lacking or rudimentary — the "dumb" rabies as contrasted 
with the furibund type. The spasms and excitement cease, the pulse 
becomes fast, small and irregular, the pupils are wide and irregular, 
sweating is profuse, swallowing becomes impossible and paralyses develop, 
mono-, para- or hemiplegic, or of the acute ascending type of Landry. 
The patient dies, unconscious, of cardiac collapse, rarely of asphyxia 
or convulsions. The third stage seldom lasts more than eighteen 
hours. 

Autopsy Findings. — Pathologists are not unanimous in regard to 
specific findings. Minute hemorrhages and special congestion of the 
medulla and cord characterize all convulsive states. Babes' s rabic tubercles 
are aggregations of leukocytes around the vessels and nerve cells. The 
latter may degenerate. Rapid diagnosis of rabies may be made accord- 
ing to von Gehuchten and Nelis, by examination of the sympathetic and 
cerebrospinal ganglia, under the capsules of which are found accumula- 
tions of epithelioid and lymphoid cells, in animals, only, which die of the 
disease. The bodies described by Negri and Pavia (1903) in the cell 
processes may be protozoal parasites or artefacts. 

Course and Prognosis. — In twelve hours to ten days — on the average 
two to four days — all untreated cases die, 10 per cent, in the first day 
and 60 per cent, in the first three days. Hogyes's is the only recovery 
verified by inoculations of the saliva. Paltauf's autopsies, on persons 
under Pasteur treatment and dying from accidental causes, indicate 
that 9 out of 10 persons bitten destroy the virus in the central nervous 
system, for the inoculated medulla gives rabies to guinea-pigs; and that 
the tenth case fails to destroy it and therefore dies. Tonin alleges a cure 
under salvarsan. 

Diagnosis. — After bites by supposedly rabid animals, microscopic 
examination of the plexiform ganglion of the vagus can be made and also 
subdural inoculations in rabbits, which die in two or three weeks with 
paralytic symptoms. Tetanus of the cephalic and hydrophobic type is 
distinguished by the invariable trismus. Hysteria (pseudohydrophobia, 
lyssophobia) in one bitten by a dog may at first cause suspicion, but 
rarely any protracted doubt; the initial spasmodic dysphagia and 
irritability are not followed by other symptoms of hydrophobia, and the 
clinical evolution alone is distinctive. 

Treatment. — Prophylactic. — Pasteur, in 1881, found the rabic virus 
in the nervous tissues. "The virus of the street," as Pasteur called 
it, varies in virulence and subdural inoculations from the brains of 



HYDROPHOBIA 297 

rabid dogs, into rabbits, killed them in periods varying from fourteen 
to twenty days. By inoculating a series of rabbits, the incubation 
period is progressively shortened to a fixed period of seven days; this 
"fixed virus" is attenuated by desiccating the spinal cord of the rabbit 
with caustic potash. Animals were inoculated with virus which had 
been desiccated for two weeks, then with virus a little stronger, until 
finally immunization was secured against inoculations which previously 
would have been fatal. In 1885 human beings bitten by rabid beasts 
were thus treated by two inoculations daily for fifteen days and immuni- 
zation was secured, for the slow rabic incubation gives ample time for 
treatment. Statistics show that the former mortality of 80 per cent, in 
untreated bites in the head or face has been reduced to 1.25 per cent.; 
the mortality of 60 per cent, in those bitten in the hands is reduced to 
0.75 per cent.; the mortality of 80 per cent, in those bitten in the cov- 
ered parts of the arm and trunk, and of 15 per cent, in those bitten in 
the leg, is reduced to 0.25 per cent. The total mortality has been reduced 
to 0.5 per cent. Treatment requires two weeks. As Park says, "it is 
a contest of speed between the passage of the virus from the wound to 
the brain by way of the nerves and the development of immunity by 
absorption of vaccines through the circulation;" if "the patient escapes 
infection up to the end of two weeks, few, following the full course, 
develop the disease (2 or 3 per 1000)." As sequences of Pasteur's treat- 
ment, neuritis, bulbar or spinal, and Landry's paralysis are very rarely 
found (Babes, 1905). One-half of those treated by Pasteur's method 
are treated unnecessarily. W. H. Park formulates the indications thus: 
(i) Keep the animal and if it has rabies, give the treatment, (ii) No treat- 
ment is necessary if at the end of the week, the dog has not developed 
rabies, (iii) If the animal has escaped, judge as far as one can by its 
conduct (giving the patient advantage of any doubt) . (iv) If the animal 
has been killed and no Negri bodies are found, give the treatment, as 
microscopic examination is negative in 3 per cent of cases, (v) If the 
dog has been killed and no microscopic examination made, give the 
treatment if rabies prevails. 

2. Primary Wound Treatment. — The wound may be sucked by 
the victim, but by no other person. It should be washed with strong 
antiseptics, burned with nitric acid (the best remedy), formalin, pure 
phenol, etc., and exposed surgically, treated with the live cautery and 
packed with gauze, so that healing may be delayed for over a month. 

3. Late Treatment. — In developed cases the mortality is 100 per 
cent., whence curative therapy is out of the question. The treatment 
of the convulsions is similar to that of tetanus, and nutrition is main- 
tained by nutritive rectal enemata. Morphine and inhalation of chloro- 
form are better than chloral and bromides and should be given until 
they show their full physiological effects. Cocainization of the mouth 
and pharynx may overcome the pharyngeal spasm incident to swallowing 
milk and water and to medication. Tracheotomy is useless for the respi- 
ratory spasm, which reaches further than the larynx and involves the 
muscles of the chest and diaphragm. 



298 INFECTIONS OF DOUBTFUL ETIOLOGY 



FEBRICULA. 

Definition.— A fever of short duration. If only of twenty-four hours' 
duration it is called ephemeral fever; when it lasts a few days, it is called 
febricula; when attended by herpes, febris herpetica; or when accompanied 
by gastric disorder, febris gastrica. 

Febricula is no morbid entity, but embraces (a) benign or abortive 
forms of various infections, such as rheumatism, typhoid, paratyphoid, 
malaria, scarlatina, tonsillitis and pneumonia; infections with the 
Bacillus coli, proteus or pyocyaneus; and (b) febrile dyspepsias, especially 
those in children. Gastric fever or febrile gastritis is possibly produced 
by toxins in the food. Sewer gas never causes gastro-intestinal fever. 

Symptoms. — The three common symptoms are (a) chill or chilliness; 
(b) sudden rise of temperature; and (c) a slow crisis. The onset is 
abrupt, usually without prodromes. The fever rises quickly to 101° to 
103°, or higher in the young, with the usual signs of toxemia, headache, 
coated tongue, anorexia and febrile urine. Herpes is frequent. Bron- 
chitis, acute splenic tumor, albuminuria and in children, cerebral toxemia, 
are sometimes present. The term ephemeral is inappropriate, as the 
average duration is three days. 

Diagnosis and Treatment. — The diagnosis is by exclusion, and the 
treatment is expectant. Rest in bed is advisable as a precaution against 
some longer and insidious malady; the bowels should be unloaded, the 
diet restricted and a drop or two of tincturse aconiti and spts. setheris 
nitrosi 5 ss given every three or four hours. 

GLANDULAR FEVER. 

Definition. — An acute infection, characterized by pharyngeal infec- 
tion, short, high fever and painful cervical lymph adenopathy. It was 
described as Drilsen fieber by Pfeiffer, in 1889. Its etiology is unknown 
but it is evidently an infection and frequently epidemic. It is usually 
seen between five and eight years of age, and during the colder months. 
Park West observed an epidemic of 96 cases in Bellaire, Ohio. Hoch- 
singer and Kretz maintain that the adenopathy is the first obvious sign 
and sequel to nasopharyngeal infection. 

Symptoms. — The symptoms begin without prodromes, with fever 
of 101° to 103°, pain in the head and neck, redness of the throat, dys- 
phagia, nausea, vomiting, pain in the limbs and abdomen. On the 
second day the cervical lymph glands become swollen and tender bilater- 
ally, especially back of the upper part of the sternomastoid. The inguinal 
and axillary glands are involved in 75 per cent, of cases. The glands 
may reach the size of an egg. After ten to twenty days the swelling 
subsides, having lasted longer than the fever, which, after a few days, 
falls by crisis. In some instances a persistent, dry cough suggests involve- 
ment of the bronchial glands, and umbilical pain of mesenteric localiza- 
tion (in about 40 per cent.) . The spleen is enlarged in 60 and the liver in 
90 per cent. Suppuration is exceptional. Acute nephritis, endocar- 
ditis, herpes and otitis media are occasionally observed. 



WEIVS DISEASE 299 

Prognosis and Treatment. — The prognosis is good. The absence of a 
rash excludes the adenopathies of varicella, scarlatina and measles, and 
the generalized glandular swelling excludes the local swelling due to 
simple pharyngitis. The treatment is expectant. 

MILIARY FEVER. 

Definition. — An acute infection, marked by fever, sweating, miliary 
eruption, nervous symptoms and precordial anxiety. It first appeared 
in England after the Battle of Bosworth (1486) and was known as the 
" English sweats" (sudor Anglicus); its mortality reached 50 to 80 per 
cent. In 1529 it caused 3000 deaths in Dantzig. There have been 200 
epidemics between the epidemic in Picardy, in 1718, and that in Poitou, 
in 1887. It is highly contagious. Short epidemics have occurred in 
Italy, Switzerland, Germany and Austria, with a death-rate of 5 to 
25 per cent. In 1906 an epidemic of over 6256 cases prevailed in northern 
France. 

Symptoms and Treatment. — In mild outbreaks the symptoms are 
fever, profuse periodic sweating and miliary eruptions. The eruption 
may be erythematous or morbilliform (miliaria rubra), or without red- 
ness of the skin (miliaria alba) ; desquamation follows. In severe cases 
there are marked cerebral toxemia, rapid pulse, precordial distress, 
palpitation, splenic tumor, prostration and hemorrhages into the skin; 
death results in a day or two. Its duration averages ten days. Convales- 
cence is tardy and treatment supportive and expectant. 

WEIL'S DISEASE (ACUTE FEBRILE JAUNDICE). 

Definition. — An acute infection, characterized by fever, jaundice, 
herpes, enlarged spleen and liver, sore throat, muscle pain and albu- 
minuria. It was especially described by Weil (1886). Nicolaysen 
describes 63 epidemics in Norway and Sweden in the last fourteen years ; 
the morbidity was 3 to 28 per cent. 

Etiology. — Its etiology is unknown, whence it may be a morbid entity 
or may include several diseases. It occurs in 90 per cent, in men between 
twenty-five and forty, especially in butchers and alcoholics, in the warmer 
seasons. The Proteus fluorescens has been found, but the intravitam 
findings are usually negative. Some cases have occurred in this country; 
the author saw 9 cases in Chicago. 

Symptoms. — The symptoms begin suddenly with fever, chill, head- 
ache and severe pains in the extremities. The fever reaches 103°; it 
remits and falls by crisis or lysis after five to eight days. The nervous 
symptoms may resemble typhoid. Jaundice develops on the third 
day, due to catarrhal angiocholitis ; bile appears in the urine and the 
stools are often acholic; the author has twice seen deep jaundice without 
bile obstruction. Muscular pain and tenderness are intense, especially 
in the calves. Articular pains are not uncommon. Herpes is very com- 
mon. The rapid pulse contrasts sharply with the slow pulse of simple 
catarrhal icterus. In 2 cases the author observed blood-stained bronchitic 



300 INFECTIONS OF DOUBTFUL ETIOLOGY 

sputum. Digestive symptoms are common, as furred tongue, vomiting, 
epigastric pain, abdominal distention and diarrhea. The liver is enlarged 
and tender in more than 50 per cent, of cases, the spleen in over 66 per 
cent., and the lymph nodes are frequently affected. The urine is albu- 
minous in over 50 per cent. ; acute nephritis is frequent; hematuria occurs 
occasionally and uremia exceptionally; the urea and the amount of urine 
are decreased during, and increased after, the seizure (Chauffard's 
nitrogenous and polyuric crises) . 

Diagnosis. — Weil's disease must be differentiated from recurrent fever, 
sepsis, typhoid, suppurative angiocholitis (q. v.) and acute yellow atrophy 
(q.v.). 

Prognosis. — Convalescence is usually established in two weeks; the 
mortality may reach 11 per cent. Recurrence in 40 per cent, may be 
anticipated if the splenic tumor persists; renal or hepatic insufficiency, 
pregnancy and hemolysis render the prognosis less favorable. 

Treatment. — The treatment is directed to (a) the intoxication, for 
which calomel and salines are indicated; cold-water enemata increase 
the renal flow, and, with it, the excretion of toxins; (b) the jaundice, 
for which salines are given to lessen duodenal catarrh; (c) the albumin- 
uria, for which a milk diet is indicated; and (d) muscular pains, for 
which heat and massage with chloroform liniment, are most beneficial. 

MILK SICKNESS. 

Definition. — A disease acquired by man from the milk or meat of 
cattle suffering from the "trembles." Cows with the disease, after 
being driven too rapidly, suffer from anorexia, injection of the eyes, 
vertigo, trembling and convulsions ending in death. Young horses 
and sheep may also acquire the disease. Milk sickness occurs chiefly 
in newly settled countries, as in the Southwestern states, and it is still 
seen in North Carolina. Its origin and pathology are unknown. Jordan 
and Harris describe a Bacillus lactimorbi. 

Symptoms. — In man the nervous symptoms are frequently conspic- 
uous, as restlessness, convulsions or coma, which appear after -a few 
days of malaise. The tongue is swollen and heavily coated, the breath 
fetid, the stomach painful and irritable, the fever low, high or sometimes 
typhoidal. The issue is either fatal, in acute forms, within a few days, 
or recovery may result after weeks. Flesh, butter, cheese and milk, 
from infected animals may, even when boiled, cause death when given 
to dogs. 

ROCKY MOUNTAIN FEVER. 

It occurs in the Bitter Root Valley of Montana and also in Wyoming, 
Nevada and Idaho. Howard Ricketts found the disease was inoculable 
and he and King found the medium of infection was the wood-tick 
(Dermacentor occidentalis) . Ricketts (1909) discovered a bacillus like 
that of hemorrhagic septicemia. Cases develop in the early spring, and 
are marked by chill, fever lasting one or two weeks, rapid pulse, epistaxis, 
albuminuria, rapid breathing, bronchitis, splenic tumor, rapid anemia, 



RAT-BITE DISEASE 301 

moderate leukocytosis, slight icterus, muscular pains and a widely diffused 
macular rash, which develops on the third day, disappears on pressure 
at first, but afterward persists on pressure. The liver and spleen are 
enlarged. Quinine may be beneficial in some cases. The death-rate 
may reach 70 to 90 per cent, in Montana, yet in Idaho it runs between 
2 and 3 per cent. T. B. McClintic died a martyr to the disease, as 
Ricketts died of typhus. 

FOOT-AND-MOUTH DISEASE. 

Definition. — Epidemic stomatitis, aphthous fever, or aphthae epizo- 
oticse is one of the zoonoses. Loeffier and Frosch have shown that the 
virus is ultramicroscopic, passing in full virulence through porcelain 
filters. The disease, first described by von Valentini, in 1695, chiefly 
affects cattle, sheep and pigs, but sometimes also goats, horses, dogs 
and even fowl. In cattle there is fever, swelling of the mouth, salivation 
and the formation of small, clear vesicles on the tongue, gums, lips, 
udders and hoofs. These vesicles soon become opaque, and bursting, 
form small ulcers; emaciation is rapid, and the milk becomes yellowish 
and mucoid. Embolism or fatal apoplexy may result. Recovery is 
usual in ten days. The disease spreads very rapidly. It is observed in 
Hungary, Germany, France, Switzerland, England and America, Chicago 
being the centre of a wide epidemic in 1914. 

Etiology and Symptoms. — In man infection occurs from diseased 
milk (as proved on himself by Hertwig), butter and cheese, but not 
by diseased meat. Open wounds may be directly infected. Cattle 
have been inoculated from man. The incubation is three to five days. 
There are fever, salivation, aphthous ulcers, angina, nausea, vomiting 
and vesicles on the skin — which have caused confusion with vaccinia. 
Hemorrhages occur in severe epidemics. Ebstein suggested that foot- 
and-mouth disease may be kindred with the ordinary aphthous stoma- 
titis of nurslings or pregnant women. Children are more endangered 
than adults. The death-rate is 2 to 8 per cent. Recovery is usual in 
three weeks. 

Treatment. — Prophylaxis concerns the boiling of suspected milk, the 
segregation of diseased animals or human subjects, and vaccination, as 
discovered by Loeffler. A dram of 5 per cent, solution of potas. chlorate, 
t. i. d., should be given, and the aphthse should be touched with borax 
or silver. 

RAT-BITE DISEASE. 

Rat-bite fever, known as Sokudu in Japan, closely resembles recurrent 
fever and in some ways, lues. The bite heals, and after two to five 
weeks, inflammation, even ulceration develops at its site, with inter- 
mittent fever, chills, headache, vomiting, an erythematous eruption, 
eosinophilia and local and general lymphadenopathy. After a fever-free 
interval of three to five days, the symptoms recur; the mortality is 
10 per cent., usually from nephritis. Crohn (1915) collected 52 cases. 
Salvarsan is recommended. 



302 METAZOAN INFECTIONS 

PSITTACOSIS. 

Psittacosis is a disease of birds, characterized by loss of appetite, 
general weakness, diarrhea, convulsions and death. It is communicable 
to man, infection being commonly acquired from parrots. The disease 
occurs in England, Germany, France and Italy. It is characterized by 
atypical pneumonia, attended by profound and usually fatal toxemia. 



METAZOAN INFECTIONS. 



DISEASES CAUSED BY CESTODES. 

Tape-worms were known to the Egyptians, Hindus and probably the 
Jews. They may cause symptoms by the presence of the mature parasite 
in the bowels or of the larval form in the viscera. 

I. Tenia Solium. — The Tenia solium or pork tape-worm (Linnaeus, 
1752) exists as the cysticercus cellulosse in hogs and rarely in dogs, 
rats or deer, as "measles." The adult form is peculiar to man. Cysti- 
cerci (the larvse), found in the intermuscular tissue, particularly of the 
undersurface of the tongue, in the masseters, shoulders, neck and dia- 
phragm, are easily seen with the naked eye and very easily with a low-power 
lens, as small, opaque, white bodies. They are vastly more frequent, in 
Asiatic and German than in American pork. Man is infected by eating 
raw or partly cooked "measley" pork; the cysticerci develop in the 
upper ileum into the tenia ("band or ribbon-like") solium (referring to 
its usual solitary appearance, though 2 or 3, and even 20 or 41, have 
been found). The worm measures 2 to 8 meters in length. Its head 
(scolex) is round, often gray or black in its upper part, is smaller than a 
pin-head, and is attached to the upper ileum; it has 4 sucking disks and 
20 to 30 hooklets, arranged in an anterior, more numerous row, and a 
posterior row, whence the name "armed" tape- worm; it has no real 
mouth. Its neck is thin and not jointed, to which the segments, "pro- 
glottides," are attached. These number 800 or 900; the segments 
measure 10 mm. in length by 5 or 6 mm. in width; those near the neck 
are narrower and shorter. About a yard from the neck they become 
squarer, and lower down they are smaller again. Each proglottis is 
hermaphroditic, containing male and female reproductive elements. 
The uterus is central and vertical, with 7 to 15 lateral branches; only 
a few of them mature, chiefly those in the lower links; the ova (31 to 
3G/x) are very numerous in each maturing segment and each one shows 
a shell and an embryo armed with six hooklets. The tenia reaches its 
full length of two to four yards in three or four months, when the lower 
segments are detached and voided; if the worm breaks and a yard or so 
appears in the feces, segments do not reappear in the feces until three 
months later. An ovum ingested by a hog or man loses its shell in the 
stomach and the freed embryo passes into the tissues, where, encysted, 
it becomes again the cysticercus cellulosse (or larva). 



DISEASES CAUSED BY CESTODES 303 

Symptoms of the Tenia Solium in the Human Intestine (Intestinal Teniasis). 
— Many, possibly most, cases present no symptoms; they may first 
develop after passing segments are noted by neurotic subjects. In other 
cases headache, itching, pupillary inequality, emaciation and dyspeptic 
disturbances arise, as anorexia (or less often ravenous appetite), nausea, 
abdominal pains, constipation or diarrhea. Stiles, in an experimental 
infection on himself, thought that he could feel the parasite move. 
Several feet of tape- worm have been vomited; in these rare instances 
the individual suffers from both the intestinal and larval stages. Anemia 
is uncommon. In children reflex convulsions are possible. The parasite 
may live for 10 to 15 years. The diagnosis is determined by the segments 
and ova and the prognosis is good. 

Treatment. — As to prophylaxis: segments of the tape-worm should 
be burned; meat inspection should be general; "interstate" meat is 
well inspected; pork should always be thoroughly cooked. Hogs obtain 
ova from human feces. 

1. To cure the disease a light and chiefly fluid diet should be given for 
two days, when food is withheld for eighteen hours; this often causes 
the parasite to release its hold on the mucous membrane; a meal of 
onions and herring may be given just before drugs are administered. 

2. A preliminary cathartic cleanses the bowel, allows more direct access 
of the vermifuge to the parasite and prevents its regaining its hold when 
once detached. 

3. Anthelmintics: Of these pomegranate (granatum) ranks first; a 
decoction is made of 3 ounces of the root with 8 ounces of water, 
reduced to 4 ounces by evaporation and taken in divided doses 
within three or four hours; its active principle is the expensive pelle- 
tierine, which is given in doses of 3, 5 to 10 grains and is followed by a 
purge in an hour (pelletierinse tannas) . Male fern (f elix mas) is almost 
equally effective; it is given as the oleoresina aspidii, or extr. felicis 
maris ether., 5iss-iiss; it may be given in syrup; both are followed by a 
saline purge in three or four hours. Castor oil is never used, because it 
promotes absorption of the male fern, which causes toxic symptoms, as 
icterus, claudication or amaurosis; Sidler collected 78 cases of poisoning 
with 15 per cent, mortality and lasting blindness in 25 per cent. ; Leich- 
tenstern advises that more than 10 gm. (5 iiss) of the ethereal extract 
should never be given to adults (3 j or less to children) ; that it never be 
given on an empty stomach or given two days in succession. The drug 
decomposes easily, whence reliable preparations must be obtained. 
Combinations may be made by giving after the decoction of pomegranate, 
spts. chloroformi (Tfl.xv) for four doses or croton oil (Tfl,ij) for one dose; 
thymol (v. i.) is effective. Search should be made for the head of the 
parasite, without removal of which treatment is unsuccessful. If it is 
not found another trial should be made after a few weeks. 

1$ — Oleoresinse aspidii, 

Tr. vanillse aa gtt. xlv 

Acacias, 

Sacchari albi aa 3J 

Aquae . 5J 

M. et fac emulsum. 
S. — Take in one dose. 



304 METAZOAN INFECTIONS 

Symptoms of the cysticercus celluloses (somatic teniasis) result when 
ova of the Tenia solium are taken into the stomach; ova may reach 
the stomach from the intestines by antiperistaltic movements during 
vomiting or indirectly by handling worms voided from the bowels. 
Cysticerci in the hog produce few symptoms. In man, symptoms depend 
largely on the number and localization of the larvae, (a) In the muscles 
and skin, a few cysticerci cause no symptoms; numerous cysticerci 
cause pain, tenderness and difficult movement. Diagnosis is possible 
only on excision of the subcutaneous nodules. In Stiles' s collection of 
155 cases the localization was muscular in 20 per cent, and cutaneous 
in 3 per cent. (6) In the brain (in 75 per cent, of Stiles's series) symptoms 
depend on their location; they are often absent; if the location is in 
the cortex, Jacksonian epilepsy is frequent, and if in the medulla, diabetes 
may develop, (c) Other localizations. They may be found clinically in 
the eye (v. Graefe) and at autopsy in the lungs, kidneys or liver. There 
is no treatment except surgery. 

II. Tenia Saginata (Mediocanellata).— This form (Goeze, 1782) is 
the most frequent of large tape-worms in America and Europe. It is 
the "fat," "unarmed" or beef tape-worm. Its cysticercus bovis is found 
in masseters of beef seven times as frequently as in other muscles or in 
the heart or brain. They are not so readily seen with the naked eye as 
the cysticerci in pork. Ingestion of rare beef containing cysticerci 
produces the Tenia saginata in man, in whom alone the adult worm is 
found. 

The intestinal parasite differs from the T. solium in the following 
points: (a) its head is larger, measuring 2 mm. and is square; it has 
no hooklets but four sucking disks, which are larger, more forward and 
are surrounded by pigment, (b) Its neck is much shorter, (c) Its 
proglottides are longer (16 to 22 mm.) and broader (5 to 10 mm.); even 
1000 segments have been found, (d) The uterus contains 15 to 35 
branches, which are less dendritic than pronged or forked; in diagnosis 
the uterus is more important than the ova or size of the segments, which 
are hard for the practitioner to distinguish (Stiles), (e) The ova measure 
30-40 by 20-30/*. (/) The parasite is larger and longer, measuring 4 
to 10 meters. Its symptoms and treatment are those of the Tenia solium. 
Ingestion of the ova or segments from human feces produces the cysti- 
cercus mediocanellata, which is common in beef but extremely rare in man. 

III. Other Teniae Occurring in Man. — The Dibothriocephalus lotus 
(Linnseus, 1782), or the Russian tape- worm, is found chiefly in Russia, 
Poland, Norway, . Sweden, Switzerland and Japan. It is rarely found 
in this country unless imported (30 cases reported, Stiles), but fish in 
Lake Superior have recently been infected. Its cysticerci are found in 
the muscles and peritoneum of the pike, trout, salmon and perch and in 
man's intestines develop into the dibothriocephalus. Its head is flat 
or ovoid, possesses no hooklets and attaches itself to the intestines by 
two lateral grooves (suckers). Its neck is long and its segments broad, 
square and may number 3000 to 4200. It is long, measuring 8 to 10 
yards. It may produce a profound anemia which in severe cases closely 
resembles the pernicious type in its general symptoms and blood findings. 



DISEASES CAUSED BY CESTODES 305 

The Tenia elliptica or cucumerina (Dipylidium caninum) is a form, 
the larvae of which develop in the lice of dogs and the adult form exists 
in the intestines of dogs, sometimes in those of cats and rarely in man. 

The Tenia flavo-punctata (Hymenolepsis diminuta), the larvae of which 
exist in beetles and Lapidoptera, exists in rats and 12 human cases are 
recorded (Rausom). 

The Tenia nana (Hymenolepis nana) is the dwarf tape- worm. It 
measures but J to 2 inches in length. Its cysticercus stage is in the 
intestinal wall of the rat and its adult stage in the rat's intestine. Stiles 
decided that it is much more frequent in man than previous accounts 
would indicate and in some places is the most common type. Its head 
contains four suckers and one row of hooklets. It may occur singly or 
in myriads. Aspidium alone is of therapeutic benefit. 

Tenia Echinococcus (Echinococcus Disease) (Zeder, 1803). — We may 
first consider the adult parasite as inhabiting the intestine of the dog chiefly 
and rarely of the wolf, fox or jackal. The head is small and is provided 
with four suckers, and from 30 to 50 hooklets arranged in a double row. 
The segments number only three or four, and only the end one matures; 
it measures but 0.6 by 2 mm. but contains even 5000 ova. The 
worm is small, measuring but 4 to 5 mm. in length, is very delicate and 
white, so that it readily escapes detection. When the ovum reaches 
the stomach of another animal, the hog and ox chiefly, and less often 
the horse, sheep or man, it loses its shell and migrates to the various 
organs. The geography of echinococcus disease and mode of infection is 
as follows: In Iceland, where dogs and men live together, every seventh 
person becomes infected. In Australia both men and sheep are often 
infected. In Europe the malady is much more common than in America, 
where the reported cases in 1901 numbered 241 (Lyon); most of these 
were foreigners. Icelanders brought the disease to Manitoba in 1874. 

Infection occurs by licking of the hands by the dog, the tongue and 
anus of which often come in contact. Infection by contaminated drink- 
ing water or vegetables is less common. 

General Symptoms and Pathology. — The small embryo, freed of its 
shell, penetrates the intestinal wall arid wanders into the muscles, peri- 
toneum or radicles of the portal vein or cava, so that any tissue or organ 
may be infected, and stops when it reaches vessels too small for it. Once 
lodged, its hooklets disappear and a cyst develops, which is small at 
first but gradually reaches large or enormous proportions; cysts may con- 
tain 30, even 70 pints of fluid. Its layers consist of a granular endocyst 
and an outer finely lamellated structureless capsule; a fibrous layer 
develops outside from reaction of the tissues to the foreign body. After 
a while a number of "daughter" cysts arise from the endocyst; these 
are first "buds" and then miniatures of the original mother cyst; from 
these daughter cysts, which number about a dozen, " granddaughter" 
cysts arise by an identical process. Allen in one case found 8000 daughter 
cysts. Finally from the endocyst of the maternal and daughter cysts 
there develop "brood capsules," in which small buds arise, which grad- 
ually become scolices (the heads of which will be intestinal teniae in the 
animal which ingests them). Some cysts do not develop scolices and 
20 



306 METAZOAN INFECTIONS 

are called sterile. In animals the daughter cysts may grow outward 
(exogenous cysts) . The well-grown cyst contains fluid (v. Liver Echino- 
coccus); it is clear and neutral, has a specific gravity of 1005-15 and 
contains succinic acid, inosite (possibly sugar) and much sodium chloride 
but no albumin, unless the parasite dies and cystic inflammation develops, 
then the fluid may become buttery, gelatinous, purulent, brownish or 
grumous; the cysts disappear as well as the membrane, though the 
hooklets remain a long time. When the parasites are alive a toxin is 
present, for collapse often develops when the cyst ruptures or is punc- 
tured (anaphylaxis). 

The parasite lives for years, in one instance for twenty years; after 
a variable time, unless suppuration intervenes, the cysts become cheesy, 
perhaps calcified or ossified. 

The parasite may rupture into the serous sacs, bloodvessels (causing 
embolism), air passages, urinary tract or externally (see pages 580 and 
665) ; in 50 per cent, it is fatal within five years. 

Visceral Localization. — In 1912 cases (the total reported by Davaine, 
Finsen, Mosler, Neisser and Cobbold) the liver was involved in 51 per 
cent., genito-urinary organs in 10, intestinal canal in 9, lungs or pleurae 
in 9, brain or cord in 7, bones in 3, heart and vessels in 3, and other 
organs in 8 per cent. Vegas and Cranwell reported 970 Argentine cases 
of which 64 per cent, were hepatic. Thomas, in 809 Australian cases of 
single hydatid cyst, found the lungs involved in 16.5 per cent. Hook- 
lets have been obtained by lumbar puncture. There are reported 142 
cases of renal echinococcus, 78 cases with localization in the bones and 
23 in the pelvic bones, 25 in the pancreas, 80 in the spleen and 55 cases 
with cardiac or pericardial localization; 23 thyroid cysts have been 
reported. 

Echinococcus of the Lung. — Many cases produce no symptoms and 
are unexpected findings at the postmortem. Dieulafoy described three 
clinical stages: (a) the initial, (6) the tumor stage and (c) the suppura- 
tive or rupture stage, (a) The initial stage often has no symptoms, 
but may be marked by scanty hemoptysis, cough, emaciation and pos- 
sibly fever, all of which may closely simulate incipient phthisis. - (b) In 
the tumor stage, there are bronchial (or weak) breathing, increased fremi- 
tus and circumscribed dulness, which occur in the lower lobes and twice 
as frequently on the right side as on the left; it sometimes causes bulging 
of the chest wall. There is a sharp transition between it and the note 
of the sound contiguous lung. Dislocation of the heart and compres- 
sion of the lung may occur. The .x-rays often confirm the physical 
signs. The dulness curves upward, but is quite different from the curve 
of pleuritic effusion which is concave upward. Tumor of the lung gives 
a larger, harder flatness. Puncture reveals a clear, aseptic fluid (v. s.). 
(c) In the third stage, as in liver echinococcus, rupture may occur into 
the pleura (in which primary disease is 25 times as rare). Pneumo- 
thorax may result. Far oftener rupture into a bronchus occurs, with 
pain, dyspnea, collapse and sudden "mouthful" expectoration of pus, 
small vesicles, lamellated cyst wall and hooklets. At the time of rupture 
a curious urticaria plevelops (Finsen) which is probably toxic, as the fluid 



DISEASES CAUSED BY NEMATODES 307 

from echinococcus cysts produces it when inoculated into animals. 
Profuse hemoptoe is common. If it comes from the liver, the sputum 
is ochre-yellow from undissolved bilirubin, even when there is no direct 
connection with the bile vessels; cholesterin is often present. The 
vesicles or cyst wall may cause suffocation. Rupture may also occur 
into the pericardium, stomach or peritoneum. In this stage hectic- 
fever is usual. 

There is an unusual form of echinococcus, the multilocular form, 
probably due to a separate worm, the clinical features of which are 
described under hydatid disease of the liver, to which it is almost 
exclusively confined. Virchow first described it in 1856. It occurs in 
Bavaria, Wurtemburg, Switzerland, Austria, Austrian Tyrol and Russia; 
6 imported cases have occurred in America. It is unknown where the 
ordinary form is most common. It is rare, few more than 100 cases 
being recorded. Sixty per cent, occur in males between 20 and 50 years 
of age. The ova are spheroidal and measure 100 to 170 micromilli- 
meters. The great difference from the ordinary form is the outward 
(exogenous) growth of the cysts. The irregular and diffuse cystic pro- 
liferation is an unfavorable feature. The cysts contain a gelatinous 
material (sometimes simulating colloid cancer), surrounded by intersect- 
ing fibrous strands, which gives the liver a porous appearance, like a 
sponge or cheese with air cavities. In some vesicles there is cheesy 
material, with some resemblance to the granulomata. The vesicles 
sometimes suppurate. 

Echinococcus cysts belong to surgery, though spontaneous recovery 
is not infrequent; the operative mortality is 10 per cent., the expectant, 
60 per cent. 

DISEASES CAUSED BY NEMATODES. 

I. The Ascaris Lumbricoides. — This most common intestinal parasite 
in man, described by Linnaeus, 1758, occurs oftenest in children and 
with relative frequency in the insane. Unlike the cestodes, no inter- 
mediate host is required. The female measures 7 to 12 and the male 
4 to 8 inches in length; it is smooth, pointed at both ends and has trans- 
verse rings and four longitudinal ridges, a white one dorsally and ventrally 
and two brownish ones laterally. The oval reddish ova measure 0.075 
x 0.058 mm. and have a thick capsule; 60,000,000 eggs may develop in 
a single female. Its mode of infection is obscure. Though they usually 
occur singly or in pairs, in the upper small intestine, they may exceptionally 
develop in such numbers that they obstruct the intestine. The ascaris 
may rarely rupture through an intestinal ulcer. It has passed through a 
perforated appendix. With or without vomiting, ascarides may pass 
from' the stomach into the esophagus, nose, bronchi, lungs, middle ear, 
the common or hepatic duct, causing asphyxia, gangrene of the lung, etc. 

Symptoms are not usually pronounced, though anorexia, salivation, 
offensive breath, constipation, colic and- diarrhea occur in some cases. 
Malnutrition is sometimes marked. The parasite secretes irritating, 
volatile aldehydes and fatty acids, which may cause constitutional 
symptoms. Irritability, grinding the teeth, muscular twitchings, con- 



308 METAZOAN INFECTIONS 

vulsions or even meningeal symptoms may develop in nervous children. 
The author doubted the existence of the typholumbricosis of Chaff ard, 
Marie and Tauchon, until in one adult case, with fever and nervous 
toxemia, instantaneous subsidence of all symptoms occurred when the 
parasites were removed. 

Treatment. — After a fast of one-half to one day, santonin should be 
given, gr. ss-j, for a child, and gr. ij, iij or v, for an adult, followed by 
a saline cathartic (never by castor oil) ; if unsuccessful it may be repeated 
on two or three successive days, though toxic symptoms sometimes 
develop, as xanthopsia (yellow vision), collapse, urticaria (which may 
result from the parasite itself), vomiting or convulsions. The fluid- 
extractum spigelian (3j) may be given with or without the santonin or 
calomel. These remedies do not kill the parasite, but merely render it 
uncomfortable. 

II. Oxyuris Vermicularis (Seat-worm, Pin- or Thread-worm). — 
The female in length measures 10 and the male 4 mm. Ingested 
ova develop in the small intestine, where the worms mature and cohabit; 
afterward they exist chiefly in the lower colon and rectum. The eggs 
remain in the mother until the worm is expelled, though she occasionally 
" aborts" in the bowel. Infection occurs in those who are the most 
uncleanly, as in children and the insane. Infection may occur from 
water and green vegetables, and reinfection is not uncommon from 
scratching the anus during sleep and thus crushing the parasite; Eich- 
horst frequently found ova in the minute fecal particles about the anus 
and Zenker repeatedly demonstrated their presence under the finger 
nails. As the parasites migrate at night, the symptoms are greatest at 
that time; they may be found on the bed sheet. The anal itching and 
rectal irritation are often excessive; periproctal suppuration may be 
excited. If a vaginal discharge moistens the perineum (and only then) 
they can wander into the vagina, causing irritation, sexual stimulation 
or masturbation. Disturbance of sleep and appetite, nervous symp- 
toms and anemia may result. Diarrhea is due to large numbers of 
parasites. 

Treatment. — Santonin may be given in obstinate cases, but - local 
measures are usually sufficient, as high enemata containing small pro- 
portions of carbolic acid, quassia or turpentine. They should be 
repeated daily for two weeks. Itching is palliated by application of 
0.5 per cent, carbolic salve to or within the anus. A thymol salve on 
the anus kills worms and eggs. 

III. Trichina (Trichinella) Spiralis; Trichinosis. — Though Tiedemann 
(1822), Hilton (1832) and Paget (1835) saw the parasite, Owen (1835) 
first fully described it. Leidy saw it in the hog in 1847. Zenker 
(1855-60) first described its pathological and clinical bearings; he found 
4 cases in 136 autopsies. 

Swine are infected probably from eating offal. From the clinical and 
etiological stand-point, the (a) muscular or larval stage in hogs should 
be considered first. The small encapsulated, "hair-like" (trichina) 
worm lies in the abdominal, diaphragmatic, psoas, laryngeal and other 
muscles. It lives for a long while, even twenty to twenty-five years, 



DISEASES CAUSED BY NEMATODES 309 

without causing symptoms; calcification rarely occurs in swine. Man 
is infected by eating smoked, "cured" or insufficiently cooked pork; 
animals may be accidentally or experimentally inoculated, especially the 
rat, guinea-pig, rabbit, less often the cat and rarely the dog. Rela- 
tive to its alleged presence in fish or worms, the trichina has been con- 
fused with other parasites, (b) The adult or intestinal stage in man is 
the next phase. When eaten by man, the small capsules (larval form 
in swine) are digested and the worms liberated; in the small intestine 
they mature (the females measure 3 or 4 mm., and the males are half 
as long) and the females are fecundated in two or three days. The 
female trichinae produce 1000 to 2000 embryos at once or possibly 
in succession, which stage requires another week (from fecundation of 
the female to birth of the embryos). At the end of the second week the 
embryos migrate, entering the lymph vessels and then the veins, by 
which they reach the voluntary muscles, which they seek for their 
glycogen. They lodge between the muscle fibers, enter them and attain 
(c) the mature larval form, which is identical with the larval stage (a) in 
hogs. They measure 0.5 to 1 mm. in length. As a result of tissue reac- 
tion against the foreign bodies, a capsule develops in about six weeks, 
which surrounds one or more parasites. The capsules at first trans- 
parent, grow opaque and, after months, calcify and later the trichinae 
calcify also. 

Frequency. — Though trichinae are about 20 to 40 times as frequent in 
American as in German swine, the disease is more common in North 
Germany where raw sausage, Westphalian ham and smoked ham are 
freely eaten. Seymour reports infections in Boston among Italians 
eating raw ham (prosciutto) . Frankel denies that German trichinosis 
results from American pork. Williams of Buffalo, in 505 autopsies, 
found trichinosis in .5 per cent. Miiller of Dresden found it in 0.98 
per cent, of 1939 postmortem examinations. Other statistics usually 
show lower figures than Muller's, and like the above, are taken from 
accidental postmortem findings. The disease occurs sporadically or 
epidemically. Perhaps a thousand epidemics occurred in America. 
In Germany the epidemic at Hedersleben numbered 337, and that at 
Emmersleben 250 cases. » 

Symptoms. — Symptoms may be absent or slight, particularly in sporadic 
cases, and with moderately severe infection, as evidenced by accidental 
autopsy finding of encapsulated parasites. 

In clear cases the symptoms are divisible into two stages: (a) The 
preliminary, g astro-intestinal stage, which begins in two or three days 
after eating the diseased meat; the symptoms are not constant either 
in sporadic or severe epidemic cases; they are anorexia, nausea, vomit- 
ing, colic and sometimes diarrhea, which may resemble the evacuations 
of cholera, (b) The invasion symptoms begin in one or two weeks and 
correspond to the parasitic migration, (i) Fever is usual, but seldom 
rigors. It results from some toxin the parasites elaborate; it may 
rise to 102°, 104° or 106°, its course is remittent and intermittent, it lasts 
a few days to even two or three months, and falls by lysis. Symptoms 
attendant on any fever may be present, as headache, febrile urine or 



310 METAZOAN INFECTIONS 

quickened pulse. In severe cases, as in Zenker's, typhoid may be sug- 
gested by delirium, epistaxis, dry tongue, status typhosus, diazo reac- 
tion (in 80 per cent.), bronchitis, albuminuria and kindred toxemic 
symptoms. Typhoid and trichinosis coexisted in the cases of Zenker, 
Fischer and McCrae. (ii) Acute diffuse myositis is always most sugges- 
tive. Its intensity varies from mild forms of "muscular rheumatism" 
to the most severe and characteristic involvement; there are pain, 
tenderness, swelling, flexion to relieve muscular tension, and edema 
(25 per cent.) in the face and other locations. The worms most curiously 
select only the striated muscles, so that the edema observed in the 
abdomen and thighs, for example, never invades the scrotum or vulva. 
The eyelids are often affected greatly and early. Invasion of the eye 
muscles causes pain on moving the eyes; pain during mastication, 
phonation and deglutition marks penetration of the masseteric, laryn- 
geal and pharyngeal muscles by the parasite; dyspnea (25 per cent.) 
results from involvement of the diaphragm and intercostal muscles. 
W. G. Thompson records frequent corneal hemorrhages. The tendon 
reflexes may disappear, (c) The blood presents two striking features: 
first, the leukocytosis (15,000 to 30,000) and second, the eosinophiles, 
normally 0.3 to 4 per cent, of the leukocytes, rise as high as 30 or 86 
per cent, and though they increase in the other parasitic diseases, this 
rise is most peculiar if not pathognomonic. The eosinophilia averaged 
over 20 per cent, in more than half the cases (Thompson) and is greatest 
at the time when the trichinae enter the muscles. (See Plate XVI, Fig. 
5.) In an experimental study Graham observed the embryos in the 
arteries of rats and in hemorrhagic lesions in the lungs, and Staubli 
found them in the heart's blood and in the blood from the ear of infected 
guinea-pigs. His method consisted in laking the blood with 3 per cent, 
acetic acid, centrifugating and examining the sediment. W. W. Herrick 
and T. C. Janeway (1909) using Staubli's method, found the parasites 
in the human blood in 2 cases of trichiniasis. The blood is best obtained 
from a vein at the elbow by means of a small syringe. They thought 
it is certain they also migrate along the connective-tissue spaces, (d) 
Profuse siveats, polyuria, paresthesia, urticaria and anemia are inconstant 
manifestations. On the 24th day a second edema appears. 

Diagnosis. — This is based on (a) the possibility of infection, as by 
eating poorly cooked pork, (b) the discovery of trichinae in the blood, the 
uneaten portions of suspected meat or perhaps in the feces or cerebro- 
spinal fluid ; (c) their detection by removal of small slivers of the biceps 
or pectorals for microscopic examination, especially the parts near the 
muscular insertion; (d) the myositis with edema; (e) signs of insuffi- 
ciency, e. g., in the ocular or diaphragmatic muscles and (/) leukocy- 
tosis with eosinophilia. 

Prognosis. — This depends on the number of parasites ingested. Chol- 
eraic and typhoidal symptoms, dyspnea and pneumonia are most ominous. 
.Moderately severe early diarrhea is favorable. Children die less often 
than adults. Of the 15,000 recorded cases, 830 resulted fatally. Accord- 
ing to Stiles, the German mortality averages 5.6 per cent. In the epidemic 
at Weimar there were no fatalities in 108 cases. In the epidemic at 



DISEASES CAUSED BY NEMATODES 311 

Hadersleben 30 per cent. died. In certain epidemics the mortality was 
70 to 100 per cent. 

Treatment. — (a) Prevention comprises the feeding of hogs with clean 
food, government inspection of meat, and thorough cooking (160° F.). 

(b) In the preliminary stage, active and repeated purgation should be 
ordered, for moderate and early spontaneous diarrhea is prognostically 
favorable; calomel should be followed by salts and castor oil; male 
fern, santonin (v. s.), thymol gr. v, t. i. d. benzene Tfl,ij-v, t. i. d. and 
oil of turpentine Tfl,v-x are recommended; glycerin is now discarded. 

(c) In the stage of muscular invasion, the fever is treated as in other 
infections, the myositis by local applications of ice and by narcotics, 
and the general nutrition by food and stimulants. 

IV. Ankylostoma (Uncinaria). — A disease, due to the hook-worm, 
whose development is favored by warmth and filth; attacking those 
coming in contact with damp earth or water infected with the larvae; 
and characterized by the ova in the stools, progressive anemia, weakness, 
and alimentary, developmental and other disorders. The uncinaria 
duodenalis (ankylostoma duodenale) exists in two forms, that of the 
old and that of the new world. Ankylostomiasis was first well described 
by Piso (1648) in Brazil and the parasite was recognized in Milan by 
Dubini (1838). It occurs chiefly in the tropics and subtropics, including 
the Philippine and Sandwich Islands; according to Thornton, it is the 
most dangerous of all tropical diseases. In Egyptian chlorosis it was 
found by Bilharz and Griesinger, and is said to be present in nearly 
every autopsy made there. It is endemic in Italy ("bricklayers' anemia") 
and also in Belgium, France, England, Germany, Hungary and the Bal- 
kans. In India it is found in even 80 per cent, of the healthy coolies and 
in 300 autopsies in Assam it was present 299 times. Stiles (1902) described 
the new-world type, caused by the Uncinaria (or Necator) Americana, 
which is also found in Africa and East Indies. Thirty per cent, of Porto 
Rican deaths result from uncinariasis, and Ashford and King state that 
90 per cent, of the rural and 50 per cent, of the urban population have 
the disease; during six months in 1905, 18,865 cases were treated in 
Porto Rico, of which 33 per cent. died. Capps in 1903 collected 50 
American cases of the European type. It is possibly the most important 
disease of our Southern States. Dock and Bass estimate that over a 
quarter of the Southern, apparently healthy, population, suffer from this 
malady. 

In the Westphalian mines, Tenholt himself treated over 4000 cases. 
It was the cause of the "tunnel anemia," observed in building the St. 
Gothard tunnel. It is disseminated by Italian and Polish workmen. 
Infection comes from the food, drinking water and earth which are 
infected by dejections from persons suffering from the disease. Looss 
and C. A. Smith proved that it may enter by the skin, producing 
the "ground itch," common in the Southern States. Dock and Bass 
believe the skin to be the sole mode of infection. The larva penetrates 
the skin in a few hours and, by way of the heart, lodges in the lungs 
and bronchi, whence it is expectorated or swallowed; in the latter case 
the larva reaching the intestine, sheds one skin and acquires a buccal 



312 METAZOAN INFECTIONS 

capsule by which it adheres to the mucosa; from the mucosa it draws 
blood and sheds its last skin. Subjects, harboring the hook-worm, 
void feces laden with ova of the parasite. In localities, most severely 
affected, the privies are commonly so exposed that swine or fowl scatter 
the ova from the dejecta over the ground; even more frequently, out- 
houses are not employed, but the infected persons defecate in the barn- 
yard, bushes, garden, fields or in the mines. The ova develop into larvae 
in the moist ground, shallow water or the soil of a mine, and attack those 
running bare-foot, enter the hands or reach the mouth. 

The male worm is 8 to 10 and the female 10 to 18 mm. in length; 
the mouth has hooks by which it adheres to the mucosa of the duodenum. 
The ova measure 30 to 60 micromillimeters ; they are oval, are covered 
with a translucent shell and differ from the flat oxyuris ova. They 
show 1 to 6 yolk segments and may number over 4,000,000. They 
develop into the larvae. 

Symptoms. — Some subjects resist the parasites they carry and present 
no symptoms. Despite their immunity, these "carriers" disseminate 
the disease. Mechanisms of the symptoms: (1) The parasites suck 
blood; Ernst and Treichtenstern describe dying worms ejecting blood, 
as a locomotive puffs smoke. (2) They also bore into the intestinal 
mucosa but destroy it and the submucosa which Looss pictures drawn into 
their esophagus and even into their intestines. (3) Their bites become 
infected (A. J. Smith). (4) It is also possible that they secrete a sub- 
stance which degenerates the bloodvessels, hinders hemostasis or operates 
as a hemolytic. Types: (i) The symptoms may be only mild dyspepsia, 
slight anemia (hemoglobin 80 or more), dull headache, etc. (ii) Moderate 
intensity; with hemoglobin 60 to 80 per cent., epigastric pain, poor 
development in the case of children and some apathy, (iii) The severe 
type, with hemoglobin 30 to 60 per cent., great dyspnea and abdominal 
pain, vomiting, anasarca and other symptoms (v. i.). (iv) The severest 
form, with hemoglobin below 30 per cent., and all symptoms extreme. 

The ground itch represents the atrium in most cases and a history of 
it is generally obtained. Around the toes, or less often on the hands or 
buttocks, an itching, very painful eruption develops, first of vesicles 
which loosen the skin and contain the larvae, then of pustules, oozing 
and fissures. In a few days the larvae reach the air passages (v. s.) and 
cause sore throat, bronchitis, cough and expectoration, which latter, 
being swallowed, allow the larvae to reach the bowel. 

Alimentary Symptoms. — The tongue exhibits ink-like patches. The 
appetite may be increased in cases of mild or moderate intensity but is 
lacking in the severest types; it is often perverted and resin-chewing, 
eating of hair, earth (geophagy), clay or pebbles, inordinate or early 
chewing of tobacco, etc., are frequently observed. Ashford and King 
find that epigastric pain or uneasiness is the most constant, suggestive 
and clear symptom. Nausea, vomiting, diarrhea alternating with 
constipation and colic are common. Occult or obvious blood in the 
stools is the rule. In the Panama case which the author saw in the 
County Hospital, there was great nausea, pain and exquisite abdominal 
tenderness; the stools contained blood, eosinophile cells, Charcot- 



DISEASES CAUSED BY NEMATODES 313 

Leyden crystals and ova. Stiles suggests a ready test for blood, by which 
parts of the stool are placed upon blotting paper; after an hour or so a 
rusty stain develops about the stool. Children become pot-bellied. In 
the subjects coming to autopsy, the feces show Charcot's crystals, eosino- 
philes, much mucus, ova, worms and blood. Reddish areas may be seen 
through the unopened gut. The bowel may appear red or chocolate 
color; Peyer's patches and the solitary follicles are often swollen; ecchy- 
moses, submucous cysts and erosions are common; and moist red areas 
are noted, either elevated or bitten by the worms, and eosinophilic infil- 
tration of the mucosa, submucosa and even the muscularis. Most of 
the parasites lodge in the jejunum but also in the duodenum and upper 
ileum. Before the death of their host, many leave the body. 

Blood Findings. — An anemia develops which is first of the secondary 
type and later resembles pernicious anemia; it is due to loss of blood 
and possibly some hemolysin from the parasite. The hemoglobin 
averages 67 per cent. (Dock and Bass) or 42 per cent. (Ashford and 
King) ; it is more reduced than the red cells (low color index) . The 
red cells range between 2 J and 3 J millions; there are polychromatophilia, 
normoblasts and microcytes. The white cells are usually not increased; 
in advanced cases there is leukopenia; the eosinophiles average 15 to 
25 per cent., but may run higher (30 to 72 per cent.). The skin is sallow, 
pasty, even lemon-color or waxy, and finally edematous. The bone- 
marrow is pale — perhaps lymphoid, gelatinous or fatty; nucleated 
cells indicate blood regeneration. 

Many, perhaps most, of the other findings are anemic? — the extreme 
dyspnea, rapid pulse (over 100), pulsating vessels, edema of the skin, 
serous sacs and brain; dulness, somnolence, headache, inertia (laziness), 
weakness and headache are common and in severer infections the vertigo 
is extreme; pains develop in the joints and sternum; marked pares- 
thesia, abolition of the patellars and weakness develop, to the simulation 
of paralysis; the pupils dilate and the eyes present a fishy look; there 
is retinal clouding, anemia and hemorrhage; and extreme apathy, 
anxiety or melancholia intervenes. Cardiac hypertrophy and dilatation 
and arteriosclerosis are frequent. The urine is copious, of low specific 
gravity, either free of albumin or highly albuminous and contains no 
casts. The heart, liver and kidneys are fatty, degenerated and enlarged; 
the spleen is not usually enlarged (save in Egyptian autopsies). The 
temperature is subnormal, sometimes with irregular runs of fever. Mal- 
nutrition and maldevelopment mark the pronounced types. Children 
grow poorly and reach puberty late and incompletely. Men of twenty 
may appear ten years old. Some are dwarfs. The pubic hair is scant, 
the beard comes slowly, the mammae are small, and in males, impotence, 
and in women, amenorrhea are common. 

Diagnosis. — The diagnosis is suggested by the anemia, dyspnea, 
dilated heart, epigastric pain, maldevelopment and history of ground 
itch, but is made certain only by examination of the stools for ova 
or worms. 

Prognosis. — The outlook depends on the stage of the malady. Uncin- 
ariasis greatly reduces the resistance to other diseases. The eosinophilia 



314 METAZOAN INFECTIONS 

measures the degree of resisting power. The mortality is 10 to 30 per 
cent. Much depends on early therapy. 

Treatment. — 1. Prevention. — Drinking water should be boiled and the 
hands should be cleansed before eating. The stools should be received 
in water-tight closets and disinfected; careless defecation in mines has 
caused wide dissemination of the disease. Mines should be disinfected 
with the milk of lime. Prevention means (i) the extermination of the 
mature worms in man, particularly in " carriers;" (ii) preventing the 
growth of ova into larvse; and (iii) guarding against infection by already 
developed larvae. 

2. Medication. — Thymol is the most efficacious remedy. After a 
preliminary purge of sodium sulphate, the patient is kept abed and as 
the peristalsis decreases, gr. xx of thymol are given in capsules and repeated 
twice at three-hour intervals. The thymol is first well triturated with 
an equal amount of sugar of milk to prevent its cohering and followed 
by a saline purge two hours afterward. The first treatment evicts 80 
to 90 per cent, of the parasites, 5 courses cure 95 per cent., and persisted 
in, "it always succeeds." As toxic symptoms (nervous excitation, 
smoky urine, dizziness, fainting, abortion or death; 11 cases in America) 
may develop, no solvents of thymol should be given, as alcohol, chloro- 
form, ether or castor oil. This treatment should be repeated once a 
week, as long as ova or Charcot-Leyden crystals appear in the stools. 
Very edematous patients do not tolerate thymol. Male fern is considered 
the best remedy by Tenholt and other Westphalian writers. 

V. Filaria. — Demarquai (1863) first found the embryos of the filaria; 
Wiicherer (1866) found them in the urine and Lewis (1872) in the blood. 

1 . Filaria Nocturna. — (Bancrofti, Cobold, 1877) . Its distribution is largely 
tropical and subtropical. It occurs in 30 per cent, of the inhabitants of 
the Samoan and Friendly Islands. In the United States it has been 
found in the South, New York, Illinois and Pennsylvania, (a) Infec- 
tion of man occurs by mosquito bites or possibly by water, contaminated 
with mosquito eggs. In the mosquito, the embryos change to the young 
adult form, (b) The next stage is the presence of adult filaria in the 
lymph channels, where they cause lymph stasis and lymphangitis. The 
female filaria measures 155 x 0.7 mm. and the male 83 x 0.4 mm. (c) The 
embryos enter the blood current from their birth place, the lymph channels; 
they are very numerous, measure \ inch in length and the diameter of 
a red blood cell. Under a low-power lens their active movements are 
easily seen. They appear in the blood only at night, usually near mid- 
night, and during the day retire to internal organs, as the lungs, but if 
the patient sleeps by day, they appear in the daytime only. (For Staubli's 
method of detection see page 310.) 

Symptoms are absent in the majority of cases of human and animal 
infection and are due to the parent worm, not to the embryos, (a) 
Chyluria or hematochyluria is due to plugging by the worm or its ova of 
the lvmphatic vessels in the peritoneum, pelvis, vesical and perirenal 
tissues. Lymph stasis, ectasia and lymphangitis result, with intermittent 
rupture into some part of the urinary tract, and the passage of milky, 
chylous urine, containing molecular albumin and fat. The amount of 



DISEASES CAUSED BY NEMATODES 315 

the urine varies; it may be normal or increased. There is usually also 
some blood. If the blood clots, vesical disturbance results. The embryos 
are often found in the blood and sometimes in the urine; there is also 
a non-filarial chyluria. The affection may last for years without im- 
pairment of health. The very rare rupture into the peritoneum causes 
chylous ascites, (b) The lymph scrotum is due to lymphatic obstruction 
by the adult worm. The scrotum may weigh 50 to 200 pounds. Rupture 
into the tunica vaginalis causes chylocele. The labia may be similarly 
involved. The embryos are often missing from the blood, being appar- 
ently confined to the local involvement by the lymphangitic thickening, 
whence the difficulty in stating the relative percentage of parasitic and 
non-parasitic cases of lymph scrotum and elephantiasis, (c) Elephan- 
tiasis usually develops in the legs, scrotum and labia, less often in the 
arms, breasts or trunk. In forms (6) and (c) there occur intermittent 
exacerbations with fever and nervous disturbance. 

2. Other Forms of Filaria. — The exact status of the Filaria diurna 
(Manson, 1891) is not known; F. per starts (Manson, 1891), which causes 
pustular eruptions (craw-craw) ; F. loa (the adult stage of Filaria perstans) 
which inhabits the conjunctiva; F. labialis; and F. oris and bronchialis 
are other forms. 

Treatment. — (a) For prevention, mosquitoes and infected water 
should be avoided, (b) No parasiticide is known, (c) Chyluria is 
treated by cinchonization, salvarsan and z-rays. (d) Lymph scrotum 
and elephantiasis may necessitate castration or amputation. 

VI. Dracunculus (Filaria) Medinensis. — This is found on the West 
African coast, the Gold Coast, in Abyssinia and South Egypt; on the 
Caspian Sea and Persian Gulf; in the East Indies, parts of India and 
South America. Guinea- worm disease (drachontiasis) developed in 
persons who had always lived in Philadelphia and Fortress Monroe. 
Man is infected by a small water flea (cyclops) which contaminates the 
water with the larvae (embryos). These embryos, measuring 0.6 mm., 
enter the stomach, bowel and probably the mesentery, where they 
copulate; the male, of which little is known, is either discharged from 
the bowel or dies in the mesentery. The female is cylindrical in form, 
measures 50 to 80 x 2 mm., has a triangular mouth, eight papillae and a 
blunt tail; its uterus occupies almost its entire length. The female, 
which is usually solitary, wanders downward in the subcutaneous and 
intermuscular tissues to the thighs, legs and in 66 per cent, of cases 
reaches the feet where, near its head, vesicles, abscesses and ulcers 
develop. Its downward course occupies a year, during which it may be 
felt subcutaneously. When the skin breaks the parasite discharges her 
embryos and then leaves the body, to die. 

Treatment. — Treatment by excision, or by 1 to 1000 bichloride injec- 
tions, seems most rational. If the worm is ruptured in efforts to extract 
it, high temperature, alarming nervous symptoms and sepsis result from 
migration of the embryos liberated in the tissues. 

VII. The Trichocephalus Dispar or Whip-worm. — This nematode is 
found most often in southern Italy and France and but seldom in this 
country; one case occurred in the Cook County Hospital. It is also 



316 METAZOAN INFECTIONS 

called trichuris trichura. It requires no intermediate host, enters with 
the food and drink and is found in the cecum and large gut. The male 
is slightly shorter than the female, which is 4 or 5 cm. in length. The 
anterior portion of the worm is thin; the posterior two-fifths is thick, 
in the male round and in the female pointed. It bores into the mucosa 
and is nourished by the blood and not by the alimentary contents. The 
eggs measure 0.05 mm., are oval and are marked by a button-like pro- 
jection. It causes few symptoms; occasionally there is severe abdominal 
pain. Three fatal cases are recorded. Male fern and thymol internally 
and benzene 3j to Oij of water as an enema are recommended. 

VIII. The Strongyloides Intestinalis. — This includes a number of 
nematodes, as the Anguillula intestinalis or stercoralis, rhabdonema, 
etc. They are found in the endemic diarrhea which occurs in Cochin- 
China. Strong reports cases from Manila and W. F. Thayer reported 
3 cases in America. A few parasites cause no symptoms. Thymol is 
almost specific. 

Enstrongylus Gigas. — The Enstrongylus gigas which occurs frequently 
in dogs and wolves, is very rare in man. It is a nematode whose ova 
appear in the urine. It causes pyelitis, hematuria, colic, tenesmus and 
sometimes chyluria. 

DISEASES CAUSED BY TREMATODES (DISTOMIASIS). 

1. Bilharzia disease (endemic hematuria) is due to the blood fluke 
(Schistosomum hematobium). Bilharz described the disease in 1851. 
It is an African and Japanese affection; it has prevailed for many cen- 
turies in Egypt, where Bilharz considered that half of the lower classes 
was affected. It is equally frequent in Uganda. Importation has 
occurred into India, the Mediterranean islands and America. Only 12 
cases have occurred in the United States. 

Children are more predisposed than adults to infection, which occurs 
through the drinking water or possibly through the skin. The embryos 
enter the stomach, penetrate the alimentary mucosa and mature in 
the veins of the pelvis, spleen, mesentery, liver, kidney and bladder. 
The male worm measures 4 to 15 x 0.6 mm., the female 15 to 20 x 0.3 mm. 
The male is rolled up like a leaf, forming a groove in which the female 
lies during copulation. Many ova are found in the urine; they are 
oval, carry a spine and contain a ciliated embryo. They die in the urine 
in a day but live for some time in water, where their life-history is still 
imperfectly understood. 

Hematuria is the most common and often the only symptom; it 
may be macro- or microscopic and occurs chiefly at the end of urination ; 
examination shows many ova and eosinophiles. Cystitis occurs in severe 
infection. Stones are not uncommon, particularly in Canton, China. 
Suppuration may develop fistulae. These clinical symptoms result from 
massive accumulation of ova in the submucosa, which leads to papillo- 
matous hyperplasia, hemorrhage, suppuration, necrosis, salt deposits 
(calculi) and rarely to malignant degeneration. Similar changes in the 
rectum cause pile-like papillomata, dysenteric evacuations and tenesmus. 



DISEASES CAUSED BY TREMATODES 317 

As complications, pyelitis, prostatitis, urinary fistulse and changes in the 
liver (thickening of the periportal connective tissue), uterus, vagina, 
seminal vesicles and renal pelvis, resembling those in the bladder, may 
develop. The eosinophiles are increased to' 10 to 50 per cent. 

Schistosomum Japonicum '(Cattoi) . This fluke is found in China, the 
Philippines and Japan. Its ova are smaller and have no spine. Living 
in the bloodvessels of the digestive tract, it induces a severe anemia, 
dysentery, ascites and cirrhosis of the liver and spleen. Epilepsy may 
develop. In the intestines, other flukes may be found — the Gastrodiscus 
(iVmphistoma) hominis and Distoma (Fasciolopsis) Buskii, in India and 
the Mesogonimus heterophyes in Egypt and Japan. 

Treatment. — Change of climate is advisable to avoid reinfection. The 
parasites usually die, though slowly, and as no local or systemic remedies 
modify their life-history, treatment must be expectant. 

2. Lung flukes cause the endemic hemoptysis, observed by Balz chiefly 
in North China, Corea, Japan, the Philippines and Formosa. The 
parasite is named Distoma pulmonale (Paragonimus westermani); it 
measures 10 x 6 mm. and is found largely in the lungs, but sometimes 
in the brain and skin. In young males dyspnea, anemia, lung induration 
and a chronic cough develop with bloody or prune- juice sputum, in which 
are found blood, dark brown ova measuring 0.08 to 0.1 x 0.05 mm., 
eosinophile cells and Charcot-Leyden crystals. The hemorrhages, which 
are sometimes profuse, result from small infarcts and cysts of ova in the 
subpleural lung tissue. Epilepsy and hemiplegia may result from brain 
embolism. The course is usually favorable, though chronic, and is not 
influenced by treatment. 

3. Liver flukes (Fasciola hepatica, Opisthorchis sinensis and at least 
four other species) enter like the above forms through contaminated 
water. The fluke is found in the upper small intestine and the biliary or 
pancreatic duct. It measures 10 to 20x2 to 5 mm. and its ova 30 x 15/jl. 
It is found in Japan and certain provinces show a mortality of 20 to 
72 per cent. (Balz and Inouye). White reported 18 cases in San Fran- 
cisco, and Brayton and Darling cases in Panama. The liver is enlarged 
and tender; icterus results from biliary stasis, for the parasites lie in 
the walls of the biliary ducts and gall-bladder; diarrhea develops, and 
the dejections contain ova and blood; anemia, ascites, anasarca, ady- 
namia and emaciation develop and death invariably results. There is 
no treatment beyond the symptomatic support of the heart. Prophyl- 
axis : avoidance of drinking or of swimming in canal water, and thorough 
cooking of fish and mussels have stamped out the plague in one Japanese 
province (Inouye). 



SECTION II. 

DISEASES OF THE CIKCULATIOK 



DISEASES OF THE HEART MUSCLE. 



INTRODUCTORY PHYSIOLOGY. 

Although convention has sanctioned the classification of heart diseases 
into those of the myocardium, endocardium and pericardium, besides 
its nervous disturbances, nearly all cardiac disorders are referable — on 
the last analysis — to failure of the heart muscle. A review of the more 
salient affections of the heart relegates many of them to a secondary place. 
Thus, valvular diseases seldom attract attention, until the overstrained 
heart muscle becomes more or less " incompetent." In pericarditis, 
the fresh effusion presses on the heart and embarrasses its diastole; or, 
when older adhesions firmly anchor the organ, the heart's systole is 
impeded. The heart muscle and the vasomotor system sustain the 
brunt of the acute infections and chronic intoxications. Angina pectoris 
is a myocardial malady, arising from disease of the coronary vessels, 
which bathe the myocardium with fresh blood. Arteriosclerosis works 
its gravest injury on the cardiac musculature. The fatty heart, chronic 
myocarditis, the senile heart, heart-block, and many of the arrhythmias 
or "neuroses" of the heart, are but instances of failing competency in 
some segment of this hollow contractile muscle. 

Until recently it was maintained that the heart mechanism was 
regulated by nervous influences (the neurogenic theory), but now the 
source of cardiac action is held to reside in the muscle itself (the myo- 
genic theory — which is possibly overstrained in our swing from one 
extreme to another). Gaskell enumerates the functions of the myo- 
cardium as five: "The muscular fibers of the heart are capable of 
rhythmically creating a stimulus (rhythmicity) , of being able to receive 
a stimulus (excitability), of responding to a stimulus by contracting 
(contractility), of conveying the stimulus from muscle fiber to muscle 
fiber (conductivity), and of maintaining a certain ill-defined condition 
called tone (tonicity)." 

The normal (or sinus) rhythm of the heart consists of the successive 
contraction of the sinus, auricle and ventricle. The stimulus to contrac- 
tion arises in the remains of the sinus venosus (the sino-auricular node 
of Keith and Flack) at the mouth of the superior vena cava; it is called 
the pace-maker of the heart. In the wall of the right auricle near the 



320 DISEASES OF THE HEART MUSCLE 

coronary sinus is Tawara's auriculo ventricular node, the origin of the 
auriculoventricular bundle of Kent and His, by which impulses are 
conducted from the auricle to the ventricle. (In pathological rhythm, 
stimuli may arise from other points than the sino-auricular node and 
initiate extrasy stoles.) Contractility is so regulated that each systole 
is forcible (to the full capacity of the heart's muscle); each beat is fol- 
lowed by a period of rest — a refractory period in which contraction 
cannot be elicited. Tonicity holds the heart in "tone," keeps its volume 
less than it would be if the myocardium completely relaxed, and prevents 
dilatation. Tone is increased, e. g., by digitalis, and lessened by severe 
toxemias and cardiac overstrain. The vagus inhibits or decreases the 
rate, conductivity, irritability and contractility and the sympathetic 
increases the rate, etc. Throughout this section, repeated reference to 
these functions will be made, as the myocardium is the key to cardiac 
conditions. 

In the balanced circulation, besides the heart and its nerves, the 
bloodvessels are important; without their elasticity and contractility 
and their vasomotor control, the circulation could not be maintained; 
and in vasoparalysis, we see the circulatory failure of certain severe 
toxemias. Respiration aids in charging the heart with blood and the 
coronary flow is directly stimulating. We are just gaining, also, a small 
conception of the part played by the organs of internal secretion, e. g., 
the chemical action of the secretion from the suprarenal glands and the 
pituitary body. 

DILATATION OF THE HEART. 

Definition. — Dilatation means distention and diminished tonicity of 
the chambers of the heart. Tonicity is that function of the heart which 
sustains a slight degree of contraction even during the diastole. Hyper- 
trophy is thickening of the walls of one or more chambers. The two 
conditions are separate in themselves, though frequently combined; 
dilatation is the incentive to hypertrophy. Lancisi (1706-1728) described 
hypertrophy and dilatation. 

Etiology. — 1. Mechanical Causes. — The normal heart may possibly 
yield to increased blood-pressure or a weak heart to normal pressure. 
Rarely, if ever, is dilatation an independent condition, (a) Valvular dis- 
ease, e.g., dilatation of the left ventricle in aortic insufficiency, or of the left 
auricle and right ventricle in mitral stenosis. Hypertrophy is inversely 
proportional to the dilatation. In combined aortic and mitral insuffi- 
ciency, the heart is enormous — the ox heart, cor bovinum, bucardia. 
(Two types of dilatation are recognized : the accommodative, in which 
it is compensatory and the dilatation of stasis). (b) Causes raising 
arterial blood-pressure, as stenosis of the aorta, arteriosclerosis and 
nephritis produce hypertrophy and dilatation of the left ventricle. 
Workers in caissons may suffer from dilatation, (c) Causes raising 
blood tension in the lesser circulation, as spinal deformity, chronic disease 
of the lungs and pleura, which produce hypertrophy of the right ven- 
tricle; of these emphysema is the most important; abdominal lesions 
are thought to reflexly raise the pulmonary blood-pressure. The lung's 



DILATATION OF THE HEART 321 

vascular area must be reduced to 25 per cent, in order to affect the right 
heart. When there is pulmonary obstruction the heart stands pneumonia, 
bronchitis and other infections poorly. The size of the heart varies 
much physiologically; during severe exercise, the systole is incomplete 
and right-heart dilatation — even tricuspid regurgitation and marked 
venous stasis — may follow. Physical training increases the power and 
reserve strength of the right heart, the "wind" and endurance. An 
equal effort in an individual out of training, or with poor nutrition, 
"breaks his wind" and produces cardiac exhaustion. Air embolism 
also produces dilatation. 

2. Nutritive Disturbances. — Dilatation may be induced (a) by 
acute infections, leading to cardiac degeneration or acute myocarditis; 

(b) by anemia or loss of fluids; (c) by chronic myocarditis, fatty heart 
or coronary atheroma, possibly following sudden heart strain; by endo- 
or pericarditis invading the heart muscle by contiguity, pericardial 
adhesions, etc.; (d) by poisons, alcohol or tobacco. 

Pathology. — Dilatation occurs (a) with thinning of the walls, simple 
dilatation, or (6) with eccentric hypertrophy (q. v.). It is most common 
in the thin-walled auricles and less resistant right ventricle. The muscle 
is lax and the heart, when held inverted by the basal vessels, may in 
extreme instances fall flabbily like a cap over the hand; the endo- and 
pericardium may almost touch. 

The papillary muscles and trabecular are flattened (pressure atrophy) 
and frequently thickened (pressure sclerosis). Microscopically the 
heart muscle may be normal, or show fatty or cloudy degeneration or 
myocarditis. There is much blood in the heart's chambers, cavse and 
other veins. In dilatation occurring during the death agony from acute 
lung disease, suffocation, etc., the right heart is chiefly affected and 
on removal of the postmortem clots the chambers seem nearly of normal 
size. 

Physical Signs. — 1 . Dilatation of the Left Ventricle. — (a) On inspec- 
tion, the apex beat is dislocated downward, to the left and is diffuse, undu- 
lating and weak, if not absent. (6) On palpation, the apex may not be 
felt even though visible; in other cases the apex and heart shock are snappy 
and feel strong to the inexperienced hand, yet contrast sharply with 
the weak, rapid and often irregular radial pulse. (A palpable impulse 
may be due to active diastole of the auricle, to passive distention of 
the ventricle by blood or to closure of the auriculo ventricular valves.) 
Albertini (1761) distinguished hypertrophy and dilatation by palpation. 

(c) On auscultation, the heart tones are weak, though sometimes snappy. 
The first apex tone is more valvular. The second aortic sound is weak 
because of poor arterial tension. In insufficient hearts, the heart tones 
sound alike, resembling the fetal heart tones (embryocardia) . An apical 
systolic murmur is sometimes due to relative insufficiency of the mitral 
valve whose normal circumference of three and one-half inches may be 
stretched to five. Decreased tonicity accounts for the dilatation and 
murmur also; these signs may be relieved by rest and digitalis. Gallop- 
rhythm consists of three tones like the rhythm of the hoofs of a galloping 
horse; according as the extra tone falls at the end, beginning or middle 

21 



322 DISEASES OF THE HEART MUSCLE 

of the diastole, we distinguish presystolic, protodiastolic or mesodiastolic 
gallop-rhythm. The presystolic type is heard in strongly beating hearts, 
being due to strong auricular contraction and is likewise heard in weak 
hearts, being due to the ventricle beating later after the auricle than 
usual, from delayed conductivity. The other two types originate in an 
extra tone developed in the ventricles, probably based on decreased 
tonicity. The protodiastolic (third) sound is heard in the majority of 
normal young individuals. Gallop-rhythm is heard in the failing hyper- 
trophied hearts of nephritics chiefly, in valvular lesions, atheroma, 
emphysema and in acute diseases; it is a sign of great danger. 
(d) On percussion, the heart extends to the left and downward, giving 
a more oval area of dulness. 

2. Dilatation of the Right Ventricle. — This is more common. 
(a) On inspection, a diffuse beat is seen to the right of the sternum or 
in the epigastrium; and (6) it may be palpated, (c) Auscultation shows 
weak heart tones, and (d) percussion outlines dulness to the right of 
the sternum. Extreme dilatation increases the tricuspid orifice from 
four and one-half to five or six and one-half inches, causing relative 
tricuspid insufficiency. 

3. Dilatation of the Auricles. — Because of the deep location of 
the left auricle physical signs of dilatation are seldom obtained. The 
changes usually ascribed to the left auricle are due to enlargement of 
the conus of the right ventricle. The distended right auricle is recognized 
by undulation to the right of the sternum, above the right ventricle, 
by dulness and sometimes by a presystolic wave. 

Dilatation of all the chambers gives the heart a trapezoid conforma- 
tion. The symptoms and physical findings of dilatation may develop 
gradually or abruptly after violent exercise, especially when the heart's 
nutrition is altered. 

Symptoms. — Subjectively, the consequences of dilatation are loss of 
reserve power of the heart (see Symptoms of Valvular Disease) . Cardiac 
insufficiency is evidenced by breathlessness or dyspnea, by cyanosis, 
cough, syncopal attacks, precordial anxiety, and, when the systole 
ceases to expel completely the blood from the dilated chambers, the 
liver enlarges and becomes tender, the lungs reveal crepitant rales along 
their bases, the legs swell and the urine, the surest gauge of cardiac 
competency, becomes less abundant. 

Diagnosis. — The diagnosis depends on the etiological factors, the 
weak tones, the increased dulness and evidences of cardiac failure. The 
absolute heart dulness in middle life is bounded by the left border of the 
sternum, the fourth or fifth rib and the left parasternal line. Percussion 
should be made lightly, using the finger-to-finger method and applying 
the passive finger firmly against the chest wall; observance of this tech- 
nique gives as accurate results as does the fluoroscope. According to 
Moritz, the normal heart measures 3.5 to 4.5 cm. to the right of a mid- 
sternal point and 7.5 to 8.5 cm. to the left. The relative dulness reaches 
from the third or fourth rib above to the apex beat and to a line drawn 
obliquely from the third left costal cartilage across the sternum to the 
fifth right costal articulation. Percussion is difficult in distorted, fatty 



DILATATION OF THE HEART 323 

or edematous chests. Various functional tests 1 are suggested, yet none 
is satisfactory except the test where a given effort causes it to decrease 
in size, stimulation inducing tonicity, or to increase in size, decreased 
tonicity on overstraining. Differentiation concerns the same conditions 
discussed under effusive pericarditis (q. v.). Rest and digitalis benefit 
dilatation, but not pericardial effusion. Consolidation of the adjacent 
lung margin can be recognized by the altered breathing and rales. 
Mediastinal tumor and aneurysm are suggested by pressure symp- 
toms. If the margins of the lung are adherent from pleural adhesions 
or emphysema obscures the outlines of the heart, dilatation is diagnos- 
ticated by the relative, more than by the absolute, dulness. Palpatory 
percussion, very lightly made, is most valuable and the feel of the increased 
dulness has greater diagnostic value than the sound elicited. Encap- 
sulated pleurisy is differentiated by careful puncture, if other signs fail. 
The fluoroscope is frequently of aid. In short chests and in 12 per cent, 
of women, the apex is seen normally at or even beyond the nipple. In 
spinal curvature the topographical relations are disturbed by visceral 
luxation, and the irregularity of the sternum and ribs makes percussion 
uncertain. In fat individuals, dulness may result from adipose deposit 
in the mediastinum. Dilatation must not be mistaken for dislocation 
due to distention of the abdomen. 

Prognosis. — The prognosis largely depends on the etiology. 

Treatment. — (a) The cause must be treated, (b) The dietetic and 
special indications of valvular disease (q. v.) must be carried out. (c) 
OerteVs treatment consists of (i) limitation of fluid ingested, and stimula- 
tion of its excretion by sweats and deep inspirations; beer must be 
interdicted. Many nervous subjects tolerate limitation of water very 
poorly, (ii) Reduction of the body weight (see Obesity), (iii) Stimula- 
tion of the circulation by exercise. Mountain climbing is said to stimulate 
the heart, develop the respiratory muscles, increase the lung capacity 
and widen the vessels. Reasonable exercise may prove beneficial, but 
rest in bed gives better results; exercise is injurious when the heart 
muscle or coronaries are diseased, or when endocarditis, pericardial 
adhesions or Bright's disease exists, (d) The Schott method consists of 
(i) baths in springs containing sodium and calcium chloride, iron car- 
bonate and carbon dioxide. The temperature should be a few degrees 
below body heat, and they should be given once daily for five to twenty 
minutes, for two or three days, and then intermitted. They may be 
given artificially, using 40 gallons of water, with 3 to 10 pounds of salt, 

1 In Schapiro's test, the normal decline of 7 to 15 beats in the heart's rate, when the 
patient lies down, is absent in decompensation. Graupner's test: Normally the pulse and 
blood-pressure rise after exertion, such as running upstairs, and if the effort is prolonged and 
arduous, the figures fall to normal or below it, but the pulse rises and falls before the blood- 
pressure begins to rise and fall ; in weak hearts the blood-pressure rise is delayed, decreased 
or absent. In Hertz's test, the patient sits and very slowly flexes and extends the right 
forearm, directing all his attention on the act but avoiding any firm contraction of the 
muscles; the physician supports the patient's elbow with his left hand and directs the move- 
ment with his right, but without aiding the movement; there is no influence on the pulse 
in normal conditions, while in pathological conditions, it is slowed 5 to 20 beats. Marey's 
and Levy's test consists of digital compression of both femoral arteries; in normal conditions, 
within three minutes the blood-pressure rises 5 to 15 mm. Hg. ; in hypertrophy, even more 
and in weak hearts, no rise (this test is not valid in neurotics) . 



324 DISEASES OF THE HEART MUSCLE 

10 ounces of pure calcium chloride and carbon dioxide generated in a 
vessel from sodium bicarbonate and hydrochloric acid. The temperature 
is then reduced to 90°, and the amount of carbon dioxide increased. 
The bloodvessels are contracted and later dilated. The pulse becomes 
slower and fuller, dilatation decreases, stasis is lessened, diuresis is 
increased and the metabolism of the muscles and heart is improved. 
(ii) Movements by the patient, resisted by the operator, dilate the vessels. 
Active exercise constricts the vessels. The Nauheim treatment has been 
unduly exploited. 

Each exercise is made against slight resistance applied by the physician. 

1. The arms are extended in front of the body at the level of the shoulder, with the 
palms touching. The arms are then moved slowly outward till they are in a line with each 
other; they are then brought back to their original position. 

2. The arm and hand hanging down with the palm turned forward, the forearm is 
flexed upon the arm (which is kept still) until the fingers touch the shoulder. The forearm 
is then extended to its original position. 

3. The arms, hanging down as in No. 2, are raised outward until the thumbs meet over 
the head ; they are then returned to their original position. 

4. With arms dependent, the fingers, at the first phalangeal joints, are pressed together, 
and the arms are then raised until the hands are above the head, after which they are 
brought back to their original position. 

5. The arms, hanging in the position of "attention," are advanced forward parallel to 
each other until they are elevated to a vertical position; they are then brought back to 
where they were before. 

6. Same as No. 1, but with fists clenched. 

7. Same as No. 2, but with fists firmly clenched. 

8. The arms, starting from the position of "attention," describe a circle by moving 
forward and upward until they are raised vertically; then each palm is turned outward, 
and the arms descend backward to their former position. 

9. The body is bent forward, and then brought back to the erect position. 

10. The body is rotated, without any movement of the feet, first to the right and then to 
the left, and then back to its original position. 

11. The body is flexed laterally, as far as possible, first to the one side and then to the 
other, and afterward restored to its original erect position. 

12. The patient, standing with the feet side by side and supporting himself by leaning 
with one hand upon any object, flexes the opposite thigh as far as it is possible, and after- 
ward extends it until the feet are again side by side; then leaning on the other hand, he 
carries out a similar movement with the other thigh. 

13. The patient, supporting himself by one hand, as in 12, and the knee being kept 
straight, each leg in turn is raised as high as possible in front of the body, and then in the 
same way behind. 

14. Supporting himself by placing both hands in front on the back of a chair, the patient 
first flexes one leg and then the other upon the thigh as far as he can. 

15. Each leg in turn is abducted as far as possible, the knees being kept straight, the 
patient resting on one or other hand the while. 

16. The arms, held horizontally outward, are rotated forward and backward at the 
shoulder-joint. 

Contra-indications are aneurysm, angina pectoris, acute cardiac insuffi- 
ciency and tendency to hemorrhage or embolism. 

HYPERTROPHY OF THE HEART. 

Etiology. — Hypertrophy of the left ventricle results from (a) valvular 
lesions wherein dilatation precedes and incites hypertrophy; (b) renal dis- 
ease; usually from a chronic interstitial nephritis (mechanical obstruction 
to the flow of blood or retention within the blood of waste substances 
which excite arterial spasm); (c) arteriosclerosis (q. v.); (d) congenital 



HYPERTROPHY OF THE HEART 325 

narrowness (hypoplasia) of the arterial system, or of the aorta at the isth- 
mus; (e) dilatation of the aorta, diffuse or aneurysmatic; (/) pericardial 
adhesions, (q. v.); (g) myocarditis (q. v.); (h) pregnancy; the placental 
circulation or increased intra-abdominal pressure increases the heart's 
work. The high diaphragm also apposes the heart to the chest wall and 
tips the apex outward so as to simulate hypertrophy; (i) overexertion; 
the "irritable heart of soldiers" is caused by forced marches, cold and 
mental excitement; the so-called idiopathic hypertrophy occurs in hard 
workers, and especially in Munich from excessive use of beer and from 
the resulting high blood-pressure; hypertrophy results from continued 
hard work, while dilatation follows sudden cardiac strain ; (j) nervous or 
toxic causes, as exophthalmic goitre and tobacco, especially strong 
Havana cigars, which cause rapid irregular heart action; (k) reflex 
hypertrophy is said to result from abdominal growths, brachial neuritis, 
etc. 

Hypertrophy of the right ventricle arises from (a) left-heart disease, 
from the intimate connection between the muscular fibers of both sides; 
(b) right-heart valvular lesions and congenital heart disease; (c) increased 
pulmonary pressure from disease of the pulmonary artery or pressure 
upon it; (d) emphysema, chronic bronchitis, spinal deformity, pulmonary 
induration, extensive pleural adhesions, etc. 

Hypertrophy of the auricles always coexists with dilatation. 

Pathology. — The muscle fibers increase even tenfold in size (hyper- 
trophy) and increase in number (hyperplasia). Hypertrophy may exist 
alone — simple hypertrophy, but more frequently with dilatation — eccen- 
tric hypertrophy. Concentric hypertrophy is rarer and some regard it as 
a postmortem condition; the ventricle may be firmly contracted in 
death from violence, cholera or hemorrhage, but it can be distended by 
the finger. The size of the normal heart is that of the fist (Laennec), 
and the normal weight is 300 gm. The heart is sometimes increased in 
weight, even 1980 gm. — the cor bovinum. The left ventricle, normally 
9 to 10 mm. in thickness, may be more than doubled in hypertrophy; the 
right ventricle measures 3 or 4 mm.; the left auricle measures 3 and the 
right 2 mm. In the fetus the ventricles are equally thick. Up to the 
eighth year, the left ventricle is relatively thicker than in adults, because 
of narrowing of the aorta at its isthmus. 

Symptoms. — Hypertrophy of the left heart may be symptomless, or 
there may be palpitation, cardiac oppression or cerebral congestion — 
tinnitus, headache or vertigo. There is frequently a tendency to hemor- 
rhage — epistaxis, cerebral hemorrhage, excessive menstruation. Polyuria 
results from high arterial tension. The causal nephritis, valvular disease, 
arteriosclerosis or emphysema presents its own symptoms. Right-heart 
hypertrophy is attended by brown induration of the lungs, hemoptysis, 
cyanosis or bronchial catarrh. 

Physical Signs. — Much confusion in the clinical description prevails 
because the signs of hypertrophy are very often confounded with those 
of dilatation, with which it frequently coexists. 

Hypertrophy of the Left Ventricle. — 1. Inspection. — This dis- 
closes (a) a strong, sometimes heaving, diffuse apex; its dislocation 



326 DISEASES OF THE HEART MUSCLE 

indicates dilatation, because thickening of the heart muscle alone gives 
no appreciable increase in the size of the heart. Rotatory retraction of 
the apex beat is sometimes seen, (b) Precordial prominence; (c) forcible 
pulsation of the vessels. 

2. Palpation. — Palpation confirms (a) the strong apex beat, detects 
(6) the palpable second aortic tone due to high tension or atheroma, and 
sometimes (c) a systolic apical thrill (transmission of the strong first 
tone), (d) The pulse is regular, full and hard in simple hypertrophy; 
in the eccentric form it is softer and more rapid; it is sometimes 
weak or almost absent in the arms, due to loss of vessel tonus, (e) 
Thrills over the peripheral vessels from high tension vibration mav be 
felt. 

3. Percussion. — Enlargement means dilatation or an atheromatous 
relaxed aorta which allows sinking of the heart. 

4. Auscultation. — This brings out (a) the loud first tone over the apex 
(but not in aortic leakage) ; (6) the accentuated, even, metallic, second 
aortic tone; (c) systolic arterial bruits from tension and vibration of the 
walls; (d) the gallop-rhythm in failing hypertrophy, especially in neph- 
ritics; (e) a peculiar clink, sometimes heard to the right of the apex; 
(/) an apical systolic murmur, frequently of the cardiopulmonary type. 
Seitz and Gendrin recorded murmurs resembling the pericardial rub, 
due to violent muscular contraction. 

Hypertrophy of the Right Ventricle. — (1) Inspection shows a 
strong, systolic impulse under the lower part of the sternum which is (2) 
palpable, as is the strong second pulmonic tone. (3) Auscultation brings 
out the accentuated second pulmonic; and (4) percussion is negative, 
unless there is coincident dilatation. 

Diagnosis. — In left-sided hypertrophy, the cardinal signs are (a) the 
tense pulse, (6) the strong apex beat and (c) the accentuated second 
aortic tone; in right-sided hypertrophy they are (1) the strong second 
pulmonic tone and (2) substernal pulsation. 

In nervous overaction of the heart, the apex is not heaving. Retraction 
of the left lung exposes more of the left ventricle, but the heart's outline 
enlarges upward and to the left. In narrow chests with poor lungs, the 
heart's dulness is wide, but hypertrophy is lacking. At puberty the heart 
is nervously unstable, the chest is thin and the heart normally wider. 
Abundant casts and blood in the urine usually indicate nephritis, but, 
if there are other evidences of stasis, such as congested liver, they are 
compatible, in the minds of some clinicians, with stasis alone. Nephritis 
may cause hypertrophy; nephritis and hypertrophy may be due to a 
common cause; or a failing heart may produce renal stasis. (See Neph- 
ritis, Differential Table.) 

Prognosis. — The immediate outlook is good because hypertrophy is 
usually a compensatory process; the ultimate outlook is bad, as the 
reserve power is exhausted. Symptoms appear gradually or suddenly 
from intercurrent fevers, malnutrition and mental or physical strain. 
Hypertrophy caused by tobacco or athletics may regress. Gallop- 
rhythm is ominous, as is the occurrence of the first and second apical 
tones close together. 



FATTY HEART 327 

Treatment. — The therapy is eminently causal and dietetic; alcohol, tea, 
coffee, tobacco, cold baths and constipation are to be avoided. Treatment 
of decompensation is that of valvular disease (q. v.). 

ATROPHY OF THE HEART. 

Atrophy of the heart is chiefly of pathological interest. 

Etiology. — The heart is at times congenitally weak and small. It 
may then be associated with small vessels, chlorosis (Virchow) or with 
hypoplasia of the genitalia (Rokitansky) . Pressure atrophy, coronary 
sclerosis, pericardiac adhesions, the senile involution and cachectic 
diseases are the most frequent causes. Anatomically, the heart is reduced 
in size and weight (even to 1| ounces), the subpericardial fat disappears, 
the pericardium wrinkles, the coronary arteries are tortuous and the 
heart muscle is pigmented. The valves, especially the aortic, may waste. 
The atrophy may be partial, as that of the left ventricle in some cases 
of mitral stenosis. 

The symptoms are indeterminate, and the diagnosis impossible. 

FATTY HEART. 

Etiology and Pathology. — Fatty heart is no distinct pathological or 
clinical entity. Two forms are recognized: (1) fatty infiltration and (2) 
fatty degeneration. 

1. Fatty Infiltration. — The Lipoma cordis capsular -e, Virchow, con- 
sists of invasion of the heart muscle by the subpericardial fat, normally 
found about the heart, in its furrows, at the tips of the ventricles and 
around the basal vessels. The fat extends in parallel lines between the 
muscle fibers, which it may wholly replace. The fatty infiltration was 
once considered primary, but it is secondary to muscle atrophy or some 
nutritive disturbance. The fat develops most in the outer layers of the 
myocardium, but may reach to the endocardium. Fatty infiltration 
is most common in obese males over forty years of age. It may occur 
after the menopause or in sterile women. High living, abuse of alcohol 
and heredity are factors. The heart is reduced 25 per cent, compared 
with the body weight. 

2. Fatty Degeneration. — This form is caused by deficient oxygena- 
tion which is either (a) general, resulting from acute infections, old age, 
cachexia, anemia, poisons, etc.; or (6) local or cardiac, from pericarditis; 
coronary disease, which most frequently produces myofibrosis; and 
from cardiac failure following hypertrophy. Most degeneration occurs 
in the left heart. The fatty heart is flabby and yellowish-brown — the 
" faded leaf" color of Laennec; the splashes and streaks of fatty degen- 
eration give the variegated " tiger" or " tabby-cat" appearance; oil 
globules in rows in the muscle fibers may replace them in part or en- 
tirely. Frequently the muscle fibers show albuminoid degeneration, the 
first step in fatty degeneration. The striations of the muscle disappear 
later, its consistence is decreased and its substance is friable. 

Parenchymatous and fatty degeneration are observed in those seg- 



328 DISEASES OF THE HEART MUSCLE 

ments of the heart where the greatest work and the most nutrition are 
demanded, as in the papillary muscles of the mitral valves and where 
pressure is greatest, viz., the septum and left conus arteriosus. 

Symptoms and Signs. — Extensive changes may occur without clinical 
symptoms; Leube details a case of pernicious anemia without cardiac 
symptoms in which the apex was completely fatty. In some obese 
subjects, cardiac embarrassment develops with dyspnea, palpitation, etc. 
The autopsy may reveal fatty heart, but far more frequently myocarditis, 
hypertrophy or coronary disease is found; i. e., there is no uniformity 
in the pathological findings, nor parallelism between them and the clinical 
signs. Though percussion of obese individuals is difficult, the heart is 
found dilated. In fatty heart, the tones are weak and distant, the 
apex beat is weak, diffuse or absent, and sometimes an apical systolic 
murmur is heard, due to irregular systolic vibration. Gallop-rhythm 
indicates cardiac fatigue. The pulse may be rapid, small and arrhythmic. 
Low temperature, sweating and bronchitis are common. Much stress 
was formerly laid on the Adams- Stokes s syndrome (see page 342). 

Prognosis. — The prognosis is grave when coronary disease, angina, 
lung edema or an irregular or very slow pulse intervenes. Sudden death 
is not uncommon from acute dilatation, pulmonary embolism, cerebral 
hemorrhage, " heart block," or rarely heart rupture. 

Treatment. — The treatment is that of obesity in fatty infiltration, 
but distinction must be made between (a) obesity with anemia, in which 
the subject is pale, with cold extremities, sweating, scanty urine, weak 
muscles and dyspnea; and (b) obesity with plethora, in which the color 
is red, the urine increased and uratic, the heart stronger, the muscles 
fairly developed and exercise possible with little dyspnea. Schott's 
treatment is beneficial in the first type, and Oertel's method in the 
latter. Saline cathartics, total abstinence from alcohol and the use of 
potassium iodide are indicated. Cardiac insufficiency is treated as in 
uncompensated valvular lesions and dilatation. Morphine should be 
used with great circumspection. 



ACUTE MYOCARDITIS. 

Etiology and Pathology. — Acute myocarditis is of the greatest clinical 
and prognostic importance. 

Acute parenchymatous myocarditis corresponds to granular and fatty 
degeneration (v. i.); the "mushroom" heart of Stokes, and the "softened 
heart" of Laennec and Louis. 

Acute interstitial myocarditis has been most studied of late years, while 
formerly the degenerations attracted most attention. It was first dis- 
covered by Leyden in scarlatina; it is found in a large percentage of 
cases of diphtheria, typhoid, acute endocarditis and rheumatism. Round 
cells are found in the interstitial tissue, with or without muscular altera- 
tion, such as vacuolization, nuclear multiplication, pigmentary deposit, 
blood extravasation and waxy changes. 

Nodes (v. page 284), inflammatory thickening of the intima in the cor- 



CHRONIC MYOCARDITIS 329 

onary radicles and perineuritis are also described. Probably inflam- 
mation is primary and degeneration secondary. 

Symptoms and Signs. — During the progress of an acute infection the 
heart's strength decreases; its tones, especially the first mitral, become 
fainter. There is often a marked presystolic impulse; the less distinct 
apex is dislocated to the left and the pulse grows more weak and irregular. 
Vasomotor relaxation is a very important element in the heart failure. 
Gallop-rhythm and embryocardia develop, and there is usually a rela- 
tive mitral leakage. Cardiac pain may be severe. These changes may 
develop during the typhoid, scarlatina or rheumatism; or occur two to 
ten weeks after the infection, as in diphtheria. Sudden death may occur 
during convalescence. Rheumatic myocarditis often leads to chronic 
fibrous myocarditis. 

Diagnosis. — The etiology is important; acute myocarditis is distin- 
guished with great difficulty from acute endocarditis (q. v.). 

Treatment. — Prophylaxis. — The patient should have absolute rest 
well into convalescence, because sudden heart insufficiency or unexpected 
death may follow effort, difficult defecation or sexual intercourse. Car- 
diants are indicated as in valvular incompetency. (See therapy of 
Typhoid, Diphtheria and Pneumonia.) 

I. Acute Circumscript Myocarditis. — This, the disease of gladiators 
(Galen), is a form of sepsis, and its embolic heart foci are usually multiple. 
It is usually caused by the pyogenic organisms. The issues are (a) 
resorption with fibrosis, (6) caseation or calcification and (c) rupture 
into the pericardium or into the heart cavity, thus producing "heart 
ulcers," embolism, heart aneurysm or abnormal communications between 
the chambers. Sudden valvular insufficiency is sometimes suggestive, 
though it is usually impossible to make a diagnosis. The treatment is 
that of the fundamental septicopyemia and the resulting cardiac insuffi- 
ciency. 

II. Fragmentation of the Heart Muscle. — There are two forms (a) 
segmentation or separation from each other of the heart fibers, and (b) 
fragmentation or rupture across the normal or degenerated muscle fibers. 
It also has been called segmentary myocarditis; it most frequently occurs 
in death from violence, but may have clinical significance in sudden or 
gradual heart weakness. (See Myolysis, under Diphtheria.) 

CHRONIC MYOCARDITIS (CHRONIC FIBROUS OR INTERSTITIAL 
MYOCARDITIS, MYOFIBROSIS CORDIS). 

Etiology and Pathology. — Chronic myocarditis is rarely a disease 
sui generis, but is a sequel of some retrogressive lesion — a secondary 
process. It compensates for destruction of heart tissue, is a measure of 
that loss and is more often a fibrosis than an inflammation. The longi- 
tudinal incision of the heart muscle discloses scar-like tissue often unseen 
in transverse sections. This tissue is seen most frequently in the lower 
two-thirds of the anterior wall of the left ventricle and the upper two- 
thirds of its posterior wall near the auricle, as glistening sunken areas 
under the pericardium or endocardium. It also occurs in the papillary 



330 DISEASES OF THE HEART MUSCLE 

muscles or septum. The scars appear as streaks or stellate plaques, some- 
times measuring three or four centimeters. The foci may be macro- or 
microscopic, circumscribed or general. Gross changes in the heart include: 

1. Hypertrophy. — This is vicarious and is inversely proportional to 
the number of scars. The relation is twofold; (a) hypertrophy often 
compensates for moderate muscular destruction; or (b) fibrosis develops 
in tired, hypertrophied hearts. 

2. Dilatation. — This follows extensive fibrosis and decreased tonicity. 
Fibrosis may neutralize dilatation. 

3. Atrophy of the Myocardium. 

4. Valvular Disease. — A relative mitral insufficiency may follow 
myocarditis in the mitral papillary muscles. Dittrich described a genuine 
heart-stenosis, a myocarditic contraction of the left conus arteriosus 
in the adult, or of the right conus in the fetus. Relative aortic insuffi- 
ciency may follow dilatation and myocarditis of the left ventricle (personal 
observations) . 

5. Heart Aneurysm and Heart Rupture. — Partial heart aneurysm, 
a localized bulging of the heart wall, is seen largely near the apex (left 
ventricle, 68 per cent, of cases), where acute myomalacia cordis or 
chronic fibrosis occurs most frequently; it is seen more rarely at the 
base or septum which may bulge into the right heart; and most infre- 
quently in the right heart. The aneurysm is usually small, but may 
equal the size of the heart; it is usually single (though four were found 
by Thurnam), and may communicate with the heart cavity by a neck- 
like constriction; its walls consist of connective tissue, which is rarely 
ossified, as in Corvisart's case. It may rupture or detach a valve. During 
twenty years ending in 1903, D. G. Hall found 112 cases recorded (26 
had aneurysm in the valves, and 25 in the coronary vessels) ; Volker 
alone made a diagnosis. Rupture of the heart (v. page 332). 

Pathogenesis. — The most frequent cause is disease of the coronary arter- 
ies, which are end arteries, and anastomose with each other only through 
their capillaries. The vessels of Thebesius, entering the muscle from 
the auricles and ventricles may carry on some collateral circulation 
when the coronary arteries are occluded. Coronary narrowing may be 
gradual, by obliterative endarteritis or by the occlusion of the vessel 
from an atheromatous plaque in the aorta; or it may be sudden and 
fatal by embolism or thrombosis in an already narrowed vessel; the 
most common location is in the left ventricle (anterior coronary artery 
which is relatively small) and in the septum. In acute coronary obstruc- 
tion, the heart muscle becomes ischemic and opaque and the necrotic 
area swells (coagulation necrosis) ; a wedge-shaped anemic infarct is less 
common. The muscle fibers become fragmented, lose their nuclei and 
disappear; this process may lead to rupture of the heart or sudden 
death. Ziegler named it myomalacia cordis. If the subject lives, scar 
tissue develops — a dystrophic sclerosis. Huchard employs the terms, 
arteriosclerosis of heart and arterial cardiopathy, to emphasize the 
causal role of arterial disease. A less frequent cause is actual chronic 
myocarditis following acute myocarditis or endarteritis due to rheumatism, 
typhoid or diphtheria. Dehio holds that myofibrosis is a result of dilata- 



CHRONIC MYOCARDITIS 331 

tion, and occurs where the muscle is destroyed, as a necessary and pro- 
tective process, conforming with Thoma's conception of arteriosclerosis 
(q. v.). 

Symptoms. — (a) In the latent type there are no symptoms and sudden 
apoplectiform death occurs in apparently perfect health, (b) Most 
cases present chronic symptoms of cardiac insufficiency. There is venous 
congestion. The pulmonary circulation suffers especially, as is shown 
by cyanosis, large infarcts, hydrothorax, edema of the lungs, bronchitis 
and dyspnea. The cardiac symptoms are precordial oppression, pal- 
pitation, cardiac asthma or angina pectoris. Examination of the heart 
sometimes gives negative results, but dilatation and hypertrophy are 
usually present (cardiomegalia) . The heart tones, at first often clear, 
become faint and irregular, so that in the resulting delirium cordis, the 
tones are disorderly and the phase of the murmur, due to relative mus- 
cular insufficiency or to arteriosclerotic dilatation, cannot be distinguished. 
The second pulmonic sound is accentuated or split and the second aortic 
tone is weak, because the arterial tension is low. The pulse is usually 
irregular; paroxysms of arrhythmia may indicate an extension of the 
sclerosis. Irregularity usually antedates cardiac insufficiency. A regu- 
lar pulse may be present throughout, or a number of regular strong 
beats is followed by a wave of rapid, tumbling heart action. The pulse- 
rate, often slow at first, increases to 90 or 100, with ominous crises of 
tachycardia. In some instances the pulse is persistently slow and asso- 
ciated with syncope (v. i. Bradycakdia) . 

Edema is, as a rule, less common and intense than in valvular disease. 
Embolism may occur. Digestive disturbances are constant. Alimentary 
autotoxemia, from carelessness in diet, may cause paroxysmal cardiac 
symptoms. Potain and Barie hold that digestive disorders induce a 
reflex contraction of the lung vessels and thus lead to dyspnea. The 
urine is that of stasis in the later stages, but early in the disease poly- 
uria may prevail from high blood-pressure. 

Diagnosis. — There are five cardinal points: (a) In the majority of 
cases arteriosclerosis is most important; it is usually diffuse, but may 
exist in the heart and not in the radial arteries, and conversely, (b) 
The heart is usually dilated and hypertrophied. (c) No valvular murmur 
exists in uncomplicated cases. The systolic apical murmur of arterio- 
sclerotic dilatation may be heard or the soft, variable bruit of relative 
mitral leakage, id) The pulse is fast and irregular. A regular pulse does 
not absolutely exclude myocarditis, (e) Dyspnea and pulmonary stasis 
are suggestive. 

Myofibrosis may be overshadowed by the more frank yet wholly iden- 
tical fibrosis of the vessels, kidneys, liver and perhaps meninges or 
adrenals (poly visceral scleroses), until one of the great trio of risks of 
diffuse degeneration intervenes — cerebral accidents, renal suppression 
or cardiac agony (angina with pain or angina with precipitate coronary 
death) . 

Differentiation is often so difficult that many clinicians limit the 
diagnosis to muscular insufficiency; fatty heart, hypertrophy and dilata- 
tion, or pericardial adhesions may be found at autopsy instead of the 



332 DISEASES OF THE HEART MUSCLE 

anticipated myocarditis. Sometimes when myocarditis is suspected, the 
heart shows nothing microscopically or macroscopically (the causes of 
heart failure are often beyond detection by the microscope) . A diagnosis 
is made by exclusion, and then is only a " probability diagnosis." In 
differentiation from the "heart of renal disease," long observation, the 
gallop-rhythm (more common in the cor renale) and uremic manifesta- 
tions are helpful; myocarditis and renal disease are frequently asso- 
ciated. From mitral stenosis: both lesions cause irregularity and a weak 
radial pulse and apex beat; when the presystolic stenotic murmur is 
absent, the loud second pulmonic sound, the loud snapping apical tone 
and the wide right heart are most suggestive of mitral stenosis. " Cardiac 
apoplexy" may be mistaken for cerebral apoplexy or embolism; the 
autopsy in cases of sudden death often discloses coronary closure with 
myomalacia cordis or fibrous myocarditis. 

Prognosis. — Since digitalis is often ineffectual and angina pectoris, 
heart rupture or coronary closure may occur, the outlook is most un- 
promising. Some patients, especially elderly subjects, may live a decade 
or more, until intercurrent pneumonia or another secondary affection 
causes their death. Early digestive symptoms are less favorable than 
early edema or congested liver. 

Treatment. — The therapy is (a) that of the causal factor , arteriosclerosis 
(q. v.) being the most common cause. Potassium iodide should be given, 
freely diluted in milk or water — 

1$ — Potassii iodidi 3iiss 

Syr. sarsaparillse co . . . . . . . 5iv 

M. et S. — One teaspoonful in a glass of water after meals. 

(b) Dietetic; stimulants should be used carefully and overexertion 
and excitement avoided, (c) The Schott treatment (v. s.). (d) Cardiants. 
Digitalis is beneficial in the early stages — less so in advanced cases, or 
when the pulse is slow. Strychnine is frequently valuable. For anginal 
seizures or hard vessels, nitroglycerin is given. Caffeine, camphor, and 
morphine should be administered for cardiac asthma. (See Therapy 
of Valvular Disease.) 

RUPTURE OF THE HEART. 

Etiology. — Rupture through the altered heart muscle occurs in myocar- 
ditis; heart aneurysm, in which it may even perforate the chest wall; 
myomalacia cordis; coronary aneurysm; fatty heart, abscess, gumma 
or neoplasm of the heart, ulcerative endocarditis, obstructive valvular 
disease and stenosis of the isthmus of the aorta. It occurs largely in 
men over sixty years of age. It may occur during sleep or may be caused 
by trauma, vomiting, great effort, excitement, delivery, coitus, or by the 
abuse of digitalis. Kroll collected 332 cases. 

Pathology and Symptoms. — (a) Rupture of a valve induces sudden val- 
vular insufficiency, (b) Total rupture is usually single, though five rents 
are recorded, and takes place in the left ventricle (80 per cent.) where the 
pathological factors come most into play. Sudden death may occur, or 



ANGINA PECTORIS 333 

death may result after a few hours to eleven to seventeen days. The 
symptoms are a sense of something giving way in the chest, great precor- 
dial pain, incoercible vomiting or diarrhea, irritation of the vagus from 
hemopericardium, collapse and death from pressure of the blood on the 
heart or vense cavse. Hemopericardium (q. v.) may be suspected because 
of greatly increased triangular dulness, faint heart tones and absent or 
weak apex beat within the left border of the dulness. 

Diagnosis and Treatment. — The diagnosis is rarely made. It depends 
on the etiology, increased dulness, cardiac insufficiency and symptoms 
of internal hemorrhage. The outlook is bad and the treatment wholly 
symptomatic; absolute rest should be enforced. 

ANGINA PECTORIS. 

This affection is usually described under cardiac neuroses but it is 
a coronary cardiopathy and its effects relate to the myocardium. Angina 
pectoris (stenocardia, breast-pang) was first described by Heberden and 
then by Hunter. Edward Jenner first recognized the connection between 
angina pectoris and coronary disease. By far the best treatises are Osier's 
classic on Angina Pectoris and Allied States, and Neusser's Ausgewahlte 
Kapitel der klinischen Symptomatologie, Heft 2. 

Definition. — An arteriosclerotic cardiopathy, characterized by (a) 
paroxysms of excruciating cardiac pain, (b) mental anguish, a sense of 
dying and (c) frequently by sudden death. 

Etiology and Pathology. — The chief and practically constant patho- 
logical finding is arteriosclerosis involving the heart muscle directly 
by coronary atheroma, or indirectly by plaques in the aorta at the 
coronary orifices. The aorta is often atheromatous without coronary 
involvement and coronary sclerosis is frequent without much change in 
the aorta. It is notable that atheroma is frequent and angina pectoris 
is rare. The etiology is that of arteriosclerosis (q. v.) — syphilis (aortitis), 
gout, alcohol, contracted kidneys, sometimes infections such as rheu- 
matism or influenza. A history of its occurrence through several gen- 
erations is sometimes elicited. It occurs chiefly in men (90 per cent.), 
usually after the fortieth year (although cases in the second decennium 
are reported) and in the well-to-do classes, professional men, hard workers 
and luxurious livers. Angina is far more common in private than in 
hospital practice. 

Symptoms.— Mode of Onset. — (a) In some cases the onset is gradual, 
and is preceded by dyspnea, especially when dressing or undressing, 
lacing the shoes, emptying the bowels, sitting up or beginning to exer- 
cise; by short, deep respiration, precordial oppression, pulmonary edema, 
bronchial catarrh, strong beating in the second or third left interspace, 
and difficulty in moving the left arm. This "cardiac asthma" is followed 
by genuine angina; both are secondary to coronary disease, (b) In other 
cases angina is the first important symptom of cardiac disease. It is 
excited by muscular effort, as walking up hill; mental excitement, as 
anger or coitus; chilling or bathing; flatulent dyspepsia or overloading 
the stomach, which by way of the vagus, may induce the attack when 



334 DISEASES OF THE HEART MUSCLE 

the patient is quiet or just going to sleep, (c) Death may be the first 
symptom. 

Paroxysm. — The attack itself consists of (1) sudden agonizing pain, 
which is lancinating and feels like an iron hand squeezing the heart. 
The pain emanates from the cardiac plexus lying behind the aorta, 
and in the nerve branches from it to the coronary arteries, whence its 
reflection to other parts, mentioned later. During the seizure the heart 
muscle is ischemic from coronary obstruction or possibly from superin- 
duced spasm of the vessel (Allan Burns, Potain). In man and in the 
horse, atheroma or thrombosis of the abdominal aorta or its branches to 
the legs, shuts off the blood necessary during exertion; with moderate 
exercise the collateral circulation is sufficient, but prolonged exertion 
produces tingling, cramps and transient paraplegia ("intermittent 
claudication"). The heart-pang is caused by an analogous cardiac 
ischemia when unusual stress is thrown on the diseased coronaries and 
the myocardium becomes exhausted (impaired contractility). The 
author observed thoracic and abdominal angina followed by claudica- 
tion. The "unutterable" pain is usually substernal and radiates to the 
left shoulder, neck and arm (to the chin, ear, jaw, occiput, larynx, even 
to the gall-bladder and renal region, spine, stomach, left leg and testis). 
Pain along the ulnar nerve to the fingers may precede the angina, or perhaps 
is associated with motor weakness or ulnar atrophy (in primitive verte- 
brates, the nerves involved would have been over the heart). Hyper- 
esthesia of the arm, chest or mammary regions is frequent, and may per- 
sist, due to reflex cord irritation. The pain produces vasomotor symp- 
toms, such as great pallor, low temperature and profuse sweating. The 
patient may fall, perhaps in a fatal syncope, or more often may support 
himself for a few seconds or minutes until the paroxysm has passed. 

(2) The mental anguish, the angor animi (Latham) is the second com- 
ponent of the seizure and consists of a sense of dying, with great anxiety, 
complete consciousness, immobile attitude with head and trunk extended, 
and perhaps inability to articulate. 

(3) The danger of sudden death is the third element. Death may come 
without pain (syncope anginosa) in the first seizure; often in the second 
or third attack; years after the initial paroxysm; or after repeated 
attacks, maybe twenty a day (the etat angineuse). Osier has called the 
anterior branch of the coronary artery the "artery of sudden death." 

Other Signs and Symptoms. — The heart is variable, sometimes nor- 
mal in rate and strength, and again tense or weak, slow or rapid or 
irregular. The left radial pulse may be smaller than the right. Dunin 
found the arterial pressure low in 45 per cent, and high in 20 per cent, of 
his cases. Delirium cordis, partial heart-block, gallop-rhythm, extra- 
systoles, pulsus alternans and shortening of the long pause are but 
signs of cardiac fatigue. 

The second aortic tone is often loud and metallic; a rough or blowing 
systolic (and sometimes a diastolic) murmur is heard over the aorta, 
which is sometimes dilated; and the left ventricle may be dilated; 
the relative mitral leakage relieves the high blood-pressure inducing 
the angina and exhausting the left heart. These incidents are simply 



ANGINA PECTORIS 



335 



arteriosclerosis and its sequences. Constitutional disturbance is very fre- 
quent, as loss of weight, color and endurance. Dyspnea is not a part 
of angina pectoris, but of heart insufficiency. The urine is often pale 
and abundant after the seizure. Dysphagia, singultus, air-swallowing or 
gastric symptoms are due to sympathetic, phrenic and pneumogastric 
participation. 

Diagnosis. — When the attack is typical and severe, there is little 
difficulty in diagnosis. Mild or early attacks may be confused with car- 
diac asthma. Angina involving the abdomen (angina abdominis) or legs 
(angina cruris) is easily mistaken and may appear first or alternate with 
the more usual angina pectoris (see Arteriosclerosis). The classical 
picture, together with hardness of the arteries and atheroma of the 
aorta, makes the diagnosis practically certain. When the heart seems 
normal, severe precordial pain means angina. 

Pseudo-angina (Latham and Walshe) is the most frequent cause of 
diagnostic error. Its varieties are (a) nervous pseudo-angina. (James 
Mackenzie regards all angina as of the genuine type; the anginal pain 
arising, e. g., in worn-out women, is due to exhaustion of the heart as 
well as of the nervous system.) Huchard's widely quoted table is substan- 
tially as follows: 

Pseudo-angina. 

Commonest in women, at any age. 

Spontaneous; often nocturnal and periodic; 
frequent. 

Less severe, lasting hours; epigastric; agi- 
tation, activity; sensation of distention. 

Neurasthenic or hysterical stigmata. 

Common. 

Never fatal. 

From neuralgia. 

Neuralgic medication successful. 



Tktje Angina vt 

Most common in middle-aged men. 

Paroxysms induced by exertion, etc.; diur- 
nal; few in number. 

Pain intense, of short duration, precordial, 
inarticulate; immobile attitude; sensa- 
tion of cardiac compression. 

No nervous symptoms. 

Vasomotor form rare. 

Prognosis grave or fatal. 

Lesions: from coronary sclerosis. 

Arterial medication. 



(b) Vasomotor angina is attended by vasomotor spasm, coldness and 
numbness in the extremities, faintness and great pain in the heart (Noth- 
nagel). It may be reflex in origin. 

(c) Toxic pseudo-angina is due to coffee, etc., but especially tobacco. 
Vasomotor symptoms, amaurosis, dyspepsia, weak, rapid or irregular 
heart action, palpitation and anginal pain are common. Functional 
tobacco angina from coronary spasm heals when tobacco is withheld; 
but actual coronary disease, due to tobacco and other heart poisons, is 
not curable, (d) The crises of tabes and precordial pain due to brachial 
or vagus neuritis, gout, etc., may be difficult to diagnosticate. 

Prognosis. — The prognosis must be given with great caution; one 
patient lived for forty years. Few recoveries are reported. 

Treatment. — The treatment concerns (a) the etiology — arteriosclerosis. 
Gout and diabetes necessitate appropriate diet and therapy. Attention 
must be directed to the question of stimulants. The possibility of 
syphilis should always be considered; aside from syphilis, the iodides 
are valuable, given two-thirds of the time, for months and years. Small 
amounts are tolerated not as well as 10- or 20-grain doses. Care in their 
use is necessary in nephritis and even then well-diluted, gastric disorder 



336 DISEASES OF THE HEART MUSCLE 

may result; Spts. glycerylis nitratis is indicated in the intervals, in 
doses of Vf[ij, four or more times daily; its effects last less than an hour. 
It may cause headache, flushing or (in iarger doses) cyanosis or pallor, 
muscular relaxation, dyspnea and irregular pulse; erythrol tetranitrate 
in doses of gr. ss. t. i. d. has a more lasting effect. (See Arteriosclerosis.) 
(b) The causes precipitating paroxysms. Prophylaxis concerns exertion, 
excitement, coitus, chilling, constipation and dyspepsia; foods favoring 
flatulency should be avoided, and a light evening meal should be taken. 
Rest is imperative, as whatever exhausts the heart, precipitates the 
paroxysm. Bromides and chloral may avert nocturnal attacks. The 
patient should be provided with aromatics to dispel flatulency: 

R- — Spiritus ammonise aromatici . . 5ss 

Spiritus chloroformi 3ss 

Spiritus glycerylis nitratis gtt. j 

Spiritus setheris compositi 5ss 

M. et S. — To be taken in hot water (as a single dose). 

(c) The paroxysm. Amyl nitrite was advised by Brunton (1867) as 
an analgesic and vasodilator; the pearls contain three minims of the 
remedy. They often operate powerfully and instantaneously, even 
when the blood-pressure is normal; sometimes they are useless. It is 
better to have the patient carry the spts. glycerylis nitratis or amyl 
nitrite with him, for the physician rarely sees the attack. Some member 
of the family should be taught to give a hypodermic of morphine and 
atropine. Morphine and chloroform by inhalation are dreaded when 
brain trouble exists, but they must be used; large doses of morphine are 
required and tolerated. A full drink of whisky, is excellent, as first aid. 
(d) Cardiac weakness is treated by ammonia, camphor, strychnine and 
digitalis; morphine is carried in one hand and stimulants in the other. 

1$ — Tr. digitalis 3iv 

Tr. strophanthi 3ij 

Tr. Valerianae q. s. ad. 5iv 

M. et S. — One teaspoonful after meals. 

Coffee dilates the coronaries and prevents cardiac weakness and the 
paroxysms. Pseudo-angina is treated according to the type. Electricity 
and arsenic are valuable. 

TUMORS OF THE HEART. 

The heart is rather insusceptible even to neoplasms in its immediate 
vicinity. Link collected 91 cases (1909). Carcinoma and sarcoma are 
the most frequent, and lipoma, myxoma, fibroma and myoma infrequent. 
They are usually secondary. Cardiac insufficiency, valvular compression, 
anginal symptoms or embolism sometimes develop. 

Parasites are most often accidental postmortem findings. Echinococcus 
occurs twice as often in the right ventricle as in the left; 55 cases are 
reported. Cardiac rupture, sudden death from occlusion of the pul- 
monary trunks, relative pulmonary insufficiency or cardiac incompetence 
may occur. The cysticercus, the pentastomum and trichina are of purely 
anatomical interest. 



NEUROSES OF THE HEART 337 



CARDIAC THROMBOSIS— THROMBOSIS CORDIS. 

This usually occurs at the time of, or after, death. 

Symptoms. — (a) Entire latency, (b) Thrombosis sometimes develops 
during life and leads to pulmonary or arterial embolism, (c) Sudden 
cardiac weakness, (d) Sudden valvular stenosis, a ball thrombus forming 
in the auricle, and occluding, e. g., the mitral orifice; it is beyond clinical 
recognition, although frequently associated with gangrene of the lower 
extremities or ascites. 



NEUROSES OF THE HEART. 

This topic is closely related to affections of the myocardium, especially 
the arrhythmias and heart-block. 

Palpitation of the Heart. — Palpitation (cardiopalmus, cardiogmus or 
hyperkinesis cordis) is purely a symptom, the patient experiencing a 
fluttering sensation; in health the patient is not conscious of his heart 
action; extreme irregularity, or the pounding action in aortic insufficiency, 
may escape the patient's notice, while the normal heart may palpitate 
after overwork or abuse of coffee. It is closely related to the hyperdiastole 
caused by vagus stimulation. 

Etiology. — 1. Nervous Causes (Hyperesthesia of the centripetal 
heart fibers)* — Nervous excitability is common especially in medical 
students, whose hearts must be examined when they first study physiology 
or physical diagnosis. Peter Frank feared aneurysm while writing his 
Diseases of the Heart. It is common in school children, from nervous 
tension, fear of examinations and public exercises; it is more frequent 
in females at puberty, climacteric or menstruation. It occurs constantly 
in exophthalmic goitre and in 50 per cent, of neurasthenics; neurasthenia 
cordis is attended by turgid face, red eyes, contracted temporal arteries 
and angioneurotic edema. Exhaustion, anemias, acute infections, lacta- 
tion, poor hygiene, incipient tuberculosis and sexual excess may produce 
palpitation. The "irritable" heart of soldiers, observed by Da Costa in 
our Civil War, associated with arrhythmia, diarrhea, emotional causes 
and physical strain and often placed under this head, is better classified 
as muscular insufficiency. 

2. Reflex Causes. — The products of indigestion and mechanical 
gastric distention, constipation, intestinal parasites, gall-stones, renal 
calculi, prostatic, uterine or ovarian disease and floating kidney are 
possible causes. 

3. Toxic Causes. — Palpitation may result from the use of coffee, 
tea, alcohol, tobacco, narcotics and from gout. 

4. Cardiac Causes. — Palpitation may occur in organically incom- 
petent hearts, viz., valvular disease, acute or chronic myocarditis. 

Symptoms. — The patient complains of " feeling the heart beat," "gone- 
ness," "fluttering," forcible or intermittent action of the heart, dyspnea 
and anxiety. Intermittent epigastric throbbing and vasomotor symp- 
toms, as flushing of the face, pale urine, etc., are not uncommon. Phreno- 
cardia, described by Herz (1909), is a syndrome composed of pain below 
22 



338 DISEASES OF THE HEART MUSCLE 

the nipple, palpitation and difficulty in breathing, and ascribed to sexual 
repression. 

Physical Examination. — Sometimes the heart is absolutely normal. 
Some authors describe palpitation under tachycardia. The heart's rate is 
often increased after exertion or fright to 100 to 150, with violent arterial 
throbbing due perhaps to stimulation of the accelerator nerves. The 
heart is rarely slowed. A series of rapid beats followed by a series of 
slower beats is somewhat characteristic. If the pulse is irregular when 
the patient is quiet it sometimes becomes regular after exertion. The 
first apex tone is often accentuated, is even metallic or may be heard by 
the physician at some distance from the patient's chest. The systole may 
sound short. The second tone at the base is more often strong than 
weak. A murmur at the base is usually functional. 

Diagnosis. — (a) The etiology, (b) Negative results of examination of the 
heart during the attacks, but particularly in the intervals. Coronary 
disease, arteriosclerosis, myocarditis, etc., are usually excluded with 
ease, but may coexist with palpitation. Palpitation is held by some 
to lead to dilatation or hypertrophy, but this is confusion of cause 
and effect, (c) If pain be present in nervous palpitation, it is more often 
lower (an "epigastric cramp") than the pain of organic lesions which 
radiates to the shoulder or arms. 

Prognosis. — The outlook is generally favorable. The old belief that 
fright could cause death is as unfounded as most popular conceptions, 
and few such instances are recorded (Bollinger, Laache). 

Treatment. — (a) If the cause is nervous, suggestion is valuable and 
repeated examinations assure the patient and avoid error. Regulated 
exercise, tepid baths with active friction, light meals, regular habits 
and possibly the rest cure are indicated. It seems from personal experi- 
ence that isolation often increases introspection. In anemic cases iron, 
arsenic and strychnine should be given. 

1$ — Ferri valeratis, 

Quininae valeratis, 

Ammon. valeratis aa gr. xx 

M. et ft. in pil. xx. 

S. — One pill after meals. 

A few doses of veratrum and belladonna often quiet the violent throbbing 
and general nervousness, probably affecting the peripheral fibers of the 
vagus. Sexual hygiene must be strictly observed. 

1$ — Fluidextr. veratri gtt. x 

Fluidextr. belladonnas gtt. xv 

Aquae q. s. ad. 5J 

M. et S. — One teaspoonful every half-hour for two or three doses. 

(b) When the cause is reflex, flatulency and constipation must be treated, 
with bromides, given well diluted. 

I^ — Sodii bromidi 3J 

Spts. ammon. aromat 5ss 

Syr. zingiberis . , 5i»j 

Aquae q. s. ad. 5ii 

M. et S. — One teaspoonful in hot water every half-hour for four doses. 



NEUROSES OF THE HEART 339 

A light evening meal of non-nitrogenous food is beneficial in children 
afflicted with night terrors or palpitation, (c) The toxic type, (d) In 
valvular disease (q. v.), belladonna and the ice-bag are indicated. Digitalis 
is of little use in the nervous type. 

Arrhythmia.— There are five major varieties: (1) Sinus arrhythmia; 
(2) extra-systole; (3) heart-block; (4) auricular fibrillation; (5) the 
pulsus alternans. 

1. The juvenile, sinus or respiratory form is found in all children at 
some time. The normal (fundamental or sinus) rhythm or contraction 
of the heart is initiated at the mouths of the great veins in the right 
auricle; this arrhythmia is a sinus irregularity and the chief variation 
is changing of the pulse-rate with respiration and, if the heart is rapid, 
shortening of the diastole. The heart function concerned in this type 
of arrhythmia is the stimulus production, and the vagus is largely con- 
cerned also (whence atropine often controls it temporarily). Hygienic 
measures are usually efficacious. 

2. Extra-systole is the most frequent irregularity, and the usual cause 
of intermittent pulse. Its causation is increased irritability of the myo- 
cardium which answers to some abnormal stimulus and initiates a "pre- 
mature," "abortive," "futile" contraction during the diastole. The 
source of the contraction is at the auriculoventricular node, or perhaps 
in the auricle or ventricle, or some point between them. In one group 
of cases, there is no heart disease and the extra-systole is physiological, 
as in young people, women at puberty or menopause, or mental or physical 
fatigue; in a second group, the cause lies in poisoning (tobacco, alcohol, 
coffee, digitalis), in reflex alimentary origin or sometimes in infections 
where it is ominous; in the third group, there is organic heart dis- 
ease, or increased arterial tension from atheroma or nephritis. If the 
extra-systole occurs early in the diastole, no change in the pulse is 
noticed, as the aortic valves are not opened and a muffled third sound 
is heard; if it falls later in the systole, the aortic valves are opened, 
two sharp sounds are heard and the pulse shows the extra beat (pulsus 
bigeminus, trigeminus, polygeminus). There is always a systolic tone. 
The compensatory (diastolic) pause is lengthened after each systole, 
because of exhaustion of the left ventricle, which becomes "refractory" 
to stimuli, and the next beat becomes delayed. The time occupied by 
the normal systole plus the extra-systole plus the compensatory pause 
equals the time occupied by two complete normal cardiac cycles. In many 
cases, the extra-systole is described by the patient as a thump, fluttering 
or stopping of the heart. What appears simple extra-systole may turn 
out after years to be arteriosclerosis with high blood-pressure. Com- 
pensation may remain normal or may break, depending on the specific 
cause (v. s.), upon which also hangs the prognosis and therapy. In 
decompensation digitalis often helps (though it is an occasional cause 
of this arrhythmia). 

3. Heart-block (v. i. Bradycardia). 

4. Auricular fibrillation is also called perpetual arrhythmia, absolute 
irregularity or nodal rhythm. All rhythm is lost and the condition is 
associated with loss of tonicity, occurring in severe, specially rheumatic 



340 DISEASES OF THE HEART MUSCLR 

heart disease with dilatation, particularly in mitral stenosis and also in 
the last stages of exophthalmic goitre and in myofibrosis; its cause 
apparently is always intracardiac but rarely coming from the acute 
infections or the use of digitalis. The auricle contracts or flutters with 
extreme rapidity but ineffectually and the bundle of His is overwhelmed 
with impulses attempting to pass to the ventricle; consequently the 
ventricle beats as it lists, irregularly as to sequence, force, equality or 
rate; these changes show disturbance in conductivity also. The normal 
auricular wave in the jugular tracing, representing auricular systole, dis- 
appears, as the auricle weakens and the curve shows 400 to 900 fine undu- 
lations from auricular fluttering (fibrillation). This gives the delirium 
cordis (permanent rapidity), temporary rapidity like paroxysmal tachy- 
cardia, and rarely a slow rate of action. A positive venous pulse appears 
in the jugulars. Mackenzie described its sudden onset in mitral stenosis 
and Lewis demonstrated that auricular fibrillation was the cause; these 
authors estimate that it is the cause of 50 to 70 per cent, of irregularities 
of the heart. Symptoms may be absent and the patient goes on unaware 
of the change; again there is breathlessness and signs of a weak right 
heart; in mitral stenosis the presystolic murmur disappears and a 
positive venous jugular pulse is detected. Rest may eliminate the 
trouble and here, more than in any other condition, digitalis works its 
marvellous effects, increasing tonicity and blocking the abortive impulses 
sent through the bundle of His by the excited auricle. Atropine may be 
used with benefit in certain cases. 

5. The pulsus alternans is a disturbance not of the rate but of the 
size of the heart beats; it shows in the sphygmogram as alternating 
high and small waves. It indicates lasting depression of contractility 
and is always serious, occurring in mitral lesions, angina, advanced 
arteriosclerosis, old rheumatic hearts, high blood-pressure and irremedi- 
able cardiac fatigue, with death in two or three years. In pulsus alter- 
nans, we may hear strong tones alternating with weaker ones. It is 
to be distinguished from the p. bigeminus, in which the second beat is 
due to an extra-systole and is followed by a longer pause. 

Tachycardia. — Definition. — Tachycardia is the usual term for rapid 
heart action, although polycardia and pyknocardia are better etymo- 
logically, for tachycardia implies quick (not rapid) heart action like 
the pulsus celer. Tachycardia is only a symptom. Some hearts normally 
beat 90 to 100 (120 in the case of Congreve). 

Etiology. — (a) Heart and vascular disease; coronary, valvular or myo- 
cardial affections. (b) Nervous affections; brain and cord disease, as of 
the medulla (vagus centre), tumors, hemorrhage, bulbar paralysis, etc.; 
vagus neuritis, compression of its trunk by tumors, irritation of the 
accelerator nerve, exophthalmic goitre, neuroses as emotional tachy- 
cardia and reflex tachycardia from uterine or ovarian conditions, (c) 
General diseases as fevers, chronic troubles (tuberculosis, cancer), and 
convalescence, exhaustion or excesses, (d) Toxic causes; tea, coffee, alcohol, 
lead, digitalis, atropine, amyl nitrite, etc. Some individuals by volun- 
tarily moving the ear or skin muscles of the neck can raise the heart's 
rate, through the spinal accessory nerve and the vagus (Tarchanoff). 



NEUROSES OF THE HEART 341 

A special variety is the tachycardia paroxysmalis described by Probsting 
and defined by Nothnagel as a slumbering of the vagus centre. Paroxysms 
of rapid heart action occur abruptly, last from a few seconds or minutes 
to days or even weeks, and usually end abruptly. It is seen mostly in 
strong, hard-working men who indulge in excesses in alcohol, tobacco, etc. 

The pulse becomes smaller and weaker, and its rate reaches 150 or 
even 280. It is usually regular, though arrhythmia may mark the 
beginning and end of the seizure. There are three types: In one the 
auricular beat precedes the ventricular, as normally; in a second, more 
frequent form, the auricles and ventricles beat synchronously (see 
nodal rhythm); in the third type, the ventricle beats independently of 
the auricle; the irritation is in the auricle, auriculoventricular bundle 
or in the ventricle, respectively. The heart often dilates. The pause of 
the heart is lessened, the systole incomplete and the diastole shortened. 
The systolic tone is often clicking. The vessels pulsate violently and the 
patient is anxious, depressed and late in the course, shows signs of venous 
stasis. The urine is of low specific gravity. An acute distention of the 
lungs like that observed in valvular disease, may be caused by vagus 
or phrenic irritation or tonic contraction of the diaphragm. 

Diagnosis. — Permanent tachycardia suggests organic disease in the 
medulla or nerve trunks. The physiology of the vagus and accelerator 
nerves is still obscure from the clinical stand-point. It has been held that 
(a) increase in the pulse up to 120 indicates sympathetic irritation 
(accelerator stimulation), which is relieved by morphine; (b) increase 
from 120 to 180 indicates paralysis of the vagus, which is relieved by press- 
ure on the vagus trunk; (c) increase over 180 is indicative of sympathetic 
irritation in addition to paralysis of the vagus. Sympathetic symptoms 
may prevail, as exophthalmos, wide pupils and interpalpebral increase. 
Evidences of centric vagus involvement may exist, such as respiratory, 
laryngeal or gastric crises, polyuria, etc.; sudden onset and cessation 
suggest a bulbar origin. 

Prognosis. — The permanent is less favorable than the paroxysmal 
form. Bouveret holds that permanent cure is rare and reported 4 cases 
of sudden death. The infrequent autopsies (only 16 out of 135 cases 
collected by Hoffmann in 1900) show degeneration of the heart muscle. 

Treatment. — Stimulation of the vagus is effected by faradization of 
the neck, holding of the breath, by Valsalva's experiment, by firm ban- 
daging of the abdomen, pressure on the right vagus, the use of the ice-bag, 
swallowing ice, induction of vomiting by apomorphine and inverting the 
patient. Morphine, asafetida, valerian and bromides are frequently of 
value. The causal factors require consideration. 

Bradycardia. — Definition. — Bradycardia, spanocardia and brachycardia 
are the usual terms for slow heart but oligocardia is a better desig- 
nation. A pulsus tardus is normal to some individuals and certain 
families in successive generations. It is often accommodative, as in 
aortic stenosis. The apparent pulse-rate must be verified by cardiac 
auscultation. Paroxysmal bradycardia may occur with weak heart, 
palpitation, difficulty in breathing or gastric distress. 

Mackenzie distinguishes: (1) normal bradycardia, where all the 



342 DISEASES OF THE HEART MUSCLE 

heart's chambers beat slowly; (2) slow heart due to missed beats; (3) 
nodal rhythm (v. %.), where the auricle ceases to beat or beats synchron- 
ously with the ventricle; (4) heart-block; and (5) vagus slowing of 
the heart — stand-still of the whole heart. 

Etiology. — The etiological factors are: (a) Acute infections; brady- 
cardia is very common during or after typhoid, pneumonia, diphtheria 
and rheumatism, probably caused by acute myocarditis (lessened con- 
ductivity or heart-block) or by a vagus neuritis, (b) Digestive disorders; 
jaundice, constipation, gastric cancer, ulcer, distention or vomiting and 
gall-stones are the most frequent causes, (c) Respiratory disease is a 
less frequent cause; emphysema occurs frequently with a slow, strong 
pulse, (d) Circulatory disease, such as aortic stenosis, fatty heart, coro- 
nary atheroma or chronic myocarditis, lessens conductivity and con- 
tractility. Dehio uses atropine to distinguish between (i) disease of 
the heart muscle, upon which the drug has but little effect, and (ii) slow 
heart due to inhibition of the vagus, in which it brings the heart to, or 
above, the normal rate, (e) Toxic conditions such as poisoning from lead, 
alcohol, tobacco, digitalis and other drugs; in cholemia and in uremia it 
is unfavorable. (J) General troubles, such as diabetes, cachexia, anemia 
or exhaustion, lessen the irritability of the heart muscle, (g) Nervous 
conditions, apoplexy, meningitis, disease of the medulla or cervical cord, 
vagus stimulation by tumors, compression of the vagus trunk, are factors 
in its development. Jacob describes an angiospastic form (bradycardia 
with chills, wide pupils, cold skin, loud, second aortic tone, etc.). 

Heart-block. — The Adams-Stokes syndrome was first described by 
Morgagni (1761) and Spens (1792) but more fully by Adams (1827) and 
Stokes (1846). It is due to disturbed conductivity through the bundle of 
His, who in 1893 found a band-like muscular bundle connecting the right 
auricle and the ventricles. It measures 18 millimeters in length, 2.5 
millimeters in width and 1.5 millimeters in thickness, and courses poste- 
riorly in the septum ventriculorum, whence it reaches the right and left 
ventricles and their valves. J. G. Wilson considers that the bundle is 
an intricate nerve pathway. According to Gaskell (1883), and especially 
Erlanger (1906), slight compression of His's bundle increases the inter- 
ventricular pause; marked compression causes intermittency in the 
ventricular contractions; complete compression results in independent 
contraction of the auricles and ventricles, known as "heart-block." 
Its causes are various; mild, transient or incomplete heart-block may 
occur after infections, as typhoid, diphtheria, etc., in old rheumatic 
hearts, arteriosclerosis, from the use of digitalis or strophanthus, or 
possibly from nervous causes, e. g., by the vagus. In the more severe 
and permanent cases, organic changes are discovered in His's bundle, as 
gummata, an endocarditic patch in Stengel's case, postdiphtheritic myo- 
carditis (A. S. Dunn), acute myomalacia cordis, tumors and changes in 
the medulla. 

Symptoms. — The complete syndrome consists of (1) bradycardia; (2) 
pulsation of the cervical veins, exceeding in rate the arterial pulsation; 
(3) cerebral disturbances, as syncope and convulsive seizures; and (4) 
accessory symptoms. The normal rhythm and stimulus to contraction 



EN DOC A RDITIS 343 

begin in the right auricle and pass over the bridge or bundle of His to 
the ventricles. Disturbance in conduction leads either to delayed con- 
traction of the ventricles or to complete " blocking" of the stimulus, when 
the ventricles beat independently of the auricles (ventricular rhythm). 

1. Bradycardia. — With the normal pulse of 70, one-fifth of a second 
intervenes between the auricular and ventricular systoles; if this interval 
is much increased, there is disturbance of conduction and the trans- 
mission of the contraction wave from the auricle to the ventricle is 
"blocked"; the auricular movements may be seen in the pulsating cervi- 
cal veins, the fluoroscope or in polygraph tracings. When the ventricular 
contractions exceed 36 a minute, there is a definite relation between the 
ventricular beat and the auricular waves (seen in the pulsating jugulars), 
as 1 ventricular to 2, 3, or 4 jugular beats; if the ventricular rate is 30 
or less, there is no definite ratio. An interval of one or two minutes may 
intervene between the ventricular contractions (or radial pulse beats). 
During the ventricular systole, a muffled sound, due to auricular contrac- 
tion, may be heard and identified with it as one watches the pulsating 
jugulars. The pulse may fall to 6 beats, 

2. Jugular pulsations are synchronous with the auricular contractions 
(v. s.) and the radial pulse with the ventricular. 

3. Cerebral disturbances are not necessarily connected with dissociated 
action of the auricles and ventricles. Attacks resembling apoplexy are 
marked by coma, pallid or congested face,* stertorous breathing, aphasia, 
etc., and are probably due to venous stasis in the brain. In other instances 
there is vertigo or epileptiform attacks ensue, from arterial anemia. In a 
personal observation the convulsive attacks came on with the eyes 
open, so that an incorrect diagnosis of hysteria had been made. 

4. Accessory manifestations embrace angina, Cheyne-Stokes's respira- 
tion, cardiac asthma, etc. 

Prognosis. — The constant is less favorable than the paroxysmal type. 

Treatment. — The causal therapy alone is of value. Morphine must 
be given with care where there is disease of the central nervous system. 
Strong cardiants are usually contra-indicated and in the Adams-Stokes's 
syndrome are actually dangerous (see digitalis, page 374). Alcohol is 
injurious. Mercury and iodides help, maybe cure, syphilitic disease 
in His's bundle, unless the gummata are sclerosed. Atropine may be of 
service in partial heart-block. 



DISEASES OF THE ENDOCARDIUM. 

ENDOCARDITIS. 

Definition. — Inflammation of the endocardium. Its clinical importance 
attaches to the fact that chiefly the valves are involved. Two varieties 
are distinguished, the acute and the chronic, Bouillaud, in 1840, first 
placed the disease on a scientific basis. 



344 DISEASES OF THE ENDOCARDIUM 

I. Acute Endocarditis. — This is a secondary, general and mycotic disease. 
Its clinical varieties — (a) malignant or ulcerative endocarditis, and (6) 
benign or verrucose endocarditis — differ only in degree; the term benign 
is relative, as most endocarditides entail serious sequels. Litten divides 
endocarditis into (a) the benign forms produced by rheumatism, chorea, 
etc.; and (b) malignant, (i) non-suppurative and (ii) suppurative or 
septicopyemic. 

(A) Malignant (Ulcerative or Septic) Endocarditis. — Etiology. — The 
heart lesion is either (1) secondary to some clearly causal infection, 
or (2) cryptogenetic, when the causal infection is not apparent; care 
in examination and at autopsy usually reveals the cause. The atrium, 
bacteriology, mode of extension and symptoms are described under Septic 
Infections. 

The disease is more frequent in women than in men, even excluding 
puerperal infections, and between the years of twenty and forty. Its 
frequency is 2 per 1000 patients. Seventy-five per cent, of cases develop 
upon an old valvular lesion by which the local physiological resistance is 
lessened. The literature contains 11 cases developing at a patent ductus 
Botalli (Hart, 1904). 

Pathology. — Malignant endocarditis in 86 per cent, involves the left 
heart which is far more frequently the seat of previous lesions and its 
arterial blood favors the growth of microorganisms; the right heart is 
involved more frequently (12 per cent.) than it is in other types of 
endocarditis; both sides are diseased in 2 per cent. 

The process may involve the walls (parietal or mural endocarditis), 
or more frequently attacks the valves (valvular endocarditis), which are 
often already indurated by previous simple endocarditis and are subject 
to greater mechanical activity. The valvular localization is embolic. 
The endocardium becomes opaque, and irregular deficits occur on the 
undersurface of the aortic or the auricular surface of the mitral valves; 
later there is injection of the endothelial coat and a grayish deposit. 
Exudation is more abundant on the mitral than on the aortic or pulmo- 
nary valves. Thrombi and excrescences develop on the erosions, whose 
removal discloses subjacent ulceration. The thrombi, especially in 
pneumococcic and gonococcic infections, consist of lamellated fibrin and 
bacteria. The vegetations may attain the size of a walnut and often 
extend from one valve to another by contact infection ; some thrombi are 
purely mechanical deposits of fibrin, but endocarditis is always mycotic. 
Heiberg first found microorganisms (1869) and Weichselbaum first 
obtained pure cultures. The following bacteria have been found : strep- 
tococcus, staphylococcus, pneumococcus, less frequently the gonococcus, 
colon, diphtheria, influenza, tubercle and typhoid bacillus, meningococ- 
cus and, very exceptionally, other bacteria. The same organism may 
produce either the benign or malignant form. Experimental endocarditis 
has been produced by inoculations of various organisms, usually after 
wounding the valves by a sound introduced through the cervical vessels, 
but also without trauma. The pyogenic organisms are said to attack 
more frequently the mitral, and the pneumococcus rather elects the 
aortic valves. The mitral valves are more often involved than are the 



ENDOCARDITIS 345 

aortic. The process may invade the aorta or the pulmonary artery. 
Destructive ulceration through one leaf of the valve may produce acute 
valvular aneurysm, which, when aortic, projects toward the ventricle, and 
when mitral, projects toward the auricle. If the necrosis destroys both 
lamellae of the valve, the perforation leads to valvular insufficiency. 
Ulceration of the chordae tendineae or papillary muscles also produces 
valvular insufficiency; necrosis of the parietes results in a "heart ulcer," 
which sometimes leads to communication between the ventricles or to 
rupture of the heart. Dislodgement of tissue particles, thrombi or bacteria 
occurs frequently, usually in the arterial circuit. The effects vary with 
the location of the infarct (see Symptomatology) and with the character 
of the microbes; i. e., emboli act mechanically, infectively or in both ways. 
Streptococci are said to produce anemic infarcts, while staphylococci 
result in suppuration. Loehlein described typical glomerular lesions due 
to the Streptococcus viridans; their epithelia swell, proliferate and 
desquamate; necrosis sets in, with ultimate organization. Pathological 
changes in other organs are those of (a) general sepsis, such as parenchy- 
matous degeneration or splenic tumor, (b) embolism, (c) stasis when the 
heart fails, and (d) the primary disease. 

Symptoms. — The clinical features vary greatly, according to the 
basic disease, embolic involvement and virulence of the microorganisms. 
The onset may be violent or most insidious. In the majority of cases 
the septic element prevails. The various types, artificial, though con- 
venient for description, are: 

1. The Typhoid Form. — The toxemic symptoms, such as apathy, 
delirium, dry tongue, distended abdomen, diarrhea and splenic tumor 
are suggestive of typhoid. The resemblance may be heightened by 
hemorrhage of the bowels, rose-like spots and the diazo reaction. Dila- 
tation of the right heart and cardiac murmurs, so important in endo- 
carditis, are not uncommon in typhoid. But at this point certain varia- 
tions arouse doubt; there is no Widal and no typhoid bacillemia and 
certain septic symptoms or cardiac signs come to the front. In the skin 
or upper air passages, emboli appear as spots with white or yellow 
centres and hemorrhagic peripheries, or as pemphigus, gangrene or sup- 
purative foci. Infarcts sometimes occur in the conjunctiva, and in the 
retina, simple hemorrhage or actual infarcts with yellow centres are 
frequently detected. The entire eye-ball may suppurate. The frequent 
splenic infarction is characterized by sudden pain, tenderness, enlarge- 
ment and sometimes perisplenitic friction. Embolism is often accom- 
panied by fever, chill and vomiting. Renal infarction is very frequent, is 
attended by pain in the loins, hematuria, albuminuria and sometimes 
anuria or dysuria. Severe nephritis is common. Cerebral embolism 
usually occurs in the left Sylvian artery and results in the usual stroke 
and hemiplegia with aphasia. Pulmonary infarcts are caused by lesions 
of the right heart or by auricular thrombi, and occasion sudden pleuritic 
pain, dyspnea, hemoptoe, temperature and possibly a small area of 
crepitant rales, pleural friction or consolidation. Embolism also occurs 
in the liver, in the mesenteric artery (with enterorrhagia and peritonitic 
symptoms), in the muscles and joints, testes and parotid; in the heart 



346 DlSEASESjOF THE ENDOCARDIUM 

and various mucosae; in the meninges, pleurae, pericardium, peritoneum 
and in the peripheral arteries, sometimes causing gangrene or embolic 
aneurysm. The pneumococcus is often the cause of this type. 

The course may be peracute, acute or chronic. Death occurs from 
sepsis, embolism or cardiac failure. 

2. The Septic or Intermittent Type. — This form runs an irregular fever- 
curve, with chills, drenching sweats and enlarged spleen. Heart symp- 
toms may be absent or the relaxation of the right heart and the murmur 
are called functional. The paroxysms are more irregular than in malaria 
and no response to quinine is obtained. Sepsis is suspected but the 
localization is not immediately determined. The streptococcus is often 
causal. Cardiac findings, embolism or clearly septic manifestations may 
establish the diagnosis. The course is usually several weeks but may 
cover several months to over a year. 

.3. The Visceral Forms. — In these cases one organ is especially involved. 
In the cardiac form, the heart murmur seems hemic, until a typical 
valvular lesion develops, or, if one already be present from older valvular 
disease, until another appears, as a diastolic following a systolic murmur. 
In the cerebral form, meningitis, apoplexy, coma or psychoses may 
dominate the clinical picture. The symptoms referable to any organ 
which is the seat of embolism may seem to indicate a primary disease; 
thus acute yellow atrophy, pernicious anemia, Banti's disease, tubercu- 
losis, nephritis, rheumatism, etc., have been incorrectly diagnosticated. 

Special Symptoms. — (1) All types of fever, from intermittent to 
continuous, are noted, although it may be absent for long intervals. 
(2) The heart is always somewhat disturbed. Its action is more frequent 
and variable, now being rapid, again slow and often irregular. The 
heart seems to beat harder and the pulse may throb, although the irritable 
overaction is attended by low arterial tension. Palpitation is frequent. 
Cyanosis is not common. (3) Respiration is always increased, from 
toxemic centric stimulation, pain or complications as septic pneumonia, 
infarcts, pleurisy, etc. (4) The digestive tract may be affected, as nausea, 
vomiting and diarrhea from the general sepsis. Embolism has been 
mentioned. The liver is enlarged, perhaps tender or the seat of friction. 
Icterus is ominous and referable to duodenal catarrh or oversecretion 
of bile (polycholia). (5) the spleen is almost always palpably enlarged 
from sepsis or embolism. (6) The urine shows evidences of the sepsis or 
stasis by albuminuria, with or without cylindruria, and of the "blood 
dissolution" and embolism by hematuria. The course may resemble 
that of subacute nephritis, present in 33 per cent, of cases. (7) The 
nervous system is irritated or dulled by the sepsis toxins; or embolic men- 
ingitis or encephalitis may intervene. (8) The muscles are frequently 
tender and inflamed and may undergo suppuration. The bones are often 
tender, particularly the sternum, and the joints tender or swollen, although 
the swelling is more frequently periarticular than intra-articular ; bac- 
teria are seldom found, whence the occasional resemblance to rheumatism. 
(9) The skin may be the seat of embolism (v. s.) or of toxic sudamina, ery- 
thema, purpura or polymorphous septic rashes. Bullae, gangrene, phleg- 
mons or bed-sores are also observed. (10) Optic neuritis is frequent. 



I - 



Endocarditis 347 

(11) The blood exhibits marked anemia; without heart findings, the 
anemia and splenic tumor have been confused with pseudoleukemia. 
The leukocytes are not often increased. Bacteria may be cultivated from 
the blood (v. pages 19 and 20). 

Bacteriological Forms. — (a) Streptococcic Endocarditis. — The strep- 
tococcus is the usual cause of rapidly fatal ulcerative endocarditis, with 
severe repeated chills and high, irregular fever; chronic infective endo- 
carditis is almost invariably streptococcic, especially the S. viridans of 
Jochmann and Schottmiiller (see page 21); this type is often latent, 
chronic and is attended by slight if any leukocytosis, great frequency of 
positive blood cultures (Libman and Jochmann, 95 per cent.) and the 
absence of suppuration; Schottmiiller designates this type endocarditis 
lenta. (b) Staphylococcic endocarditis is less frequent. The course is 
acute and attended by high fever, pustules in the skin, disseminated 
hemorrhages and septic infarcts, especially in the kidneys, (c) Pneamo- 
coccic endocarditis is usually acute but may last over one year; frequently 
follows pneumonia (q. v.), less often cholecystitis; begins with gradual 
fever rise associated with chills; and is often attended by suppurative 
meningitis, (d) Gonococcic endocarditis (Ricord, 1847) may result from 
Neisser's coccus or from mixed infection. Cases of recovery are instanced. 

Diagnosis.— Bamberger's remark still holds: "The diagnosis of acute 
endocarditis is seldom easy, usually difficult and often impossible." 
Without physical changes in the heart, the diagnosis is only presumptive. 
A proper etiology, malaise, weakness or emaciation, the presence of an 
old valvular lesion, fever or other evidences of sepsis, signs of cardiac 
insufficiency, such as irregular, weak pulse with apparently strong cardiac 
shock, and dilatation are strongly suggestive and may be confirmed by 
continued observation, embolism, change in the valvular murmur and 
positive blood cultures. The difference between malignant and benign 
endocarditis is that the former is septicemic (bacillemic) or pyemic. 
Actual hypertrophy of the heart not only requires time for development 
but adequate nutrition, of which the acuity of the disease seldom admits. 
The misleading visceral forms have been discussed -(v. s.). In 37 per cent, 
of cases, the heart is negative, in 44 per cent, the murmur is systolic 
and in 5 per cent, diastolic. Absolute certainty rests upon our ability 
to diagnosticate by physical signs, the presence of a mitral regurgitation 
(q. v.) which is the most frequent form, or of an aortic regurgitation (q. v.), 
plus the signs of sepsis of which the disease is a part ("arterial pyemia"). 
The valvular murmur may disappear after embolism. (See Typhoid, 
differential table.) 

Diastolic murmurs are very rarely functional and their appearance 
is therefore especially suggestive. Acute myocarditis may produce a 
systolic murmur, but is usually attended by marked early muscular 
insufficiency, weak heart shock and irregular pulse, weak systolic mur- 
mur and a moderately accentuated second pulmonary tone; fatty and 
cloudy degeneration of the myocardium is the rule in acute endocarditis, 
besides which the muscle may suffer from coronary closure or embolism, 
stasis and direct involvement, by contiguity, through inflammation 
or ulceration. 



348 DISEASES OF THE ENDOCARDIUM 

Prognosis. — Satterthwaite's figures show 5 per cent, of recoveries. It 
depends on the bacteriology, the number of infarcts and their location, 
the variability of the heart murmurs (which may indicate danger of 
embolism), and the intensity of the sepsis. Recovery from the gonor- 
rheal form is relatively frequent. Musical murmurs with fever are 
usually ominous. Apparently mild endocarditis may become severe. 
The course may be rapid or severe, of a few days' duration, or a slower 
evolution of over a year. 

Treatment. — (See Benign Endocarditis and Septic Infections.) 

(B) Acute Verrucose or Benign Endocarditis. — This variety is more 
frequent, constituting 1.5 per cent, of clinical cases, and is always 
secondary. It differs from the malignant type in degree of virulence 
only. 

Etiology. — (a) Rheumatism (q. v.), its most frequent cause, accounts 
for 60 to 85 per cent, of the cases. Over 20 per cent, of rheumatic patients 
develop endocarditis; in children it is very frequent, for in them the 
heart "resembles an articulation." Muscular rheumatism, angina or 
erythema nodosum may occasion endocarditis, (b) Chorea: 30 per cent, 
of clinical and 82 per cent, of fatal cases are complicated by endo- 
carditis, (c) Of other specific infections, scarlatina ranks first, causing 
10 per cent, of endocarditides, and active or latent foci in the tonsils, or 
elsewhere, rank not far behind. Endocarditis is far more uncommon after 
typhoid, diphtheria, measles, erysipelas, gonorrhea, variola, syphilis, 
grippe, tuberculosis, etc. (d) Occasionally it is associated with trauma, 
burns, cancer, Bright's disease, gout or diabetes, (e) It is most common 
in males between the years of twenty and thirty. 

Pathology. — The vegetations are verrucose, wart-like, papular or 
even pedunculated, are usually small and occur at or above the lines of 
closure of the valves, whereby their function is impaired and valvular 
insufficiency or stenosis results. At times the vegetations are cauliflower- 
like or condylomatous. They are grayish, gelatinous and transparent; 
they become whiter and firmer with age and consist of two strata, the 
deeper being granulating endocardium and subendocardial tissue and the 
superficial layer consisting of thrombi from the coagulable elements of 
the blood. The signs of active inflammation, such as redness or swelling, 
are usually lacking, redness being sometimes confused with postmortem 
imbibition of hemoglobin from the blood. Vegetations must not be con- 
fused with Albini's nodes, seen in infants and children. The vegetations 
are at an early stage, cellular from leukocytic exudation and tissue pro- 
liferation and usually contain bacteria (see Ulcerative Type); the 
inflammation is probably primarily embolic in the myocardium, and 
affects the valves secondarily. The outgrowths becoming detached, 
emboli are released and produce mechanical hemorrhages or anemic 
infarcts, not suppurative infarcts as in the ulcerative type. The fate 
of the vegetations is (a) embolism; (b) organization with bare possi- 
bility of restoration to normal; (c) more often, organization %oith valvular 
lesions resulting from retraction, induration and calcification; (d) being 
a locus resistentia? minoris, endocarditis may be recurrent; (e) the inflam- 
mation may lead to malignant endocarditis. 



ENDOCARDITIS 349 

Localization. — The vegetations are largely on the same surface of the 
same valves as in the first type, and in the left heart; conditions in fetal 
life predispose to endocarditis on the valves of the right heart, or on 
fetal openings or defects. The mitral valves are most affected (50 per 
cent, of the cases alone or 80 per cent, when combined with other lesions), 
next the aortic (13 per cent, alone or 40 per cent, when combined with 
other lesions), and far less frequently, the tricuspid and pulmonary valves 
and the walls, chordae or parietes. 

Symptoms. — The symptoms are not characteristic unless the valves 
are considerably involved. Simple endocarditis therefore is found far 
more frequently at autopsy than at the bedside; i. e., it is very often 
latent. An increased pulse may indicate palpitation, a valvular lesion or 
a myocarditis, though the latter is the more likely cause. Daily examina- 
tion of the heart in such diseases as rheumatism may reveal a gradual 
involvement of the endocardium, with moderate fever, cardiac unrest, 
oppression, palpitation or insufficiency. Pain is generally pleuritic or 
pericarditic. A valvular bruit often follows muffling or irregularity of 
the cardiac sounds, and is still later followed by the signs of mitral or 
aortic insufficiency (q. v.). In marantic causation, as cancer and tuber- 
culosis, murmurs are generally absent. The infrequent diastolic mur- 
murs are more distinctive than the systolic, for they are rarely functional. 
Embolism is very important, as in the first type, but mechanically rather 
than bacteriologically. 

Diagnosis. — Conservatism in diagnosis is necessary and acute benign 
endocarditis is much too often diagnosticated. The most conspicuous 
symptom is fever, though it is not characteristic and may blend with 
that of the causal disease; the most important findings, objectively, are 
the signs of valvular heart disease; for these findings one must often 
wait, because in many cases the evolution alone is final. More stress 
should be placed upon the results of percussion than on the murmur itself. 
The murmurs are mistaken for functional murmurs accompanying febrile 
relaxation of the heart chambers or myocarditis, which also always 
accompanies endocarditis. 

Recurrent endocarditis shows not only the fever and other symp- 
toms caused by the fresh lesions, but also the hypertrophy of the older 
valvular lesion. An aortic diastolic or a mitral presystolic murmur 
is more likely to indicate an old lesion. With repeated examinations 
fresh murmurs may be heard in addition to the old ones. (See Mitral 
Insufficiency and Ulcerative Endocarditis.) 

Prognosis. — (a) As to life, the outlook is generally good, unless (i) 
emboli lodge in important structures, such as the basilar or coronary 
arteries, or (ii) the process becomes malignant, (b) As to complete recovery, 
(i) valvular lesions are usual which are anything but "benign"; (ii) 
fresh recurrent endocarditis is very common; and (iii) complete recovery 
is uncommon, though not unknown. 

Treatment. — The treatment of the two forms of endocarditis is 
considered together, (a) Prophylaxis resolves itself into the treatment 
of the causal acute infection, such as rheumatism or sepsis. The admin- 
istration of salicylates in rheumatism shortens the rheumatic attack. 



350 DISEASES OF THE ENDOCARDIUM 

(b) Rest spares the heart and probably lessens the percentage of cases 
involved. Psychical, physical and cardiac rest is the prime essential, 
and requires that the patient lie, not sit, in bed for many weeks after 
temperature and cardiac weakness have wholly disappeared. Should 
relative recovery occur, the general care of the heart's strength must be 
insisted upon as in chronic valvular disease and, with intercurrent 
affections or with the appearance of temperature, the patient must be 
confined to bed. Senac (1749-1783) recognized the causal importance 
of inflammation in heart disease, the necessity of avoiding strain and of 
regulating the amount of fluid and food ingested, the relations of liver 
and stomach disturbance and the advantages of mental quietude, (c) 
The sepsis is treated by moderate doses of quinine, with three ounces of 
red wine every four hours; bichloride of mercury and other antiseptics 
are futile; there may be some virtue in hexamethylenamine. (d) The 
irritable heart may be quieted by the ice-bag. Sinapisms sometimes act 
favorably but blisters are to be avoided. Cardiac stimulants should 
be employed with caution; digitalis is only indicated when tumultuous 
heart action threatens to induce embolism, (e) Symptomatic treatment: 
For nervous symptoms, sodium bromide is indicated. Sulphonal and 
trional are to be avoided when the heart weakens. Hydrotherapy, 
aside from simple sponging, is inadvisable, for the joints and muscles are 
very tender and movement may provoke embolism. Diarrhea of septic 
origin should not be checked at once, because it is nature's effort at 
elimination. A light diet should be given because of the fever. Potassium 
iodide is often administered as a resolvent after the acute stage has 
passed. (/) Vaccines and serums injure more often than they help. 

II. Chronic Endocarditis. Chronic Valvular Disease. — Etiology. — Val- 
vular disease constitutes 5 per cent, of all diseases. It most often develops 
from (a) acute verrucose endocarditis and in 60 per cent, the cause is 
rheumatism. One-half the cases of valvular disease are in children and 
over one-third occur between 20 and 30 years of age. Some apparently 
primary cases are seen mostly in young or adolescent subjects and in 
women, but doubtless some minor or forgotten infection explains this 
group, (b) Atheroma is an important cause; it is promoted by over- 
exertion, as in the working classes, by advanced years or by chronic 
nephritis, gout, diabetes, syphilis, alcoholism and lead poisoning. It is 
more common in males. Chronic valvular disease may develop from 
other causes than actual endocarditis, e. g., from (c) rupture of the 
valves; this occurs most often in the aortic valves during supreme physical 
efforts and is favored by previous valvular lesions, although sometimes 
observed in normal valves. Healing is rare, (d) In relative valvular 
insufficiency the normal valves are unable to close their orifices because 
the heart is dilated; it is most commonly tricuspid and mitral, and more 
rarely aortic and pulmonary. Relative stenosis is not clearly established. 
(e) Other rarer causes are aortic aneurysms, neoplasms, valvular aneurysms 
and cardiac thrombi. 

Pathology. — Small grayish-red swellings are sometimes seen in the early 
stages. Foci of endocardial thickening and retraction (endocarditis 
retrahens) develop, in which calcification, and even ossification, of the 



ENDOCARDITIS 351 

valves may be present. The valves become opaque, rigid, unable to unfold* 
adherent to each other or distorted by their own thickening and retraction 
or that of the chordae or papillary muscles. Acute exacerbations may 
occur and then the ordinary vegetations appear. Embolism occurs in 
30 per cent, of cases. The myocardial changes are hypertrophy, dilata- 
tion and myocarditis. The valves most often involved are the mitral 
(78 per cent.), especially in adolescence, then the aortic (20 per cent.), 
especially in syphilis and arteriosclerosis, and finally the tricuspid (1 
per cent.) and the pulmonary valves. Combined valvular lesions occur 
in 33 per cent, of cases. The process often extends by continuity of sur- 
face from the mitral to the aortic valves. When one valve is but moder- 
ately involved, the others of the same valvular orifice may compensate 
by stretching to cover the defect, especially in aortic disease. In fetal 
cases the right heart is more frequently involved. 

Valvular insufficiency is caused by (a) thickening and retraction or 
even calcification of the valves or the chordae tendinese and papillary 
muscles; (b) massive vegetations; (c) growing together of the valves, or 
of the valves with the wall of the heart or aorta; or adhesions between 
the papillary muscles and tendons; (d) valvular aneurysm, perforation, 
rupture or tearing of the tendons or muscles. Valvular stenosis (stenosis 
of the orifice) results from (a) adhesions between the valves, (6) retraction, 
calcification, fibrosis of valves or ring of insertion and (c) vegetations. 
Combined valvular insufficiency and stenosis are very common. 

Symptoms. — The symptoms of valvular disease are (a) the cardiac 
findings peculiar to each lesion, which will be first considered, and 
(b) the general symptoms more or less common to all forms of cardiac 
insufficiency, the description of which will follow the individual lesions. 

Aortic Insufficiency (Corrigan's Disease). — Aortic regurgitation was 
described by Cowper (1705), Vieussens (1715) and Hodgkin (1829), but 
the first full description was Corrigan's (1832). 

Etiology. — 1. The endocarditic form explains 27 per cent, of cases. 
The sinuses of the valves may fuse, vegetations are present, or the valves 
grow together at their margins and shrink; this is more frequent than 
valvular perforation or ulceration, which is rapidly fatal. If calcifica- 
tion develops there may be coincident stenosis of the aortic orifice. 
The endocarditic form usually follows a previous mitral lesion, occurs at 
an earlier age and is not attended by the arteriosclerotic changes in the 
aorta and coronary arteries which characterize the atheromatous form. 

2. The atheromatous form accounts for 44 per cent, of leakage. Ather- 
oma may be slight in the aorta and located mostly on the valves. It 
is a slow, degenerative process with marginal valvular retraction (see 
Arteriosclerosis); it is caused by excessive use of alcohol, by con- 
tinued hard work or athletics. It is often, therefore, seen in middle-aged 
men. The valves may adhere to the aorta. Their edges are rounded 
and present no endocarditic masses. The atheromatous process may 
overlie or actually invade the coronary orifices; this is obviously 
dangerous. Coincident stenosis is uncommon. 

3. The syphilitic form explains 29 per cent. In half the cases of pure 
aortic leakage, the aorta shows a luetic mesa-ortitis and about three- 



352 DISEASES OF THE ENDOCARDIUM 

quarters show the Wassermann test (pages 208 and 219). The following 
forms are infrequent: 

4. Relative insufficiency occurs mostly in cases of aortitis, aneurysm 
and arteriosclerotic dilatation of the root of the aorta; the aorta relaxes 
one centimeter in circumference after the fortieth year. It may also 
occur in cases of dilatation of the left ventricle, resulting from hypertrophy, 
myocarditis or renal disease. 

5. Congenital Defects. — These are rare; absence of a valve may be in 
part compensated for by the others, though anatomical anomalies pre- 
dispose to sclerosing endocarditis. 

6. Trauma. — Only 46 aortic cases are recorded in a total of 72. 
Mechanism. — From aortic incompetence, a diastolic regurgitation of 

blood into the left ventricle takes place from gravity and contraction 
of the aorta. Blood currents are caused by the blood flowing (normally 
from the left auricle and pathologically from the aorta) into the left 
ventricle, thereby producing the diastolic murmur. The left ventricle 
becomes dilated to accommodate its added volume and hypertrophied to 
propel the normal plus the regurgitated blood; the heart may weigh 
50 ounces ("ox-heart" — cor bovinum). The hypertrophied left ventricle 
suddenly forces a large amount of blood into the arteries, and thus 
causes the many arterial phenomena (Stewart believes that the amount 
of regurgitated blood is small). 

Physical Signs. — 1. Inspection. — (a) Precordial prominence is ob- 
served chiefly in plastic chests and in the endocarditic type and therefore 
mostly in women and children. Mensuration confirms the prominence 
(the right chest normally measures nearly an inch more than the left). 
(b) The heart shock is powerful and diffuse, (c) The apex beat is dislocated 
downward (6th, 7th, 8th interspace) and outward, beyond the nipple or 
anterior axillary line. It is heaving, pulsating and superficial. The lung 
is pushed back and slight rotatory systolic retraction of the chest wall is 
seen. These findings are referable to the dilated and hypertrophied left- 
heart. If the leak is slight, there may be little or no dilatation or hyper- 
trophy, clinically. The apex also lies low in arteriosclerotics, from relaxa- 
tion of the aorta, (d) Pulsation in the first and second right intercostal 
spaces is usually dynamic, because the blood expelled with extra force 
causes dilatation of the aortic arch, (e) The peripheral vessels pidsatc 
with unusual violence; pulsation in the jugular fossa or abdominal aorta 
may simulate aneurysm, and the temporals, carotids and radials attract 
attention before the patient undresses. The crossed leg may pulsate and 
the head may throb (Musset's nodding). These are all caused by ventri- 
cular hypertrophy, the extra volume of blood thrown into the vessels or an 
accommodative dilatation of the peripheral vessels. Pulsation may 
also be seen in the retina spontaneously or by pressure on the eye-ball, 
as occurs also in Basedow's disease. The liver may pulsate, though this is 
rare because a strong heart action with stasis is necessary. (The liver 
also pulsates in tricuspid incompetency from venous filling of the organ.) 
Pulsation also may occur in the spleen, tongue, palate and penis; the 
pupils may contract and dilate rhythmically. (/) The capillar ij (Quincke's) 
pulse occurs in over 80 per cent, of cases; it is also seen in health, fevers 



ENDOCARDITIS 



353 



or anemias. It is a symptom of overfilling of the arteries and capillary 
dilatation and is best observed when the hypertrophy exceeds the dila- 
tation; it disappears when the heart weakens. It is elicited by exerting 
slight pressure on the tips of the finger nails, on the lips by a glass slide 
or by rubbing the forehead until it is red; there is a systolic reddening and 
a diastolic paling in these parts. It is sometimes found in the retina, 
palate or in complicating erysipelas, (g) The passing over of the blood 
from the arterioles into the veins may produce the centripetal venous 
pulse — most obviously in the forearm, and caused by relaxation of the 
vessels, as in fevers, nervous lesions and chlorosis; by delicate skin; and 
full heart action, (h) The arteries are actually lengthened, (i) Patients 
often assume the dorsal decubitus, for gravity increases the leakage; sub- 
jects with mitral insufficiency usually sit. The findings by inspection are 
practically pathognomonic. 

2. Palpation. — (a) The hand corroborates the results of inspection — 
as the heaving, throbbing apex and the diastolic impulse, (b) A diastolic 
thrill over the base is infrequent, occurring mostly in cases of endocarditic 
origin, (c) In the jugulum, especially in arteriosclerotics, the widened aorta 




Fig. 21. — Sphygmogram of case of uncomplicated aortic leakage. 



can be felt, (d) The pulse findings may seem paradoxical; the arteries 
are filled violently (the pulsus durus), though the tone of the vessels is 
less than normal. Oppolzer is reputed to have secured his professorship 
in Vienna by his diagnosis of aortic leakage from placing his hand on a 
patient's foot. 

The radial artery is suddenly filled, the "pistol pulse" or pulsus celer, 
due to hypertrophy of the left ventricle. The heart action is quicker, 
at the expense of the diastole, shortening of which is favorable, since 
less time is allowed for the leakage. The condition of the heart muscle 
and pulse depends on the etiology of the case ; hypertrophy is marked in 
the endocarditic form, but in the atheromatous type, coronary atheroma 
and fibrous myocarditis lessen the myocardial activity, render the pulse 
atypical and make the prognosis less favorable. The sphygmographic 
tracing shows the high up-stroke with an acute apex (the pulsus alius). 
The dicrotic wave is ill-marked and the pulse rapidly recedes (the "col- 
lapsing pulse''), due to the inability of the aortic valves to hold the 
receding blood. (Stewart's explanation is: a reflex dilatation of the 
peripheral vessels and heart stimulation by the increased pressure within 
the left ventricle.) .The collapse of the pulse is sometimes increased by 
23 



354 DISEASES OF THE ENDOCARDIUM 

lifting the arm. This pulse is strongly suggestive but also occurs in 
fevers or anemias. The typical findings are altered by atheroma; other 
valvular lesions (aortic stenosis or mitral regurgitation) ; or by heart weak- 
ness. When the pulse findings precede the murmur, it is claimed that 
the lesion is due to disease of the aorta. Thrills may be felt over the 
peripheral vessels. The peripheral pulse is. delayed in half of the cases, 
because the regurgitation continues into the first part of the systole. 
The systolic blood-pressure is higher, and the diastolic is lower, than 
normal . 

3. Percussion. — (a) The heart area is increased downward and to the left; 
the axray shows the heart rather horizontal, "recumbent" or of an 
"egg form." Dulness reaches the second or third rib to the left of the 
sternum (see Plate X, Fig. C). The dulness extends slightly beyond the 
apex and is due to dilatation of the left ventricle; the right heart may be 
crowded somewhat to the right, although dulness to the right of the 
sternum is infrequent. The papillary muscles are found flattened and 
thickened at autopsy, from the pressure of the regurgitant blood. (6) 
A small area of dulness in the first and second right interspaces denotes 
mechanical dilatation of the arch, from the cardiac hypertrophy. 

4. Auscultation. — (a) A diastolic murmur is heard over or to the left 
of the sternum at the level of the second or third rib, and increased 
downward along the sternum, for the regurgitant column follows this 
direction (Plate X, Fig. C). It has a blowing, deep and less often sawing, 
musical or whistling sound (which latter suggests a relative aortic leakage). 
When slight, it may easily escape recognition; when well developed it is 
very characteristic, sounding like the word "who." It may best be heard 
with the bare ear again'st the chest. It sometimes disappears before 
death when the heart is weak and the lesion great, but generally corre- 
sponds to the degree of leakage. It rarely reaches the neck, abdomen or 
axilla. Valvular rupture may produce a murmur which can be heard 
at a distance, (b) A slight systolic murmur over the aorta is common, 
but the too frequent diagnosis of aortic stenosis (q. v.) is not justified. 
It is soft in the atheromatous and often harsh in the endocarditic type. 
Its various explanations are: rough aorta or valves; physiological stenosis 
(the rigid valves lying between a wide aorta and a dilated ventricle); 
vibration of the aorta; or leakage continuing into the beginning of the 
systole, (c) Weakness or absence of the second aortic tone is explained by 
imperfect closure of the valves. As the second tone is normally heard 
over the carotid artery, it should be listened for there, because it is 
removed from the murmur and the second pulmonic tone. If it is pres- 
ent, one or more valves are closing, though probably imperfectly. By lift- 
ing the stethoscope a little from the skin over the aortic region, the second 
sound, previously obscured by the bruit, may be heard, (d) The first 
mitral tone is often weak or lost, because the papillary muscles are flattened 
and indurated by the regurgitant column, or a mitral systolic murmur 
may replace the first tone, (e) An apical presystolic (Flint's) murmur is 
due to aortic leakage continued in the systole, or to pressure on the 
mitral valves, which hinders the flow of blood from the left auricle into 
the left ventricle (Flint, 1862). Thayer found it in GO per cent, of 74 



O n~ 




ENDOCARDITIS 355 

cases, and in less than one-quarter of these was there coincident mitral 
stenosis. (/) Arterial tones and murmurs result from vibration of the 
vessel wall; the tones may become murmurs, when there is great differ- 
ence in tension. The systolic vessel tone is increased by the larger 
volume of blood and increased ventricular action, and is most plain 
when the vessels are not sclerotic. The femoral systolic tone is convertible 
into a murmur on pressure. Traube's double femoral sounds consist of two 
spontaneous tones" (produced without pressure), most satisfactorily 
explained by sudden change in tension. They are heard best when the 
heart is strong and the vessels soft. They may be confused with the 
double venous (Friedreich's) tones, heard over the vein in tricuspid 
leakage. Duroziez's double murmur consists of two murmurs, elicited by 
slight pressure and due to the progress and recession of blood in the 
artery. These phenomena also occur in other conditions. 

Diagnosis. — Physical examination by inspection, palpation, percus- 
sion and auscultation, in the order named, prevents error in the inter- 
pretation of murmurs. The cardinal findings are: (a) dilatation and 
hypertrophy of the left ventricle; (6) the pulsus celer and alius; (c) the 
arterial phenomena; and (d) the diastolic murmur. 

Comparing the types, endocarditic aortic insufficiency is generally 
rheumatic and occurs in younger subjects; precordial prominence and 
diastolic thrill are more common; the heart muscle hypertrophies and 
the pulsating vessels are more conspicuous; the pulse is more typically 
" pistol-like" and collapsing, as the vessels are not sclerosed; the capillary 
pulse and vessel tones are more frequent; on auscultation the diastolic 
murmur is rather harsher and nearer the valves, Flint's murmur is more 
common and if a systolic aortic bruit is heard, it is often harsher and 
coincident aortic stenosis is more frequent. 

In the atheromatous form, sexual excesses, manual work and alco- 
holism are more evident. Syphilis is declared by the immobile pupil, 
lightning pains of tabes or Wassermann reaction. As arteriosclerosis 
readily involves the heart, anginal pains, myocarditis or dyspnea may 
stand forth. The dilated aorta is more frequently palpable in the jugulum 
and allows the heart to sag lower in the chest. The diastolic murmur 
is more characteristically deep and blowing and the vascular phenomena 
are considerably modified by the rigid arteries. 

Relative aortic regurgitation is difficult to differentiate from the val- 
vular; the murmur is a short, presystolic or postdiastolic, almost pathog- 
nomonic "huff" after the second aortic tone. The pulse is frequently 
small, tardy and tense, but not quick. The murmur varies from time 
to time, sometimes short, then longer, sometimes blowing, and again 
coarse. 

Diastolic murmurs are rarely anemic (cardiopulmonary or functional) ; 
such bruits exist, however, in the cava and other veins ; they are uneven 
and stronger in the beginning of the diastole. Aortic aneurysm (q. v.) 
may cause confusion. In mitral lesions, the capillaries are poorly filled 
and the skin is cyanotic; in aortic regurgitation the arterioles are over- 
filled and the skin is pale, perhaps red. In mitral disease, congestion of 
the lungs, brown induration and dilatation of the right heart obtain; 



356 DISEASES OF THE ENDOCARDIUM 

these are absent in aortic leakage; a hemorrhagic nephritis may take 
the place of the analogous brown induration of the lungs of mitral lesions. 

Relative healing by vicarious stretching of sound valves, by increasing 
stenosis and by calcification is possible but infrequent. 

Aortic Stenosis. — Stenosis of the aortic orifice, a better term than aortic 
stenosis, is the rarest of left-heart lesions; its frequency as a solitary 
lesion is 2.5 per cent. It may occur congenitally from constriction of the 
conus arteriosus (Dittrich's genuine heart stenosis), It occurs, however, 
largely in the aged; the valves become interadherent or fibrously thick- 
ened from atheroma or chronic endocarditic calcification, or retraction 
at the valvular insertion obstructs the orifice. Acute endocarditis, with 
massive vegetations, may produce some stenosis. It is usually associated 
with aortic incompetency. 

Mechanism. — The rigid valves narrow the orifice and at the obstruc- 
tion a systolic murmur originates. The resistance to the onward flow 
of blood from the left ventricle leads to its hypertrophy. The pulse 
becomes small and slow because of obstruction. 

Physical Signs. — 1. Inspection. — Some precordial prominence may 
be seen in yielding chests. The apex beat is sometimes strong and 
dislocated to the left, but often no apex is seen on account of diminution 
of the heart's recoil. 



Fig. 22. — Pulse tracing in stenosis of the aortic orifice. 

2. Palpation. — (a) A pronounced systolic thrill is often felt over the 
second right interspace, sometimes over the heart and cervical vessels. 
(b) The pulse is infrequent (pulsus rams), because the systole is prolonged 
and the coronary arteries are poorly filled; small (p. parvus) from ob- 
struction to its flow; tense (p. durus) from hypertrophy of the left 
ventricle; and slow (p. tardus) with tardy up-and-down stroke and some 
retardation. 

3. Percussion. — Concentric hypertrophy (with the left ventricle smaller 
than normal), and simple hypertrophy, which are the more common as 
the stenosis is purer, give no change on percussion. Slight dilatation to 
the left is sometimes present, especially with aortic regurgitation, nephritis 
or atheroma. 

4. Auscultation. — (a) The systolic murmur over the aortic area is 
generally long, sawing, whistling or musical and is transmitted with the 
blood current into the arch, the descending aorta in the back, its vessels 
(Plate X, Fig. A), or over the entire heart or even at some distance from 
the chest. It is not proportionate to the intensity of the lesion and 
disappears with broken compensation, (b) The second aortic sound is 
weak, from poor filling of the aorta and weak closure of the altered valves, 
or absent in coincident aortic regurgitation; (c) when the second aortic 
sound is absent, the second mitral tone, or indeed all the heart tones, are 
weak or absent, (d) The systolic tone over the aorta is scarcely to be 
beard. 



ENDOCARDITIS 357 

Diagnosis. — The lesion may be favorable — a healing of an aortic 
regurgitation. Aortic stenosis is a frequent surprise at autopsy, having 
run a latent course. Diagnosis should be reserved, without these cardinal 
signs: (a) systolic murmur with propagation into the large vessels or 
over the entire heart; (b) a systolic fremissement over the aortic area; 
(c) the small, tense, tardy, slow pulse, in contrast to the strong apex beat. 
As the lesion is uncommon, its frequent diagnosis implies confusion 
with (i) accidental murmurs which are variable, (ii) Acute endocarditic 
vegetations, give a soft murmur which becomes harsher if actual stenosis 
ensues, (iii) Atheroma of the aorta, or acute aortitis, where the murmur 
is more localized over the aorta, the second aortic tone is metallic and the 
pulse proportionate to the apex beat. Atheroma, the most frequent 
cause of diagnostic error, is very common, while experienced clinicians 
see few cases of pure aortic stenosis, (iv) Aneurysm (q. v.), which is often 
distinguishable by its pressure symptoms. 

Mitral Insufficiency. — Mitral insufficiency (incompetency, regurgita- 
tion) is the most frequent valvular lesion and more often endocarditic 
than atheromatous. It is (a) valvular, from adhesions between the valves 
or chordae and ventricular wall, from vegetations, from thickening with 
retraction, from valvular aneurysm or perforation, or from shrinkage or 
rupture of the papillary muscles or chorda? ; (6) muscular, from relative 
insufficiency due to such ventricular relaxation that the valves do not 
cover the orifice; this form is common in hypertrophy with dilatation, 
resulting from hard work, nephritis, syphilis, alcoholism, myocarditis 
and adherent pericardium; (c) rupture of the mitral cusps is very un- 
common. Barie collected 35 cases of valvular rupture, of which 45.7 
per cent, were aortic, 45.7 per cent, mitral and 8.6 per cent, tricuspid. 

Mechanism. — During the systole, a backward flow occurs through 
the incompetent valves into the left auricle, which, as it also receives 
blood from the lung veins, first dilates and later hypertrophies as far as 
its thin musculature admits. The left ventricle dilates because it receives 
in the diastole the usual inflow of blood plus the regurgitated blood 
and, responsive to the dilatation, it hypertrophies because its work is 
increased. In aortic lesions, the first and greatest strain is felt in the 
left ventricle, but mitral lesions, by congesting the lungs, throw most 
work on the right heart. The stasis in the left auricle is transmitted to 
the pulmonary veins, capillaries and arteries, thus leading to increased 
blood-pressure in the pulmonary circuit, because (a) of this backward 
pressure, and (6) of the onward pressure from the right ventricle, which 
dilates and then hypertrophies. The lungs are enlarged, their vessels 
dilate and may become atheromatous, possibly causing infarcts in the 
lungs and fibrosis (brown induration). When the final atonicity of the 
right ventricle, i. e., broken compensation, occurs, relative tricuspid 
leakage from dilatation, cyanotic induration of the liver and kidneys, 
edema, etc., result. 

Physical Signs. — 1. Inspection. — (a) The apex may be normally 
located or displaced to the left — even into the axilla, when the heart lies 
lower than normal. A normally strong apex beat in mitral insufficiency 
is evidence of hypertrophy, (b) Systolic pulsation in the second, left inter- 



358 DISEASES OF THE ENDOCARDIUM 

space indicates a wide pulmonary artery from stasis, and (c) a diastolic 
shock there is due to closure of its valves; (d) precordial prominence 
occurs in yielding chests from dilatation; (e) pulsation, either epigastric 
or to the right of the sternum, results from dilatation and hypertrophy 
of the right ventricle. (J) The enlarged veins pulsate during the diastole 
from stasis, and sometimes during the systole from tricuspid incom- 
petency. 

2. Palpation. — (a) The apex is dislocated to the left; (b) the pulmonary 
artery pulsation and (c) the diastolic shock of the forcibly closing pulmonary 
valves are very often palpable; by placing one finger over the valves and 
another over the apex the two shocks alternate; (d) pulsation is felt to 
the right of the sternum from right ventricle dilatation; (e) a systolic 
apical thrill is often palpable but not pathognomonic. (/) In pure cases 
the pulse is about normal in tension, or weakens with decompensation. 
Irregularity is not common. 

3. Percussion. — (a) Dilatation of the right ventricle is commonly fol- 
lowed by hypertrophy, in compensated cases, as the right heart bears the 
stress of this lesion. Dilatation causes dulness and palpatory resistance 
to the right of the sternum (see Plate X, Fig. B). The .r-rays show the 
typical round heart. Hypertrophy without dilatation is usually found 
in the early and well-compensated lesions, (b) The left ventricle usually 
dilates to respond to the increased amount of blood, and hypertrophies 
because of increased work or the raising of arterial pressure by carbon 
dioxide. 

4. Auscultation. — (a) The systolic murmur is due to abnormal eddies 
in the left auricle or to the vibrations caused by them in the mitral valves; 
it most often gives a blowing sound, best heard over the apex, which is 
less covered by the lung, but at times is localized over the left auricle, 
where it originates and is heard especially in early lesions. It is transmitted 
chiefly to the left toivard the left interscapular region, and more rarely to. 
the aorta, carotids and abdomen (see Plate X, Fig. B); at times it is 
heard intermittently, in certain postures only, and it may disappear 
with weakening of the heart. In very rare cases it is entirely absent. 
(6) The first mitral tone is usually absent because the valves cannot vibrate'; 
if present it is referable to conduction from the tricuspid valve or to 
contraction of the ventricle. When obscured by the murmur, it may 
sometimes be heard by lifting the stethoscope a little from the chest 
wall. In extreme leakage, the murmur replaces all tones, (c) The 
second pulmonic sound is accentuated, " hammer-like," and is a measure 
and result of the right ventricular hypertrophy (Skoda). It sometimes 
reaches the vessels of the neck. When the tricuspid valves become 
relatively insufficient, it usually weakens. The second tone is sometimes 
split, {d) A systolic murmur over the pulmonary area is propagated from 
the apex or is due to vibrations in the distended pulmonary artery. 

Diagnosis. — The cardinal features are (a) the systolic murmur, (b) 
accentuated second pulmonic tone and (c) right-heart changes. 

Excepting the etiological diagnosis and the clinical evolution, there 
are no positive criteria by which we can differentiate a muscular (relative) 
from a valvular insufficiency, though in the former the murmur is mnvo 



ENDOCARDITIS 359 

variable, lessens with digitalis and is not associated with a diastolic- 
stenotic murmur, since pure valvular insufficiency is exceptional, and 
there is usually, anatomically at least, some mitral stenosis. An organic 
valvular defect is probable when the apex, dislocated to the left, is 
forcible. 

From the functional (accidental, hemic or cardiopulmonary) mur- 
mur, the diagnosis is usually easy. The murmur is inconstant, usually 
systolic, often basal, often depends on posture, is circumscribed, is not 
typically transmitted, follows fever, anemia and emphysema, is often 
associated with the venous hum in the neck, but is never associated with 
typical mitral changes in the heart tones and right ventricle. The 
intensity, timbre or fremissement of the murmur must not alone be 
depended upon. 

In chlorosis, we may obtain a hemic murmur, apparently large heart 
(because the lungs are poorly expanded), and a displaced apex (high 
diaphragm); deep breathing decreases the heart's dulness. 

Pericardial friction (q. v.) may simulate endocardial murmurs. 

FrantzePs rules aid in accuracy: (1) Never make a diagnosis just 
before death. (2) Remember the great infrequency of right-heart lesions. 
(3) Avoid complicated diagnoses. (4) Subordinate the murmurs to 
other physical findings. 

Mitral Stenosis. — Anatomically pure stenosis of the mitral orifice, 
without associated mitral leakage, is rare. In one group, especially 
in young girls, the stenosis is clearly endocarditic and the valves are 
irregular, calcareous and deformed. In another group, in old subjects 
of both sexes, the sclerosing process is probably endocarditic; and in the 
last group, almost exclusively observed in women, the nature of the 
lesion is uncertain; some rare cases are associated with congenital 
defects. The mitral valves are grown together or the ring constricted — 
Corrigan's "button-hole contraction"; the orifice in extreme cases is 
funnel-shaped. 

Mechanism. — The stenosis obstructs the diastolic discharge of blood 
from the left auricle, which consequently dilates and later hypertrophies. 
The enlarged auricle or pulmonary artery may compress the adjacent 
bronchus or recurrent laryngeal nerve. The stasis is propagated back- 
ward through the lungs to the right ventricle, whose dilatation and 
hypertrophy cause the large right heart and the increased pressure 
in the lesser circulation. The effects on the right heart and lungs are 
more severe than in mitral insufficiency. The right auricle also dilates 
when the later venous stasis follows. Thrombi in either auricle may dis- 
lodge and produce pulmonary or arterial infarction. The arterial system 
is poorly rilled. 

Physical Signs. — 1. Inspection. — This reveals (a) precordial dis- 
tention, (b) epigastric pulsation and (c) a diffuse cardiac shock; (d) the 
apex beat may in comparison be small, and (e) two impulses may be seen 
in the second left interspace; one is systolic, from systolic filling of the 
pulmonary artery, and the other is diastolic, from pulmonary valve closure 
under high tension. All these findings depend on the right-heart hyper- 
trophy and dilatation. 



360 . DISEASES OF THE ENDOCARDIUM 

2. Palpation. — Palpation confirms the above, especially (a) the apex 
beat, which is often weak in comparison with the diffuse heart impulse, 
(b) the snap of the second pulmonic sound, (c) the pulsating right heart, 
and also (d) a presystolic (more rarely diastolic) thrill, fremissement 
cataire, which is usually limited to the apex, ends with the snappy first 
apex tone, and is felt sometimes only in the left lateral posture or after 
exertion. Its mechanism is identical with that of the murmur (q. v.). 
(e) The pulse is often irregular in pure stenosis, because dilatation inter- 
feres with cardiac conductivity and is usually small and of low tension, 
because the aorta is poorly filled; its weakness contrasts conspicuously 
with the active heart impulse. It may seem hard. The pulse and sphyg- 
mogram are not pathognomonic. 

3. Percussion. — (a) The right ventricle in the earlier stages may be 
only hypertrophied, which does not show on percussion. Dilatation 
without hypertrophy exists in few cases fortunately, for the prognosis 
is then poor. Most commonly hypertrophy and dilatation coexist, the 
latter giving increased dulness to the right, as in mitral insufficiency. 
(6) The left ventricle in many cases of dominant stenosis shows concentric 
atrophy, so that at autopsy it looks like a mere appendage to the huge 
right heart, as shown also in the x-ray examination. It is sometimes 
both hypertrophied and dilated, because of stasis with increase in the 
blood of carbon dioxide, which raises the blood-pressure; or because of 
other lesions, as mitral leakage, (c) The auricles are distended, much of 
the dulness under or to the right of the sternum being due to the dilated 
right auricle and that above and to the left, to the left ventricle and 
widened right conus arteriosus. Increased dulness, due apparently to 
dilatation of the various chambers is often caused by their disloca- 
tion by the wide right ventricle. The left auricle is best determined by 
radiography. 

4. Auscultation. — (a) An apical presystolic murmur occurs at the 
end of the diastole with the systole of the hypertrophied auricle which 
forces the blood through the narrowed ring; corresponding with its 
energy, it is loudest at the incipiency and ending of the auricular systole 
(crescendo murmur). It so closely precedes the ventricular systole 
that it is almost invariably called systolic by students. It is usually 
rolling, sounding like r-r-r-, after which comes the loud first tone, 
sounding like p (r-r-r-p). It is poorly propagated as a rule, corre- 
sponding to the localized thrill, but may in exceptional cases be heard in 
the axilla or back. It is often absent even with great stenosis, when the 
auricle and ventricle contract together and when the heart weakens. 
It is rarely diastolic (diminuendo murmur). (b) Marked accentuation 
of the second pulmonic sound is the proof and measure of hypertrophy 
of the right ventricle from pulmonary congestion. Its absence is a poor 
prognostic; it usually weakens when relative tricuspid leakage lessens 
the tension in the lungs, (c) Splitting or reduplication of the second 
pulmonic sound is due to difference in tension in the two arterial trunks, 
the aortic valves closing first and more weakly ; it is best heard at the base 
and is often propagated into the neck or axilla, (d) The loud first mitral 
tone is explained in various ways; viz., by difference in tension of the 



ENDOCARDITIS 



361 



valves during the systole and diastole or by a vigorous contraction of 
the left ventricle upon little blood. It is sometimes heard at a distance 
of several feet, (e) The second mitral tone r weak because of poor filling 
of the aorta or because the right heart pushes forward; it may be split 
at the apex (the " postman's knock") ; the cause is disputed. 

Diagnosis. — The cardial signs are (a) the presystolic thrill and bruit; 
(6) the involvement of the right heart; (c) the accentuated second 
pulmonic sound; and (d) loud first apical tone. 

The thrill and bruit are also found in aortic insufficiency, in which 
the vascular phenomena and the involvement of the left heart are suffi- 
ciently distinctive, though one out of every three cases of aortic leakage 
is complicated by mitral stenosis. The bruit is also heard in lesions 
leading to dilatation of the left ventricle, such as adherent pericardium, 
and in auricular contractions. 

Pure mitral stenosis is often overlooked in asthenic women, because 
the lesion is so benign; characteristic are the positive findings — loud 
apical tone, murmur and a third tone — and the negative findings — 
absence of hypertrophy, dilatation and systolic bruit. 

An absence of the murmur indicates a slight lesion; a presystolic 
murmur argues for a strong left auricle; a diastolic murmur indicates a 
severe stenosis; when tricuspid leakage intervenes, the murmur of 
mitral stenosis is either absent or diastolic, because both auricles are 
atonic. Absent murmur with irregularity is indicative of the most 
serious lesion. When the left auricle is strong, it may suppress the 
systolic murmur of a coincident mitral leakage; when the auricle weakens, 
the systolic murmur appears. Auricular fibrillation (page 339) indicates 
severe disturbance in cardiac function. 



DIFFERENTIAL TABLE OF THE COMMON CHRONIC VALVULAR LESIONS. 





Aortic 




Mitral 






insufficiency. 


Aortic stenosis. 


insufficiency. 


Mitral stenosis. 


Etiology. 


Arteriosclerosis 


Often _ arterio- 


Endocarditis 


Endocarditis. 




chiefly. 


sclerosis. 


chiefly. 




Pulse. 


Pulsus celer. 


Pulse small, slow , 


No characteristic 


Small and often irreg- 




Water-hammer, 


tense. 


alteration — often 


ular. 




collapsing. 




normal. 




Left Ventricle. 


Hypertrophied and 


Hypertrophy 


Some hypertrophy 


No essential or regu- 




dilated greatly; 


usually concentric. 


and dilatation. 


lar change; may be 




heaving apex. 






small. 


Right 


No change. 


No change. 


Hypertrophy and 


Both marked, also in 


Ventricle. 






dilatation marked. 


auricles. 


Murmur. 


Diastolic ; blowing 


Harsh systolic mur- 


Systolic at apex, 


Presystolic (oftener 




over sternum near 


mur over aortic 


blowing, trans- 


than diastolic) , 




second rib; pro- 


area with systolic 


mitted into left 


apical, accompanied 




pagated toward 


thrill; propagated 


axilla and behind 


by presystolic thrill, 




apex. 


into neck. 


scapula. 


fairly localized. 


First Mitral 


Usually weak. 


Strong usually. 


Usually present.per- 


Loud and sharp. 


Tone. 






haps covered by 
murmur. 


clearly palpable and 
following murmur. 


Second Aortic 


Weak or absent. 


Weak only. 


Somewhat weak. 


Somewhat weak. 


Tone. 










Second Pulmo- 


Not accentuated. 


Not accentuated. 


Loudly accentuated 


Accentuated and 


nary Tone. 






and often palpable. 


often split. 


Peripheral 


Violent pulsation ; 


Absent. 


Absent. 


Absent. 


Vessels. 


capillary pulse; 
arterial tones; skin 
red. 




Skin cyanotic. 


Skin cyanotic. 



In conjunction with this table, Plate X should be consulted. 



362 DISEASES OF THE ENDOCARDIUM 

Pulmonary Insufficiency. — The rare pulmonary insufficiency of which 
Barie has collected 58 cases, is often combined with pulmonary stenosis 
or other rare right-heart anomalies. It is (a) congenital, resulting from 
fetal endocarditis or from supernumerary or rudimentary valves; (b) 
acquired, from atheroma, rheumatism or septic ulceration; or very 
rarely (c) relative from extreme intrapulmonary blood-pressure or from 
embolism of the pulmonary trunk. 

Mechanism. — The mechanism is analogous to that of aortic insuffi- 
ciency except that the right heart suffers instead of the left and the 
arterial phenomena are manifest in the area of the pulmonary artery. 

Physical Signs. — 1. Inspection. — The dilated and hypertrophied right 
heart pulsates to the right of the sternum. A systolic, dynamic pulsation 
may be seen over the dilated pulmonary trunk. 

2. Palpation. — This determines the diffuse right-heart impulse and a 
diastolic thrill over the pulmonic area; the apex and radial pulse are 
normal or weak. 

3. Percussion. — The right ventricle is dilated because of the regur- 
gitant column of blood and hypertrophied to maintain the onward flow 
under this burden (Plate X, Fig. E). 

4. Auscultation. — A diastolic murmur is propagated down the sternum 
over the right ventricle, and maybe confused with aortic leakage, aneurysm, 
functional venous murmurs, congenital anomalies of the vessels or patent 
foramen ovale. The second pulmonic and the second tricuspid tones 
are weak or replaced by the murmur. The bruit is but rarely heard in 
the neck and the normal second arterial tone is heard over the carotids. 
A systolic murmur is heard in 25 per cent, of cases over the pulmonary 
trunk, due to vibrations in its walls or to coincident stenosis of the 
pulmonary ring. A double tone has been heard over the lung, as well 
as variation in the respiration during the systole — a capillary pulse 
in the pulmonary vessels. 

Pulmonary Stenosis.— The etiology will be considered under diagnosis 
and under congenital heart lesions. 

Mechanism and Physical Signs. — 1. Inspection. — There is precordial 
bulging, a diffuse heart shock from hypertrophy and dilatation of the 
right heart, and a weak or absent apex beat. 

2. Palpation. — Palpation confirms the above and reveals a systolic 
thrill in the left second interspace. The pulse is weak. 

3. Percussion. — Percussion shows an area of increased dulness over 
the right heart from dilatation. 

4. Auscultation. — On auscultation, a loud and whistling or musical 
systolic murmur, caused by the stenosis, is often heard, and the first 
and second pulmonic tones, hence also the second tricuspid, are weak 
or absent from poor filling of the pulmonary artery and from valve 
alteration. (See Plate X, Fig. E.) 

Diagnosis. — The more frequent form is (a) the congenital, due to 
malformation, myocarditis or endocarditis, and usually associated with 
open ductus Botalli or foramen ovale. The obstruction may be below 
the valves, from myocarditic scars narrowing the conns arteriosus, in 
which case 1 the second pulmonic sound is accentuated; or it may be at 



ENDOCARDITIS, 363 

the valves or in the trunk of the artery. Congenital cyanosis and 
acquired pulmonary tuberculosis are common, (b) The acquired valvular 
form is rare. Atheroma or gummata may be causal. The thrill is 
far less frequently felt in acccidental murmurs, which are most com- 
mon over this area because the thin walls of the artery vibrate easily. 
These "functional" murmurs are so common as to justify extreme caution 
in the diagnosis of right-heart lesions in the adult. Functional murmurs 
may occur in health, fevers, anemia or as the cardiopulmonary murmur. 
The organic murmur rarely reaches the jugular or cervical vessels. The 
left heart is frequently atrophic. When the acquired stenosis is beyond 
the valve in the pulmonary trunk or lungs, the murmur is best heard 
along the right border of the sternum or in the back, and the second 
pulmonic sound is loudly accentuated, from which points a diagnosis 
occasionally may be made. In atresia of the orifice 80 per cent, of the 
subjects die in the first year. 

Tricuspid Insufficiency. — Etiology. — (a) The congenital form occurs in 
0.8 per cent, of valvular cases. The venosity of the blood in the right 
heart tends to prevent endocarditis, except in fetal life when the blood 
is arterial. Myocarditis or ulcerative endocarditis may exceptionally 
occur, (b) Of acquired forms, the relative insufficiency is very common, 
resulting from (i) valvular lesions of the left heart, especially mitral 
stenosis; (ii) obstructive lung lesions, as induration or emphysema; 
(hi) and in severe anemias, in which, however, cyanosis and dyspnea 
are absent. 

Mechanism. — The high pressure in the lesser circulation leads to dilata- 
tion and hypertrophy of the right ventricle. Extreme dilatation stretches 
the tricuspid orifice so that the valves cannot cover it, and relative 
leakage occurs. The leak into the right auricle produces its dilatation 
and hypertrophy, a systolic murmur and a systolic pulse in the veins 
of the neck and liver. 

Physical Signs. — 1. Inspection. — (a) A systolic pulse in the jugular 
veins is due to systolic entrance of blood into the veins from the right 
ventricle through the insufficient valves; it is also a sign that the auricle 
and ventricle contract together or that the auricle is paralyzed. It is 
presystolic-systolic and is known as positive to differentiate it from the 
negative or diastolic venous pulse which is observed in many other con- 
ditions, and either physiologicallv, as on deep inspiration (damming 
back of the blood by the auricular systole) or pathologically, as in stasis. 
It i 3 seen best on the right side because of the more direct vertical connec- 
tion with the right innominate vein. It may cease when the heart grows 
weak. Digitalis may cause it to reappear in cases of relative and some- 
times of organic leakage. It is best seen in the dorsal decubitus. If 
the carotid be compressed as low down as possible, or the pulsating 
jugular vein be compressed at the middle; the upper part will then 
pulsate if the carotids beat against it (transmitted pulsation) and the 
lower part will beat if the pulsation is in the vein itself. It is sometimes 
seen in the inferior vena cava or peripheral veins, (b) A liver pulse, systolic 
in time, is venous regurgitant in origin, (c) The right heart pulsates 
widely, while the apex beat is weak. 



364 



DISEASES OF THE ENDOCARDIUM 



2. Palpation. — (a) This establishes the systolic phase of the venous 
pulse, and (b) the systolic venous pulsation of the liver, which expands in 
the bimanual examination and is easier to find than the jugular pulsa- 
tion. It must not be confused with an arterial liver pulse, which occurs 




Fig. 23. — Negative (diastolic-presystolic) venous pulse. (After Riegel and Sahli.) 

in aortic leakage and exophthalmic goitre, but is less expansile than 
throbbing, (c) A systolic thrill over the tricuspid area; (d) tones or 
thrills over the peripheral veins; and (e) a weak apex and radial pulse 
are also found. 




Fig. 24. — Positive (presystolic-systolic) venous pulse. (After Riegel.) 

3. Percussion. — This shows increased dulness to the right, from dis- 
tention of the right auricle and ventricle. Changes in the left heart 
may indicate an older valvular lesion which causes the tricuspid leakage. 
(See Plate X, Fig. D.) 




Fig. 25. — Illustrating the influence of respiration on the positive (presystolic-systolic) 
venous pulse of the jugular vein. (After Kovacs.) 

4. Auscultation. — (a) A faint systolic murmur is heard over the tri- 
cuspid region; the causal mitral murmur is higher pitched, more super- 
ficial and louder and is heard in the back. The murmur is absent when 
the right heart is so weak that it fails to produce the necessary vibration 
or eddy, (b) The second pulmonic sound is weak because the pulmonary 



ENDOCARDITIS 365 

circuit is poorly filled, but varies with the changing activity of the right 
ventricle, (c) Over the cervical veins may be heard a systolic tone refer- 
able to closure of valves in the veins; the tone may be double, or pre- 
systolic-systolic ; or venous murmurs may replace the tones. 

Diagnosis. — The relative insufficiency is diagnosticated by (a) the 
etiology, (b) the large right heart, (c) the faint systolic murmur, (d) 
the positive venous pulse in the neck, disappearing under digitalis and 
rest and (e) the weak second pulmonic tone. Rest or digitalis very 
often brings out the causal mitral lesion. The " safety valve" action 
of the tricuspid valves is compensatory; guarding the door between 
the venous and arterial circuits, their insufficiency indicates serious 
cardiac failure. 

Tricuspid Stenosis. — Rarer than tricuspid insufficiency, it occurs alone 
in only 10 per cent, of the cases; it is more often associated with insuffi- 
ciency, or with aortic or mitral stenosis; the latter is coincident in half 
the cases. In half the cases there is a history of rheumatism or chorea; 
three-quarters occur in women. Obstruction of this orifice induces 
hypertrophy and dilatation of the right auricle, with dulness to the 
right of the sternum. In the single lesion the other heart chambers and 
the large vessels are small. The pulse and second pulmonic sound are 
weak; a diastolic or presystolic murmur and thrill to the right of the 
sternum are detected if the heart is sufficiently strong, but they are often 
absent. The lesion is most serious, because it taxes the weak auricle 
and greatly engorges the venous system. In the jugular vein there is 
a presystolic wave. The diagnosis was made in but 10 of the 187 cases 
on record. (See Plate X, Fig. D.) 

Combined Valvular Lesions. — These occur, clinically, in 33 per cent, 
of valvular cases, but anatomically, a pure lesion is rare, and doable 
lesions are found oftener than physical signs would indicate. Single 
lesions occur most often on the arterial valves. One lesion may follow 
another; for instance, stenosis may gradually result from insufficiency, 
sometimes with good results; or combined lesions may develop simul- 
taneously. 

(a) Combined mitral lesions are most frequent, though one lesion 
usually predominates; (b) combined mitral and aortic lesions, e. g., 
aortic vegetations reaching the nearest mitral cusp, are next in frequency ; 
(c) double aortic lesions are less common; (d) combined aortic, mitral 
and tricuspid lesions, e. g., stenosis of each orifice with no signs other 
than slowing of the circulation, occur in 16 per cent., and (e) combined 
mitral and tricuspid lesions (especially relative tricuspid insufficiency) 
occur in 9 per cent. 

Diagnosis. — The diagnosis depends upon the character of the pulse, 
the quality and direction of transmission of the different murmurs, and 
the hypertrophy and dilatation of the right or left heart. Skoda's rule 
was that a murmur is usually most intense at its point of origin, except 
in cases of aortic insufficiency; and Oppolzer held that when listening 
to the mitral and pulmonary valves, murmurs transmitted to them disap- 
pear as examination is made more to the left, while murmurs due to 
lesions on these valves remain; on listening further to the right, the 



300 DISEASES OF THE ENDOCARDIUM 

true tricuspid and aortic murmurs remain and those which are transmitted 
disappear. Avoidance of too complicated diagnoses leads to the most 
practical results. 

(a) Aortic insufficiency and mitral insufficiency lead to dilatation and 
hypertrophy of both ventricles; the combination is frequent in children; 
the aortic findings as to pulse are frequently modified; the mitral insuffi- 
ciency may be relative (muscular) or organic (valvular), which is deter- 
mined only by continued observation. (6) Aortic stenosis and mitral 
insufficiency are next in frequency and are the most common combination 
in adults; less blood reaches the arteries than in simple aortic stenosis; 
the right heart suffers disproportionately, whence the severity of this 
complication. The systolic murmurs differ in location, transmission 
and quality. (c) Aortic insufficiency with mitral stenosis is a relatively 
frequent and favorable combination, because the left ventricle is usually 
less dilated; both may produce presystolic apical murmurs and there- 
fore the state of the right heart and the second pulmonic tone are all- 
important diagnostically. (d) In combined aortic and mitral stenosis 
the greater the aortic stenosis the more is the hypertrophy of the left 
ventricle; the more dominant the mitral stenosis the less is its hyper- 
trophy and the greater is the dilatation and hypertrophy of the right 
ventricle. 

General Symptoms of Valvular Disease and Decompensation. — The 
heart possesses not only a certain reserve power but in favorable instances 
its musculature hypertrophies. Every hypertrophy is more or less tem- 
porary in its compensation and ultimate cardiac failure is inevitable, 
either temporarily, " disturbed compensation," or permanently, "loss 
or rupture of compensation," the asystole of French writers. Failing 
cardiac competency is attended by (i) changes in the heart itself and 
altered movement of the blood; (ii) symptoms in organs remote from 
the heart, as the congested liver, etc. ; and (iii) reflex symptoms, as hyper- 
algesia over the heart or liver. All lesions tend to reduce arterial tension, 
increase venous pressure, retard the capillary flow and promote embolism. 
The blood stagnating in the veins may cause capillary resistance and 
therefore raise arterial pressure, even though the circulation is embar- 
rassed; in stasis, also, the cyanosis may raise arterial tension, from poor 
aeration of the blood. Mackenzie maintains that heart failure may 
develop without fall in arterial pressure, but here there is no loss of 
tonicity; when the heart becomes atonic (dilated), the blood-pressure 
falls to rise again when tonicity is restored. Dilatation of the compen- 
satory type appears first and incites hypertrophy ; as hypertrophy reaches 
its limit, the dilatation of the second type appears — the dilatation causing 
stasis. Circulatory disturbances may be spontaneous or induced by 
psychical excitement, physical exertion, intercurrent disease, recurrent 
endocarditis, malnutrition or excessive use of alcohol or tobacco. 

1. Constitutional Symptoms. — Anemia is frequent (aortic insufficiency); 
Andral spoke of a "heart cachexia;" polymorphonuclear leukocytosis 
is present in half the mitral cases; the body temperature may be sub- 
normal from slow circulation. Fever is due to recurrent endocarditis, 
embolism or intercurrent disease. In tricuspid stenosis the red cells 



ENDOCARDITIS 



367 



may be increased (polycythemia). The nails are sometimes clubbed. 
Skin hemorrhages are due to "blood dissolution" or less frequently to 
embolism. 

2. Cardiac Signs and Symptoms. — Apart from actual changes in the 
chambers, such as dilatation and hypertrophy, the heart itself is not 
well nourished in " breaking compensation/' for it receives less arterial 
blood and is engorged with venous blood. The importance of the integ- 
rity of the heart muscle and its functions is suggested in the introductory 
paragraph (page 319). Dilatation indicates failure of tonicity; irregu- 
larity is disturbance of rhythmicity; and disturbance in contractility 
has its obvious results. Cardiac insufficiency develops when the reserve 
force and functions of the heart are prematurely exhausted. The heart 
muscle is in some cases fatty, and in others is the seat of myocarditis 
about the arteries or cyanotic induration about the veins. These changes 
are less the cause thaa the effect of broken compensation. Here and 
there pressure-atrophy occurs, as in the papillary muscles (aortic regur- 
gitation). The rhythm is frequently disturbed, especially in mitral 
lesions (stenosis). The sphygmogram sometimes shows two ventricular 
contractions occurring very close together, pulsus bigeminus, of which 
every second weaker beat is due to an extra-systole (v. page 339) ; when 




Fig. 26. — Pulsus bigeminus. 



the pulse intermits to the finger, the tones of the abortive contraction 
may be heard over the heart with the stethoscope, the weaker wave 
failing to reach the periphery. The appearance of the pulsus alter nans 
signifies serious disorder of contractility (v. page 340). In general, 
the pulse beats are fewer than the heart beats. The gallop-rhythm is 
sometimes heard (Bouillaud, 1847), as described on page 321. In great 
irregularity, as in auricular fibrillation of mitral stenosis (page 339), 
tones and murmurs are indistinguishable (delirium cordis). The pulse 
is slow (the bradycardia of aortic stenosis) or faster than normal, tachy- 
cardia (mitral lesions); advanced decompensation may be marked by 
heart-block (page 342). 

Among the complications are pericarditis (aortic lesions) and recurrent 
endocarditis. Palpitation is frequent, yet it may be absent with the 
greatest heart alteration. A sense of tension over the heart is not infre- 
quent, and pain like angina pectoris occurs in aortic oftener than in 
mitral disease. 

3. Nervous Symptoms. — These are not frequent. Syncope (aortic 
stenosis especially) occurs with arterial anemia of the brain, cerebral 
arteriosclerosis, and sometimes with extra-systoles. Epileptiform seizures 
are also due to brain anemia and occur in Adams-Stokes's disease, nodal 
bradycardia and vagus stand-still of the heart. Venous congestion is 



368 DISEASES OF THE ENDOCARDIUM 

evidenced by epistaxis, vertigo, tinnitus or muscce volitant'es. Brain 
hemorrhage is infrequent (mostly in aortic insufficiency). Chorea and 
embolism of the Sylvian arteries are sometimes observed. The psychoses 
are delirium, mania, melancholia and suicidal tendencies, and are usually 
of unfavorable import; stasis, inanition, carbon dioxide narcosis and 
renal inadequacy are their cause. Retinitis hemorrhagica and simple 
retinal hemorrhages result from stasis and anemia. 

4. Respiratory Symptoms. — Lung stasis is sometimes confused with 
independent lung disease. Cyanosis occurs more often in mitral than in 
aortic disease and is most intense in lesions of the pulmonary orifice. 
Recurrent laryngeal paralysis, described by Ortner, is commonly explained 
by pressure of the dilated left auricle or pulmonary artery. Bronchitis 
and hemoptysis are most common in mitral affections. Bronchitis results 
less from congestion in the lesser circuit than from congestion in the 
cava superior, into which (and the azygos) the bronchial veins empty. 
Though usually bilateral, it may predominate on one side from local 
causes, as pleural adhesions. Hemoptysis results from lung stasis with 
vessel rupture, from embolism emanating from right-heart clots, throm- 
bosis in the pulmonary and less frequently in the peripheral veins, or 
from sclerosis of the pulmonary artery. Mitral stenosis may simulate 
phthisis, by hemoptysis and dulness over and below the clavicle, with 
rales, due to pressure on the left bronchus by the distended left auricle 
or pulmonary artery. The sputum may resemble that of pneumonia, 
though it is darker, more venous and less viscid. It contains the " heart- 
disease cells." They are large granular delicate cells with oval nuclei, 
which often contain hemosiderin or more rarely hematoidin; they are 
probably alveolar epithelial cells and also occur in other lesions than 
brown induration (as emphysema, asthma, pneumonia and phthisis). 
(See Plate XI.) Pulmonary edema (q. v.) is (a) due to weakening of 
the left ventricle while the right heart beats more strongly, (6) changes 
in the bloodvessels from stasis or (c) far less frequently is inflammatory. 
Crepitant rales are frequently heard. In mitral disease the lungs fre- 
quently become distended and rigid from engorgement of the capillaries, 
and closely resemble emphysema if not identical with it (von Basch's 
Lungenschwellung und Lungenstarrheit) . Brown induration or cyanotic 
induration of the lungs has for its anatomical basis, (a) capillary engorge- 
ment, often with fatty change in the intima, (b) increased interalveolar 
and perivascular connective tissue, (c) hemorrhage into the lung from 
vessel rupture, (d) consequent pigmentation of the lungs and sputum 
by the altered blood pigment, and (e) the "heart-disease cells." Dysp- 
nea, the "cry of distress of the myocardium" (Sansom), is caused by 
the increased intrapulmonary blood-pressure, the bulging of the turgid 
capillaries into the alveoli, pressure of the heart, ascites, hydrothorax, 
edema, bronchitis or infarcts. The intimate mechanism of dyspnea is 
obscure: the disturbed circulation, poor exchange of the inspired air 
and lung air ; decreased elasticity of the lung ; a reflex from the coronaries 
or aorta which causes spasm of the pulmonary vessels; or sclerosis 
of the right coronary artery. It may come on without exertion when 
there is constipation or poor digestion; or it may occur especially at 



PLATE XI 



xm 



V wyWT 



m 



& %^ ] 



&!> 




* 



OH 



Heart Disease Cells, showing Alveolar Epithelial Cells, Loaded 
Down with Granules of Hematin. (Simon.) 



ENDOCARDITIS 369 

night when the voluntary deep and diaphragmatic respiration of the 
waking hours is not in play, whence the respiratory centre becomes 
anemic. Dyspnea may be an air hunger or sense of suffocation; an 
inability to hold the breath; continued labored breathing; or appear as 
gasps, in sudden break of compensation. The dyspnea is not expiratory 
as in asthma but is mixed in type; the breathing is more rapid. The 
gallop-rhythm is rarely absent, and threatens relapse of the dyspnea; 
arteriosclerosis and nephritis are important elements in its production. 
Exertion not only increases the heart's work but the carbon dioxide and 
fatigue substances from the muscles irritate the respiratory centre, and 
the respiratory muscles ultimately become tired. Cheyne- Stokes's breath- 
ing (aortic stenosis) results from cerebral anemia, arteriosclerosis and 
uremia. Hydrothorax results from pressure on the azygos veins or pul- 
monary veins by the distended auricles. 

5. Gastro-intestinal Changes. — Gastralgia, anorexia, hemorrhagic infil- 
tration, vomiting or hematemesis, results from passive congestion and 
may be mistaken for independent gastric disease, such as cancer or 
ulcer. Delayed digestion and constipation are usual. The secretion 
of hydrochloric acid is normal except in marked weakness of the heart. 
Intestinal hemorrhage may result from capillary congestion, rarely 
from embolism of the mesenteric artery, and most infrequently from 
mesenteric venous thrombosis (q. v.). 

6. Changes in the Liver. — The liver suffers stasis through the congested 
cava and hepatic vein; this leads to cyanotic distention of the central 
veins of the liver lobules (appearing dark) and to cloudy and fatty degen- 
eration of their periphery (appearing lighter), the "nutmeg liver/' 
particularly in mitral disease. Pigmentation occurs and connective tissue 
develops in the liver and its capsule (perihepatitis, "iced liver"). Small 
granulations develop on its surface and in some instances a liver shrinkage 
results from " cyanotic induration" (cardiac cirrhosis). The liver is 
symmetrically large before edema appears; when disturbed compensa- 
tion is being restored, it is one of the last symptoms to disappear. Occa- 
sionally, from local changes, a tumor-like enlargement of the liver may 
simulate cancer. There is a feeling of tension and weight in the right 
hypochondrium and the organ is tender and variable in size; it may become 
smaller from rest and digitalis. Its edge is rounded and not hard except 
in the late stages. (See Differential Table of Hepatic Diseases.) 
The icterus viridis is a combination of cyanosis and mild icterus of the 
"urobilin" type; it is rarely sudden except in the infrequent embolism, 
which may cause a clinical picture resembling acute yellow atrophy. 
Decompensation is probably augmented by deficient hepatic and renal 
functions. Ascites is usually late and secondary to the liver congestion; 
its early appearance is indicative of independent liver disease or peritoneal 
affections. 

7. Changes in the Spleen. — The spleen is at times swollen from embolism 
or liver disease, but is often hard and small. 

8. Changes in the Kidneys. — The kidneys are enlarged from hyper- 
emia and the capsule strips readily. The stellulas Verheynii and glo- 
meruli are prominent. Epithelial degeneration follows malnutrition 

24 



370 DISEASES OF THE ENDOCARDIUM 

and cyanotic induration occurs in cases of long standing. Deformity 
from the stellate scars of healed embolism, and fresh infarcts are often 
encountered. 

Renal symptoms are greater, the higher the venous and the lower 
the arterial blood-pressure. The urine is decreased — its daily amount 
being a gauge of the heart's force; it is of higher specific gravity (1.020) to 
1.030), very acid, and highly colored from urates and increased uric acid; 
the urea is decreased and also the chlorides; albumin is frequent; and 
red disks are usually due to embolism or acute nephritis. 1 The kidney 
functional tests 'give fair results, compared with nephritis. Krehl found 
granular as well as hyaline casts, contrary to the usual experience. 
Chronic nephritis may coexist. (See Differential Table of Diffuse 
Renal Diseases.) Rest and digitalis increase the amount of urine and 
decrease or remove the albumin. In women profuse menstruation 
frequently results from stasis. 

9. Embolism. — In about one-third of the cases embolism occurs as in 
acute endocarditis but its effects are wholly mechanical. Though most 
common in the kidney (77 per cent.) and spleen (54.7 per cent.), it also 
occurs in the left Sylvian artery (22.7 per cent.), extremities, retina, 
liver, aorta (with paraplegia) and mesenteric vessels (in 1 per cent.). 
In the lungs it results from right-heart clots or thrombosis in the large 
peripheral or pulmonary veins. The visceral features of embolism will 
be discussed under Diseases of the Brain, Lung, Kidney, etc. 

10. Edema. — This results from venous stasis transmitted to the 
lymph vessels and interspaces, and from changes in the vessel walls 
from alteration of the blood (capillary dystrophy). It appears first in 
the connective tissue of the lower extremities (right leg): it disappears 
over night; and it extends upward to the vulva or scrotum, abdomen, 
chest and serous sacs (ascites, hydrothorax, hydropericardium and 
hydrocephalus). The loss of fluid to the system is unfavorable; the 
anasarca impedes the arterial circulation, threatens life from involve- 
ment of the glottis or lungs, increases the tendency to secondary infec- 
tions and may lead to hypertrophy of the connective tissue about the 
genitalia — cardiac elephantiasis. It is most common in mitral disease. 
The prognosis is less favorable if the liver becomes very large before 
edema appears. 

11. Changes in the Joints. — Swollen joints and tabes dorsalis (aortic 
insufficiency) are occasionally associated with valvular disease. 

Prognosis of Valvular Disease. — Patients may live for years with 
compensated valvular affections; a case of aortic leakage lived thirty- 
eight years and one of mitral leakage lived for sixty-six years. Though 
prognostic circumspection is necessary, pessimism leads to even more 
errors. The chronic course is influenced by the following conditions: 

1. State of the Heart Muscle. — The myocardium is the basis of hyper- 
trophy and compensation. Myocarditis and coronary disease are most 
unfavorable, for digitalis then has less effect on the heart muscle. In 

1 Bittorf and Kohler demonstrated cells resembling the heart-failure cells of the sputum. 
In 60 per cent, of patients with chronic passive congestion, "heart-failure cells" are found. 



ENDOCARDITIS 371 

cases where digitalis has immediate effect, the prognosis is favorable. 
Great dilatation or dilatation without hypertrophy is most unfavorable. 

2. Sex. — The prognosis is generally better in women, because they are 
less exposed to infections, physical strain and coronary disease. Preg- 
nancy as a rule is a rather unfavorable complication. Peter advises, 
"In girls (with valvular lesions), no marriage; in wives, no pregnancy; 
in mothers, no nursing." 

3. Age. — In the first decade of life the prognosis is poor, even though 
the heart and coronary vessels are young, because hypertrophy and 
dilatation are extreme, exercise is difficult to regulate, the valvular 
lesion tends to recur and the endocarditis develops into carditis (pan- 
carditis). After puberty the outlook is better. 

4. Valve Involved. — Opinions vary widely. In aortic insufficiency, 
the outlook depends on the type, being fair in the endocarditic and 
ominous in the atheromatous or luetic type. Subjects of mitral insuffi- 
ciency have the more favorable prospects. Broken compensation is 
more likely to be restored in mitral insufficiency than in mitral stenosis 
or in aortic lesions. Marked mitral stenosis is less favorable, although 
it is often found in women at an advanced age. Aortic stenosis is also 
found at an advanced age. Combined or multiple lesions, with some 
exceptions, are unfavorable. The writer observed a complete recovery 
from a double mitral lesion, after eight years. Pulmonic lesions predis- 
pose to early tuberculosis. 

5. Mode of Life. — The social scale, hygiene, necessity of hard work, 
psychical excitement, alcoholism, exposure and the individual constitution 
are most important factors. 

6. Unfavorable Symptoms. — Angina pectoris, embolism, persistent 
palpitation, dyspnea and irregular pulse are unfavorable symptoms. 
The "reserve heart power" of Martius is not present in all cases (failure 
of the coronary vessels to increase their caliber). 

7. Favorable Conditions. — These are good general health, proper living 
and absence of rheumatic tendencies, endocarditic (not atheromatous) 
origin, sound ventricles and arteries, and freedom from stasis in the 
lungs, liver and kidneys. 

8. Sudden Death. — In most cases, sudden death occurs in aortic affec- 
tions from coronary disease, especially in subjects over thirty with com- 
bined aortic and mitral disease, or when valvular disease is associated 
with emphysema, myocarditis, contracted kidney or aneurysm; it may 
also result from cerebral or pulmonary embolism, thrombosis cordis, 
heart rupture, sudden ventricular dilatation and glottis edema. 

9. Intercurrent or Associated Disease. — Tabes, syphilis and chorea have 
been mentioned. The acute fevers greatly tax the myocardium. Tuber- 
culosis (q. v.) is found in 8 per cent, of autopsies. 

Treatment of Valvular Disease. — (^4) In Compensated Lesions. — In 
compensated lesions medicinal treatment is unnecessary. With some 
exceptions, the patient is informed of the nature of his trouble that his 
cooperation may be enlisted. The mode of life is important, i. e., regular, 
orderly living, as free as possible from psychical or sexual excitement, 
worry or hurry, especially in aortic cases. Much depends on the social 



372 DISEASES OF THE ENDOCARDIUM 

status of the patient. The diet should be simple but not too schematic. 
Tobacco and alcohol should be interdicted as a rule; red wine, brandy or 
cognac are permissible in some adults and in the aged. Coffee may be 
given in the morning but should not be strong, for cardiac irregularity 
frequently results. A breakfast of milk may be taken before rising, 
and the noon meal should be the heartiest of the day. Nitrogenous 
food is best, with light carbohydrates, as toast; foods which ferment, 
such as cabbage, beans or brown bread, should be avoided and the 
amount of fluid ingested should be moderately restricted. Foods which 
load the stomach heavily are prone to elevate the diaphragm, and every 
meal somewhat taxes the heart. A light meal at night is the best precau- 
tion against gastric and cardiac oppression during the sleeping hours. 

Exercise. — Exercise in cases not too far advanced is advisable, 
for it reflexly stimulates the heart muscle. Palpitation, recurrent endo- 
carditis and intercurrent fever necessitate keeping the patient in bed. 
Moderate massage and deep breathing are beneficial. Tepid are more 
beneficial than cold or hot baths. 

Climate. — High altitudes are avoided, although moderate elevations 
are tonic. The seashore often disagrees with rheumatic or catarrhal 
subjects. A warm climate should be chosen for the winter. 

(B) Broken Compensation. — Broken compensation may be acute, 
gradual or terminal, as by coronary occlusion, and is evidenced at first 
by symptoms not necessarily cardiac, as fatigue, vague thoracic or 
abdominal pain or hyperesthesia, so-called neurasthenic symptoms, 
inertia, heaviness of the limbs, etc. The greatest therapeutic success 
follows the recognition of these extracardial evidences, not awaiting the 
severer signs of stasis, e. g., dyspnea, irregular pulse and dilatation. 
The indications are as follows: 

1. Absolute Rest in Bed. — Liebermeister's case of severe cardiac 
disease which recovered while in bed with a broken leg, is an example 
of compensation restored without digitalis. Rest is imperative in inter- 
current fevers, bronchitis, recurrent endocarditis and cardiac insuffi- 
ciency. Bed-sores can be prevented by water-cushions and cleanliness. 
Some patients are obliged to sit up because of dyspnea. The head may 
be propped up by back-rests, but they should have side supports so that 
falling to sleep will not waken the patient. 

2. Diet. — Karell's treatment is a low calorie diet — a glass of milk 
every four hours; its effects are often striking in dyspnea and it rests 
the tissues, reduces the fluids ingested, is poor in salt and lessens alimen- 
tary intoxication. 

3. Saline Purgation. — Epsom or Glauber salts 5ss-j in concentrated 
form should be given in the morning or compound jalap powder 3 ss-j 
at night. These remedies deplete the portal circulation and relieve the 
heart. Constipation increases the size of the left heart. 

4. Venesection. — When indicated by extreme venous engorgement 
evidenced by cyanosis, orthopnea, dilatation or tricuspid leakage, one 
pint may be drawn. The effects are often transient but are sometimes 
wonderful. Venesection raises low blood-pressure by relieving the 
heart, and lowers high blood-pressure due to excess of C0 2 in the blood. 



ENDOCARDITIS 373 

In two cases apparently moribund, no blood could be obtained from the 
arms and the external jugular veins were opened; the patients lived 
more than a year afterward. Venesection is not to be left until the 
patient is in extremis. 

5. The Oertel and Schott Methods. — (See page 323.) 

6. Digitalis. — Digitalis w T as first recommended by Wm. Withering 
(1775) and its physiological action demonstrated by Traube. Digitalis 
attaches itself to the heart muscle, and becoming fixed in the tissue, it 
is slowly given off and eliminated. Operating on the myocardium, 
vagus, vasomotors and other muscular tissue, it aids the heart to elicit 
and coordinate all its latent power, but the drug cannot augment the 
absolute power of the heart. 

Its general indications are: (a) Dilatation; digitalis restores tonicity, 
to the heart muscle upon which the drug exercises its main influence, 
i. e. y it overcomes dilatation, (b) Irregularity, or functional dissociation, 
is often corrected by digitalis; it stimulates the function "rhythmi- 
city" by action on the heart muscle, the ganglia and the peripheral 
filaments of the vagus. In about 80 per cent, of patients helped by digi- 
talis, there is continuous irregularity due to auricular fibrillation (Mac- 
kenzie); in this condition, the auricles contract rapidly and disorderly 
and convey impulses to the ventricles more rapidly than normal ; digitalis 
regulates by decreasing conduction through the bundle of His, thereby 
protecting the ventricles from undue stimulation from the auricles 
(page 339). Digitalis does not help extra-systoles, (c) Rapid, weak, 
heart action: digitalis slows the heart by action on the vagus. It tends 
to abolish abortive cardiac contractions and synergizes the systole of 
the chambers (increased contractility), as is shown by the strong systolic 
spasm of the heart in cases of digitalis poisoning. The slower and stronger 
systole empties the heart chambers more completely, forces the venous 
and arterial blood into the main arteries, and squeezes the venous blood 
out of the heart muscle itself, thereby improving the intrinsic circulation 
of the heart. The slower, more complete diastole allows better filling 
of the heart and drainage of the engorged veins. Digitalis raises the 
arterial tension by increasing the working power of the heart and by 
its centric and local action on the vasomotors; often arterial pressure 
is not raised and then digitalis probably equalizes the distribution of 
the blood and lessens tension due to edema and poor aeration of the 
blood. The most marked vasoconstriction is in the splanchnic area. 

It is seen then that digitalis increases tonicity, rhythmicity and con- 
tractility, while lessening excitability and conductivity. All in all, aside 
from details, digitalis is indicated for cardiac insufficiency of whatsoever 
type; which fact must be kept in view, when we consider its contra- 
indications. 

In the individual lesions: (a) in mitral stenosis the longer diastole 
drains the left auricle and lung vessels and the stronger systole forces 
the retarded blood through the stenotic orifice; particularly in this 
lesion auricular fibrillation arises; (6) in mitral insufficiency the best 
results are obtained; the leaking cusps are better coapted and the 
stronger systole fills the aorta and pulmonary artery; (c) in aortic 



374 Diseases of the endocardium 

stenosis, when dilatation occurs or the hypertrophy is inadequate, digitalis 
is valuable; (d) in aortic regurgitation it is theoretically contra-indicated, 
since it increases the diastole and hence the leakage; it is, however, 
as valuable in aortic decompensation as in mitral. 

Digitalis is contra-indicated (a) in balanced compensation; (6) when 
the vessels are fragile, as in aneurysm, and advanced atheroma on 
account of the risk of brain hemorrhage; (c) in fatty degeneration of 
the heart, except when resulting from stasis and malnutrition; (d) in 
vascular contraction. In this last instance, it is combined with nitro- 
glycerin, strophanthus or potassium iodide, to "unlock the arteries." 
The drug is not absolutely contra-indicated in the high tension of 
arteriosclerosis and nephritis, for paradoxical as this may seem it may 
relieve by lessening dyspnea and carbon dioxide narcosis and equalizing 
the circulation, (e) Of late, irregularity of the heart is considered a 
contra-indication, especially by Mackenzie, who stops digitalis as soon 
as irregularity develops. In partial heart-block digitalis may work harm; 
it may prove beneficial in some cases of complete heart-block. Mackenzie 
discontinue^ digitalis in severe cases of mitral stenosis, where the presys- 
tolic murmur disappears or when systolic waves appear in the jugulars, 
for then some heart-block has developed. Extra-systole is also a contra- 
indication. (/) Idiosyncrasy: individuals react differently to the drug, 
some exhibiting hypersensitiveness (v. i., toxic symptoms). (g) As 
Janeway pertinently remarks, digitalis is indicated only in ventricular 
weakness and not in paroxysmal tachycardia, nephritic edema, inflam- 
matory effusions or palpitation, (h) Digitalis may fail to operate unless 
rest, free purgation, venesection and mechanical removal of the anasarca 
have been first employed. (The Leipzig School uses digitalis on the first 
sign of decompensation.) Many of these contra-indications are relative 
only, since digitalis is indicated by cardiac insufficiency of any of the 
five types of Sahli (cardiac, pulmonary, high-pressure stasis, vasomotor 
or splanchnic insufficiency) ; it may be tested out, then, in decompensa- 
tion due to acute endocarditis (where experimental evidence favors 
its use), chronic myocarditis, arteriosclerosis, hypertension, coronary 
disease, tachycardia, etc. 

Toxic Manifestations. — Gastro-intestinal symptoms are generally 
from stasis; sometimes vomiting is due to rejection of the drug by a 
disordered stomach, or later, to toxic irritation of the stomach or the 
medulla, by the absorbed drug; there may be diarrhea, with green stools. 
Digitalis causes contraction of all unstriped muscular tissue (gastric, 
intestinal, vascular). It may cause delirium, headache, diplopia, blind- 
ness to green colors, blueness of the scleras, exophthalmos, precordial 
oppression, palpitation, extreme weakness, pallor, renal suppression, 
violent cardiac overaction, or convulsions. 

Cumulative action may attend the use of any efficient preparation, 
since the heart never becomes anesthetic to digitalis; digitalis prepara- 
tions, without cumulative action, are inert. It is averted (a) by inter- 
mittent administration, although some patients tolerate digitalis con- 
tinuously for months or years, as Thomeyer's patient who in eight and 
a half years, took over 15 ounces of pure digitalis; (/;) by great care 



ENDOCARDITIS 375 

in ambulatory cases; (c) by care in cardiac dropsy, on relief of which 
toxic quantities may be resorbed from the tissues; (d) by care in inter- 
current febrile affections, for toxic effects often follow the fall of tempera- 
ture; toxemia considerably neutralizes the slowing action of the vagus; 
(e) by withdrawal on the appearance of vomiting, syncope, reduced 
urine or irregular or very slow pulse, a sign of danger; here atropine 
may be advantageously combined with the digitalis. 

Preparations and Administration. — Among the standardized official 
preparations, the powdered leaves stand first; the powder deteriorates 
little, even after eight years and is given in doses of gr. j-iss. The 
tincture (Tfl,x) deteriorates but much less than the infusion (5 j-ij). For 
hypodermic use, the fluidextract (Tfl,ij), well diluted, is least irritating. 
Beginning with small doses of digitalis to avoid sudden overtaxing of 
the heart, the dosage is increased; Withering, who discovered digitalis, 
pushed the drug until it acted on the pulse, kidneys, stomach or bowels, 
etc., its effects appearing in two or three days. 

1$ — Infusi digitalis 5ii.i 

Spts. aetheris nitrosi 3.i 

Potas. bicarbonatis 3ss 

Aquae 5ij 

M. et S. — One tablespoonful after meals. 

The infusion is excellent for rectal use when the stomach is irritable. 
Regarding the active principles there is the greatest confusion. The 
tincture is thought to be the best cardiant because it contains digitalin 
and digitoxin. The writer has found digitalin almost inert. Digitoxin 
in the author's hands has often strengthened the weak and irregular 
heart when digitalis has failed (gr. 4^ t. i. d.); it easily disorders the 
stomach, and often cannot be given for more than six or eight doses. 
Frankel finds the therapeutic and toxic doses very similar and fears its 
use. Digitoxin is often advantageously combined with champagne. 
Cloetta's digalen is a soluble non-irritant digitoxin, and may be given 
intravenously, 1 c.c. equalling 0.3 mg., or -j\-$ grain. The preparation 
acts promptly, though it is somewhat irritating when given hypoder- 
mically. Cumulative effects are least likely when the kidneys are 
intact. Digipuratum is an active purified product, from which is elimi- 
nated the digitonin — the element irritating the stomach and intestines; 
it is given in powder or tablet form (0.1 gm., grains iss) every twelve 
hours, or as a fluid in sterilized tubes for emergency intravenous use. 
Rapid absorption, lack of alimentary irritation, and free diuresis are 
claimed for it. Like digalen and digitalone it is expensive. 

Combinations are suggested in the following prescriptions (v. i.)\ 
7. Other Cardiants. — (a) Strophantus, ITlv-x of the tincture every 
eight hours, may be given. Advantages: it is more rapid in action 
than digitalis, perpetuates the effects of digitalis and is indicated in the 
irregular heart of mitral disease; in children under twelve years; in 
cases where we are waiting for the digitalis to act; and in dilatation 
where the blood-pressure is high. Disadvantages: it is less certain and 
less energetic; it is inferior in edema and does not give tone to the vessels. 



376 DISEASES OF THE ENDOCARDIUM 

The tincture deteriorates rapidly in dilution or aqueous compounds. 
Of late strophanihin, gr. -fa once daily, has been recommended for intra- 
venous administration. It is said to be rapid in action and efficient. 
Its therapeutic dose and toxic dose are not far apart and it is inferior 
to digitalis. It must be used with caution in nephritis, high arterial 
pressure and bradycardia. Its toxic symptoms are those of digitalis 
poisoning, including irregularity, partial heart-block, vomiting, etc. It 
is eliminated by the bowel. It may not be used if digitalis has been 
recently employed, (b) Strychnine stimulates the vagus, vasomotors 
and the nervous, gastric and blood-making tissues (v. page 76). Given 
carelessly, it may irritate the heart, decrease the urine by spasm of the 
renal vessels, or even induce rupture of the vessels, (c) Sparteines sul- 
phas is given in capsule because of its bitterness (gr. \-\ every eight 
hours); larger doses may be given, gr. j-iss; it seems also to quiet the 
nervous system but is inferior to digitalis. It does not contract the 
vessels. 

8. Symptomatic Treatment. — (a) Dropsy. — Saline or hydragogue 
catharsis often relieves moderate edema. Digitalis is often combined with 
calomel, or blue mass and squills (Guy's pill, also known as Addison's 
or Niemeyer's). 

1$ — Digitalis gr. x 

Massse hydrargyri . gr. vj 

Scillse gr. x 

M. et ft. capsulse x. 

S. — One after meals for one or two days. 

Mercurials must be used with the greatest care. The author saw, in 
consultation, a case complicated by nephritis in which the tongue sloughed 
off after 5 grains of calomel had been given. Desperate stomatitis 
may result in alcoholic, myocarditic or nephritic subjects. Calomel 
acts by its conversion into bichloride, which often incites a bichloride 
nephritis. In isolated luetic aortic leakage, mercurials may prove 
specific. Excess of digitalis is held to suppress the urine by inducing 
renal spasm. It is better to use potassium salts, as potassium acetate 
gr. xxx, t. i. d., which are less abundant in the tissues than the sodium 
salts. Diuresis following digitalis is associated with increase of sodium 
chloride elimination; restriction of salt has few benefits. Caffeine 
with digitalis is beneficial in dropsy when the pulse is slow, the mind 
dull and the digestion sluggish; anginoid pains are often relieved by it; 
it may cause nervousness or insomnia (therefore given early in the day), 
irregular pulse (therefore combined with rum or brandy), or biliousness; 
gr. v should be given, but not for more than three days— 

1$ — Caffeinse citratse . 3ss 

Sodii benzoatis 3ss 

Aquae 5iij 

M. et S. — One hypodemrieful ( 5ss) as indicated. 

Caffeine stimulates the bulbar vasomotor centre, and also the per- 
ipheral vasomotor system, whereby some elevation of arterial pressure 
is accomplished; it also acts as a direct renal stimulant; and in shock 



ENDOCARDITIS 377 

and collapse surpasses strychnine and camphor (Rhomberg). Diuretin, 
■ sodiosalicylate of theobromine (5j-iss daily) may act marvellously or 
not at all, operating on the renal cells directly, and possibly also on 
the heart and vessels. Theocin sodium acetate is easily soluble in water, 
and in doses of gr. iij may act when others of this type fail. Canadian 
hemp (fluidextr. apocyni Tfl,xv) is hard to obtain pure but sometimes 
justifies Benjamin Rush's term, " a vegetable trochar." Sweats and 
the use of pilocarpine are both dangerous and injurious. Mechanical 
drainage is recommended, by scarification, by multiple knife or pin-pricks, 
or by Southey's capillary tubes; but the best method is by a single, 
long, deep incision down to the bone, by which a quart to a gallon of fluid 
seeps away in a day (and up to 40 gm. of albumin). Ascites, from 
heart disease alone, rarely necessitates puncture; it is indicated chiefly 
in coincident liver cirrhosis or chronic peritonitis. ' Hydrothorax is far 
more important, and thoracocentesis should not be delayed when dyspnea 
is urgent. 

(b) Anemia. — Digitalis with iron and arsenic, or the latter two drugs 
alone, often produce remarkable improvement. 

1$ — Digitalis gr. xx 

Ferri reducti 3ss 

Arseni trioxidi gr. ss 

M. et ft. pilulae, xx. 

S. — One pill after meals; take for a week only. 

(c) Insomnia. — It is often difficult to relieve insomnia or unrestful 
sleep, broken by nightmare or sudden "heart starts." Spts. chloroformi, 
spts. camphorse and spts. etheris compos, aa 3 ss are often helpful. Sul- 
phonal, gr. xx in hot milk at bed-time, may be tried but is somewhat 
dangerous in stasis, when used more than three nights in succession. 
Chloral hydrate is excellent in high tension. In morphine we place our 
chief reliance. 

{d) Dyspnea. — The ice-bag, chloral, and spiritus glycerylis nitratis Tflj 
are of value for high tension. Morphine may be given in the early stages 
without hesitation and especially at night, for restlessness and dyspnea; 
it is excellent while waiting for digitalis to act. It is almost specific 
and lessens the irritability of the respiratory centre. Heroine hydro- 
chloride (gr. tV - i) operates similarly, but in some instances apparently 
it can be used longer than morphine. Opiates require care in weak heart 
or Cheyne-Stokes's breathing. Dyspnea is often renal or due to right- 
sided hydrothorax, chronic bronchitis or excessive dilatation, when the 
appropriate treatment is catharsis, paracentesis, potassium iodide or 
digitalis, respectively. 

(e) Respiratory Symptoms. — Cough, cyanosis, pulmonary edema and 
hemoptysis are usually cardiac symptoms (pulmonary engorgement or 
brown induration) and are relieved by the cardiants. 

1$ — Ammonii carbonatis 3J 

Tr. hyoscyami 3iv 

Potassii iodidi 3J 

Tr. digitalis ' 3j 

Infusi calumbffi q. s. ad. 5vj 

M. et S. — One teaspoonful every four hours. 



3?S DISEASES OF THE ENDOCARDIUM 

Expectorants usually nauseate. Hemoptysis is often beneficial, being a 
species of lung venesection and is seldom urgent or fatal. Pulmonary 
edema necessitates phlebotomy, a 30-grain dose of lead acetate, gr. 
T ^o of nitroglycerin and gr. J of morphine. 

(/) Palpitation and Pain. — For palpitation and throbbing, the ice- 
bag is the best calmative; a precordial blister or a few minims of tr. 
belladonnas and tr. aconiti are often helpful, with morphine, if necessary. 

1$ — Fluidextracti belladonnse gtt. xv 

Tr. digitalis 5j 

Aq. laurocerasi q. s. ad. §j 

M. et S. — One teaspoonful two or three times daily. 

A light evening meal and laxatives are helpful. Iodide of potash and 
nitroglycerin relieve the pain, weakness, pallor or headache of aortic 
lesions. 

(g) Gastric Symptoms. — These are ominous when the liver is enlarged 
and there is not much edema. They are due to portal stasis more often 
than to digitalis, which should then be given by rectum. Phenol, gr. J 
every half-hour for five doses, and rectal nourishment are indicated. 

CONGENITAL HEART DISEASE. 

These infrequent cases are complicated and occur largely in the right 
heart, upon which more work devolves in fetal life. The causes are 
(a) developmental errors, by far the most frequent cause; (b) fetal endo- 
carditis, nearly always sclerotic; (c) fetal myocarditis or (d) adult endo- 
carditis developing upon developmental anomalies. They occur largely in 
males. 

1. Pulmonary Stenosis. — This, by far the most frequent congenital 
lesion, occurs in various forms: (a) Stenosis or actual atresia of the 
orifice itself; the second pulmonic tone is weak or absent; (6) Constric- 
tion of the conus arteriosus which obstructs the flow of blood, and may 
make, as it were, a second ventricle; the second pulmonic sound is 
clearly heard, (c) The pulmonary artery beyond the valves is narrowed 
or atresic — a grave type. The second pulmonic sound is usually heard. 

The physical signs are hypertrophy and dilatation of the right ven- 
tricle, a thrill over the pulmonic area, and a systolic murmur prop- 
agated into the neck when there is a defect in the interventricular septum 
(when a defect is lacking, the right ventricle is atrophic and the subject 
rarely lives over a year). Other congenital abnormalities are common: 
If the stenosis arises before the end of the second fetal month, the inter- 
ventricular septum fails to close in 75 per cent, of cases and is pushed to 
the left, so that the aorta may partly or entirely originate in the right 
ventricle. If the closure develops after the second month, the foramen 
ovale remains patent (6 per cent.). Upon these openings acute endocar- 
ditis is prone to develop. The ductus Botalli usually remains patent, and 
conducts blood from the aorta to the pulmonary artery and lungs. Should 
the ductus Botalli and the pulmonary orifice be closed, collateral circu- 
lation is possible through the esophageal, pericardial and bronchial 
arteries. The right ventricle usually hypertrophies and the left atrophies. 



CONGENITAL HEART DISEASE 379 

2. Defects of the Interauricular Septum. — The foramen ovale is open 
to some extent in 44 per cent, of all autopsies and in 33 per cent, of con- 
genital heart lesions; it usually closes in the first week of life, but fails 
to adhere when low pressure in the left auricle exists. Entire absence of 
the septum, the most extreme defect, is called the "reptilian heart" or 
cor biloculare when the interventricular septum is also absent or the 
cor triloculare when the ventricular septum is present. Its patency is 
almost a necessity when the valvular orifices are narrowed or closed or 
when the great vessels are transposed. Several cases have been found 
in subjects over seventy years of age. Symptoms are absent or are 
those of the more important associated trouble. Rare occurrences are 
presystolic murmur at the level of the third or fourth ribs; "crossed 
or paradoxical embolism," e. g., in the brain from a clot in the leg, passing 
directly from the right to the left auricle; and positive venous pulse in 
mitral regurgitation. 

3. Defects of the Interventricular Septum (Maladie de Roger, 1879). 
They are observed in 37 per cent, of congenital lesions and may be 
single, associated with pulmonary stenosis, or result from myocarditis. 
The deficit occurs oftenest in the upper "undefended" part of the septum. 
When wholly absent, the heart has but three chambers (cor triloculare 
biatriatum) . Symptoms are absent, complicated or ambiguous. At 
times the signs are those of mitral leakage without pulmonary stasis. 
A loud, prolonged systolic murmur and thrill are found over the upper 
third of the precordium. 

4. Patency of the Ductus Botalli. — The duct usually closes within the 
first month, because the pulmonary blood-pressure is lowered after 
birth. Patency occurs in 26 per cent, of congenital heart lesions and is 
favored by other congenital lesions or by atelectasis or pneumonia in the 
newborn. It leads to increased blood tension in the lung. The diag- 
nosis has been made in 50 cases. The second pulmonic sound is accent- 
uated, and the artery is frequently dilated, whence the dulness in the 
second left interspace, with thrill, pulsation and long vibratory systolic 
murmur which may reach the cervical vessels or the fourth dorsal vertebra 
behind. Sometimes the vessel compresses the recurrent laryngeal 
nerve. The arrays show the large artery and the wide right heart ("round 
mitral heart"). It is distinguished from pulmonary stenosis by the 
greater cyanosis of the latter lesion, the less frequent propagation to the 
neck and the absence of the second pulmonic sound. 

5. Persistent Isthmus Aortse. — The fetal narrowing, described by Paris 
(1789), is located in 46 per cent, below the duct, 37 per cent, at the duct, 
and 17 per cent, over it, and is characterized (a) by hypertrophy of the 
left ventricle (50 per cent.) to overcome the stenosis, and sometimes by 
a systolic murmur in the interscapular region; (Jo) by largeness and ful- 
ness of the aorta above the isthmus and of the arteries of the head, neck 
and arms (25 per cent.) ; (c) by a small, retarded, abdominal and femoral 
pulse (below the isthmus); (d) by a pronounced collateral circulation 
between the branches of the aortic arch and those of the thoracic and 
abdominal aorta (internal mammary, inferior thyroid and transversalis 
colli arteries). Maud Abbott finds 198 cases on record. 



380 DISEASES OF THE ENDOCARDIUM 

The pathologist makes the diagnosis, as he cuts through the large 
vessels in the chest and abdomen, and the clinician suspects the lesion 
when he feels these thrilling large vessels or hears the murmur. Broken 
compensation may intervene, though latency is common. Aneurysm, 
and mediastinal tumor are frequently confused with it. The aorta 
ruptures in 12 per cent, of cases. The lesion is twice as common in the 
newborn as in adults. 

6. Aortic Atresia or Stenosis. — Moon (1912) collected 129 cases of 
congenital atresia. If the lesion is developmental, the interventricular 
and -auricular septa are open; if endocarditic or myocarditic, they are 
closed, provided the lesion develops after the third month of fetal life. 
The left ventricle hypertrophies in stenosis or atrophies in atresia, while 
the right ventricle hypertrophies in order to force the blood from the 
pulmonary artery through the ductus Botalli into the aorta. 

7. Tricuspid Stenosis or Atresia. — In developmental or inflammatory 
atresia, both septa are open and the right heart is atrophic. Tricuspid 
insufficiency is most rare. 

8. Transposition of the Arteries and Veins. — In this lesion the fora- 
men ovale remains open; the aorta originates in the right heart. 

9. Valvular Anomalies. — The semilunar valves, especially the pul- 
monary, may be increased in number from three to five; or they may 
be decreased to two, which occurs especially in the aortic valves/ Acces- 
sory or abnormal valves are particularly prone to endocarditis. Mitral 
anomalies are rare. 

10. Anomalies in Location and Development. — These are absence of 
the heart (acardia), double heart, or ectopia cordis, where the heart lies 
in the abdomen, or chest (with fissured sternum). 

Dextrocardia (dexiocardia), described by Servius (1643), occurs with 
situs viscerum inversus; the mitral valve has three cusps, the tricuspid 
has but two; the pulmonary veins empty into the right auricle; the 
pulmonary artery arises from the left, and the aorta from the right, 
ventricle ; the aorta runs to the right of the spine and esophagus and 
to the left of the cava; the innominate artery and vena azygos are on 
the left and hemiazygos is on the right; the right lung has two lobes, 
the left three; the bronchial fremitus is greater on the left side, the left 
bronchus being larger; the spleen, liver, stomach and colon are trans- 
posed; the right kidney and testicle are higher than the left. The 
heart is rarely transposed alone. Pollock and Jewell (1909) collected 
323 cases. 

Symptoms of Congenital Heart Disease. — Intense cyanosis develops 
chiefly in transposition of the great vessels, pulmonary stenosis with 
interventricular defects and in pulmonary and tricuspid atresia. Morbvs 
cwruleus is general or limited to the nose, fingers, etc.; the purple skin 
is due to mixing of the arterial and venous currents, to sluggish circula- 
tion or to impaired function of the red cells. Sometimes the cyanosis is 
paroxysmal. A most striking increase of the red cells up to 10 or 12 
millions (polycythemia rubra) is seen in some cases, probably as a com- 
pensatory effort. The hemoglobin may register 230. Dyspnea, cough, 
convulsions and marked clubbing of the fingers and toes are frequent. 



PERICARDITIS 381 

The temperature is often subnormal. Mental and physical development 
is incomplete and exophthalmos, swelling of the face, lips and nose and 
of the optic disk are frequent. Edema and stasis are not frequent. 
Coincident maldevelopment occurs in 10 per cent, of cases in the stomach, 
colon, kidney, etc.; imperforate anus, hypospadias, cryptorchismus, 
polydactylia, hare-lip, spina bifida and anencephalus also occur. The 
murmurs are usually systolic and rough, although very complicated 
lesions may exist with normal heart tones; in a few instances the fetal 
murmur was heard before birth. The dulness concerns the right ventricle 
chiefly. 

Prognosis. — The lesion is incurable and compensation is incomplete. 
The patient in 25 to 40 per cent, of cases succumbs to cardiac failure 
or to pulmonary tuberculosis in the second decade (81 .per cent.), hence 
Rokitansky's rule, that cyanosis protects the lungs from tuberculosis, is 
not absolute. 

Treatment. — The treatment is symptomatic. The body should be 
kept warm; baths should be employed to guard against colds; mental 
and bodily - strain should be avoided ; and in general the therapy of 
adult valvular disease should be followed,, except that the heart stimu- 
lants must be used with considerable caution. 



DISEASES OF THE PERICARDIUM. 

PERICARDITIS. 

Definition.— An inflammation of the pericardium. Known anatomic- 
ally to Morgagni, it was first described clinically by Senac (1749). 

Etiology. — The so-called primary cases are tuberculous, rheumatic or 
septic. Cold, exposure and -trauma only reduce the physiological resist- 
ance to bacterial invasion. Pericarditis is mycotic, the organisms of 
suppuration, pneumonia and tuberculosis being most frequently found; 
perhaps toxins alone may excite inflammation. 

Pericarditis is secondary (a) to infectious diseases, of which rheumatism 
(40 per cent.) is foremost, particularly when many joints are involved 
in rapid succession, usually developing within half a week to two weeks. 
It may be the only manifestation of rheumatism. It occurs with recur- 
rent rheumatism", endocarditis and sometimes chorea. It is commonly 
serofibrinous. 

It is common in pneumonia, septicopyemia, puerperal fever, ulcera- 
tive endocarditis, osteomyelitis, scarlatina — more rarely in other exan- 
themata — and in pulmonary or multiple serous tuberculosis. In children 
scarlatina and rheumatism are most important. 

(b) It is secondary, by contiguity, to disease of adjacent organs; to 
pleurisy, pneumonia and aneurysm; to disease of the ribs, myocardium 
and endocardium, sternum, bronchial glands, spine, esophagus, stomach, 
spleen, liver, peritoneum; and to cervical cellulitis. 



382 DISEASES OF THE PERICARDIUM 

(c) It is secondary to certain diseases of the pericardium, as tuber- 
culosis, carcinoma and other processes. In 30 per cent, of Matter's 
" cryptogenetic" cases, tuberculosis was found at autopsy. Scaglios 
(1904) could find but 8 cases of primary pericardial tuberculosis. 

.(d) It is secondary to cachexia? or dyscrasiw, e. g., nephritis (especially 
contracted kidney), gout, diabetes, carcinoma, alcoholism, blood diseases, 
etc.; and often as a terminal infection; this chiefly adult type easily 
escapes clinical recognition. Pericarditis is most frequent between the 
fifteenth and thirtieth years. 

Fibrinous (Plastic) Pericarditis. — A strict division into dry (plastic) 
and exudative (effusive) pericarditis is impossible, because these forms 
are usually combined. Dry (plastic, fibrinous) pericarditis is circum- 
scribed over the base and large vessels, or is diffuse, and consists patho- 
logically of vascular injection, punctate ecchymoses, loss of the smooth, 
glistening appearance of the serous membrane, and exudation of plastic 
lymph in small particles or irregular lamellae, which may appear smeared 
as with butter, spongy, shaggy or hairy (cor villosum) . Some fluid is found 
in the meshes of fibrin. Stripping off of the fibrin may reveal tubercles. 
The subjacent myocardium often suffers infiltration and degeneration. 

Symptoms. — Symptoms are lacking in most cases; pain is inconstant 
and when present is by no means characteristic. 

Physical Findings. — Inspection and percussion are negative. The 
writer has seen a strong apex beat where the autopsy revealed a fibrin 
deposit an inch in thickness. Palpation and auscultation may disclose 
a friction fremitus, fully described under : 

Pericarditis with Effusion. — This form has been called the second 
stage, the fibrinous form being the first stage. The fluid may be serous 
with much or little cellular or fibrinous admixture (serofibrinous); the 
hemorrhagic type is observed in the aged, in scurvy, cancer, tuberculosis, 
purpura, hemorrhagic exanthemata or Bright 's disease, the exudation 
being tinged with fresh or altered blood; the purulent type is usually 
fibrinopurulent rather than purely purulent, and is often associated 
with pyemia or contiguous suppuration; the effusion may be 'putrid, 
when caused by pyemia, carcinoma of the esophagus or stomach, "or 
lung cavities. Sixty-seven per cent, of pericarditides are serofibrinous, 
19 per cent, hemorrhagic and 14 per cent, purulent. The pathological 
sequences of pericarditis are fatty and cloudy degeneration, inflammatory 
infiltration, or actual exulceration of the heart muscle; rupture of a puru- 
lent exudation externally into the tissues of the chest, or possibly into 
neighboring organs or cavities; inflammatory extension outside of the 
pericardium (pericarditis externa), to the mediastinum or pleura; for- 
mation of polypi, which may, in rare cases, become foreign bodies; com- 
plete resorption of the exudate and restitutio ad integrum, which is a 
rather uncommon issue; organization of connective tissue, either as local 
adhesions, mostly near the fixed base of the heart, because the heart's 
movements may detach apical adhesions, or as general obliteration of the 
sac (concretio pericardii) ; and, finally, desiccation of the exudate, leaving 
a cheesy mass which may calcify. Endocarditis is less a sequence than an 
associate or cause of pericarditis. 



PERICARDITIS 



383 



Symptoms. — No symptom is diagnostic. Total latency of symptoms 
obtains in 55 per cent, of cases. Daily examination of the heart in those 
diseases likely to cause pericarditis may save many diagnostic errors. 
Irregular fever may exist from the disease or the causal affection. It 
is often absent, especially in terminal pericarditis, and the temperature 
may be subnormal, even in purulent effusions. High fever is infrequent. 

Dyspnea or thoracic oppression occurs in 90 per cent., due largely 
to heart compression by the exudate or extension of inflammation to 
the myocardium, and less frequently due to vagus irritation, phrenic 
neuritis, venous, pulmonary and arterial compression. It is remarkable 
that patients sometimes walk into the hospital with enormous peri- 
cardial effusions. The respirations are increased. 

Pain. — Painlessness in pericarditis is the rule and is often absent in 
secondary pericarditis and is more common in small effusions; severe 
pain oftener indicates pleurisy than pericarditis. Like Andral, the 
writer has observed anginal pain radiating to the shoulder, arm and 
neck. Epigastric pain may precede pain elsewhere (Gueneau de Mussy) 
and the writer observed initial pain over the appendix. Barlow's patient 
put on a belt to relieve his pain. Precordial tenderness is at times present, 
and palpitation is common. 

Delirium, restlessness, mania, convulsions, psychoses or even coma 
may be due to pericarditis or to complicating uremia or endocarditis. 
The symptoms may suggest gastritis, while pericarditis is found on 
examination. Vomiting, singultus, dysphagia, recurrent laryngeal 
paralysis and tracheal cough are pressure symptoms. 

Physical Findings. — On these rests the diagnosis: 

1. Inspection. — Precordial prominence, voussure, first noted by 
Corvisart and Louis, may develop when the chest is plastic, as in women 
and children, and when the intercostal muscles are inflamed or paretic. 
The left chest often moves less, since that lung is usually compressed. 
The apex beat is somewhat lower when exudation depresses the dia- 
phragm; it is more to the left and the dulness transcends the apex to the 
left (see Percussion). The greater the effusion, the weaker the apex 
becomes, and disappearance of the previously distinct apex beat is all- 
important. There may be only an indefinite, diffuse cardiac impulse. 
On bending forward, the apex beat or cardiac impulse usually reappears. 
The interspaces may bulge. Collateral edema of the chest wall and 
undulation due to the heart itself are most rare. Graves and Stokes 
described tumor-like extrusion of the compressed lung above the clavicle. 
The upper edge of the first rib can be felt at its sternal attachment, being 
separated from the clavicle (Ewart's "first rib sign"). An epigastric 
tumor-like bulging of the luxated liver was noted by Auenbriigger and 
Corvisart. The veins of the thoracic wall are large. The decubitus 
is usually half-erect, dorsal or left-sided, to spare the sound lung; the 
attitude is fixed and there is abdominal inactivity during respiration. 
During convalescence the apex may retract during the systole, from 
adhesions. 

2. Palpation. — The friction-rub is often felt. Palpation localizes the 
apex. Disappearance of an apex beat previously observed, and the presence 



384 DISEASES OF THE PERICARDIUM 

of a strong radial pulse, are very important; mere absence of the apex is 
observed in many conditions. Tenderness beside the ensiform, or between 
the attachments of the sternomastoid, is due to inflammation of the 
phrenic nerve. Fluctuation is never felt. 

3. Percussion. — Dulness was first described by Auenbriigger. In 
good-sized effusions, nearly all the dulness is absolute. Three to five 
ounces of fluid are usually necessary to produce distinct physical signs. 
There are two complementary recesses in the pericardium : one over the 
basal vessels, where the fluid may accumulate, in which case it is early 
revealed by a triangular dulness, whose apex is directed downward 
(Skoda, Oppolzer), which may compress the large vessels; and the other 
in the fifth right intercostal space (Rotch, Ebstein), where the fluid 
exudate replaces the relative liver dulness; Epstein's angle, the right- 
angled junction of the right border of the heart and the liver, becomes 
more obtuse. Extensive exudates produce a triangular, pyriform or 
trapezoidal dulness, broad nearest the diaphragm and with the blunt 
apex near the manubrium (see Plate X, Fig. F.). Though the outline 
is roughly triangular, the right border is more vertical than the oblique 
left border, which is beyond the apex beat, if the latter remains visible 
(Skoda). The dulness may even reach the interclavicular notch, the 
right nipple, the left axilla, or Traube's semilunar space, and compress 
the lungs and depress the diaphragm. The apex beat shifts abnormally 
when the patient lies on his side, because the distended pericardial sac 
permits greater cardiac movement. Skoda taught that the heart falls 
back in the fluid, but the heart lies above the fluid and close to the chest 
wall. The dulness varies with fluctuations in the effusion and with re- 
sorption. The pericardial dulness is least typical when the effusion is 
covered by emphysematous lungs, or when an adherent lung cannot be 
pushed back by the effusion. In the erect posture, the dulness may be 
one-third to one-half as broad again as when in the dorsal position; 
it also is not so high; these signs may also occur in enlarged heart and 
valvular disease. Change of the dulness, especially when the patient 
lies on the right side is uncommon physiologically, whereas the shifting 
in the left decubitus is of minor value. 

Dulness may persist from cardiac dilatation, massive adhesions or 
pulmonary retraction. The effusion may be enormous (10 quarts, 
Kyber; or 8 pounds, Corvisart), and may lead to a diagnosis of pleurisy, 
or pleurisy plus pericarditis. As the normal pericardial sac holds only 
G50 to 800 c.c, the pericardium must be greatly relaxed by the inflam- 
mation, to allow such large effusions. 

4. Auscultation. — Auscultation reveals the chief and most reliable 
diagnostic sign, the pericardial friction due to attrition of the inflamed 
pericardial surfaces, first fully described by Collin, Laennec's assistant, 
in 1824. (a) It is usually a " to-and-fro ff rubbing not exactly synchronous 
with the systole or diastole, which character is most clear when the 
heart is slow. It is less often single, and then is late in the systole; it 
may be triple, i. e., presystolic, systolic and diastolic. It depends less 
on the intensity of the inflammation, than upon the accidental quality 
and location of the effused lymph. It is often absent in very soft fibrin- 



PERICARDITIS 



385 



ous deposits, hemorrhagic or purulent inflammation. In contradistinc- 
tion to pleurisy, where the effusion of fluid abolishes the primary friction, 
it usually persists, even with great exudation (Stokes), especially at the 
base, since here the heart may touch the parietal pericardium, (b) In 
quality, it may be harsh, soft, like a gentle interrupted scratching of the 
ear with the finger, creaking, crunching, musical or even metallic (reso- 
nance from the stomach or intestines), (c) In location, it is most often 
heard over the base or the tricuspid region, where it is especially signifi- 
cant. It may also be heard over the apex, or possibly most clearly at 
the angle of the left scapula, (d) It is very superficial and close to the 
ear, not deep as in endocardial murmurs. Superficiality of the friction 
sound is absent when partial adhesions exist anteriorly, and the peri- 
carditis is most intense behind the heart, (e) Its propagation is not 
wide (il nait et meurt sur place, Jaccoud), though it has been heard at a 
distance of nine feet. The murmur usually ceases abruptly when the 
stethoscope has been removed a short distance. It does not follow the 
same lines of propagation as in valvular heart disease. Propagation along 
the sternum is common. In children or sometimes in adults, the author 
has heard it over the whole chest. Coincident hydrothorax (Graves) and 
cardiac hypertrophy — almost exclusively in chronic nephritis — by bringing 
the heart closer to the chest wall, diffuse the friction more widely (Stokes) . 
(/) Inspiration usually increases the murmur, due to the closer apposition 
of the pericardial leaves, caused by the wedge of expanding lung (Traube). 
(g) Moderate pressure usually increases the friction, especially in plastic 
chests. Change of posture, e. g., leaning forward, often makes the* 
murmur clearer (Corrigan, Stokes), (h) The murmur is variable, now pres- 
ent, now absent, now systolic, or again systolic and diastolic, varying in 
acoustic properties, or changing with change of posture; it is often 
short-lived, lasting sometimes but two to six hours. Disappearance of 
the rub is explained by regression, adhesions or weak heart. As a rule, 
the heart tones gradually become more or less weakened and distant. The 
x-rays outline the pericardial effusion; Maragliano comments upon the 
absence of pulsation in the gastric bubble. 

Secondary Physical Signs. — Cardiac incompetence is due to the mechani- 
cal hindrance, by the fluid, of the diastole, especially of the auricles ; then 
the face is pale; it is also due to myocardial degeneration; then the face 
is cyanotic. The signs of cardiac incompetence are hepatic and renal 
stasis, ascites, dyspnea, cerebral anemia (syncope), edema of the lungs, 
etc. The pulse at first undergoes irritative acceleration, but lasting 
frequency indicates myocardial change; rarely is it normal or slow (to 
36), as a result of compression; dicrotism is frequent; there may be the 
pulsus paradoxus, weakening or intermitting with each inspiration 
(Traube). A very strong or water-hammer pulse may suggest under- 
lying aortic disease. Irregularity is occasional, as is the pulsus differens 
and difference in the pupils. Lung compression is frequent. Bamberger 
observed a small area of compression, the size of a dollar, at the\ngle*of 
the left scapula, where bronchial breathing, dulness (or tympany) and 
increased fremitus are noticed; the compression clears up when the 
patient assumes the knee-chest posture. Pleural puncture excludes the 
25 



386 DISEASES OF THE PERICARDIUM 

possibility of fluid, and the absence of crepitant rales excludes pneumonia. 
Bamberger's sign also occurs in hemopericardium. There may be tym- 
pany (or dulness) under the left clavicle and to the left (and sometimes 
to the right) of the heart in fair-sized effusions. Ewart describes tubular 
breathing near the right mamma. Tracheal compression and thrombosis 
of the innominate veins may result from compression. The second pul- 
monic sound may be early and sharply accentuated. The second tone 
may be split. Metallic heart tones may be due to an adjacent cavity, 
pneumothorax or the distended stomach and intestines. A systolic 
murmur over the aorta has been explained by pressure or inflammatory 
relaxation interfering with its normal vibration. 

Diagnosis. — Differentiation rests upon the friction, dulness and apex 
beat. Puncture alone reveals the character of the exudate. Fibrin for- 
mation and serous exudation usually coexist. 

1. The pericardial rub is practically pathognomonic of pericarditis 
(von Dusch). (It occurs very rarely in cholera, pericardial tubercles, 
cancer, soldier's spots, hypertrophied heart, and the heart beating 
against an inflamed diaphragm or peritoneum.) 

(a) In distinguishing it from endocardial murmurs, its acoustic quality, 
superficiality, lack of rhythmic precision, variability, slight propagation, 
palpatory differences in the rub, its basal location and increase by press- 
ure or inspiration are most decisive. Valsalva's experiment — i. e., a 
long inspiration followed by expiration with closed glottis and tense 
abdominal muscles — intensifies pericardial friction and decreases endo- 
cardial murmurs. Frequently pericarditis is a complication or coordinate 
phenomenon of endocarditis which may become manifest only after the 
pericarditis subsides. 

(6) In pleuropericardial (extrapericardial) friction originating in an 
inflamed pleura, friction depends not only on respiration, but also on 
the heart's action. The distinction lies (i) in the close connection of the 
pericardial rub with the cardiac activity, persisting during expiration, 
and (ii) in the location of the pleuropericardial friction along the lingual 
lobe, in its intimate relation to respiration and in its cessation in extreme 
inspiration or expiration (inspiration also augments true pericardial 
friction). Valsalva's test is also useful (v. s.). Pericardial friction toward 
the base or sternum is less often confused with pleural friction. Differ- 
entiation is difficult when the basal vessels beat against a tuberculous 
cavity or pneumonia. 

(c) In precordial emphysema the crackling sounds of interstitial emphy- 
sema (air) in the anterior mediastinum resemble rales, but closely follow 
the heart's action and are often metallic. The condition of the heart 
tones is decisive. 

(d) Pericardial splashing (see Pneumopericardium). 

(e) Crepitant rales are easily differentiated. 

2. The dulness of pericardial exudation is typically pyriform or 
triangular. The markedly increased relative cardiac dulness should be 
considered rather than the absolute dulness (which is often little altered 
in pleural adhesions or pulmonary emphysema). 



PERICARDITIS 



387 



(a) Hydropericardium and effusive pericarditis may be confused, 
because the friction may disappear, and fever may be lacking (chronic 
pericarditis). Hydropericardium is distinguished by its etiological 
factors (q. v.), hydrothorax which almost always develops first, by lower 
dulness, by resorption under digitalis and purges; and by absence of 
friction ; paracentesis reveals the usual differences between exudates and 
transudates in their opacity, specific gravity and percentage of albumin 
(see Pleurisy). 

(b) Hemopericardium, resulting from trauma, rupture of a coronary 
artery or ventricular or aneurysmal rupture, is usually sudden, is attended 
by syncope and blood is removed by puncture. 

(e) Pneumopericardium (q. v.). 

{d) From cardiac dilatation the differentiation may be most difficult, 
expecially when there is dilatation plus hydropericardium, in which 
case drastics, digitalis, friction, the history and evolution only, may 
decide. In dilatation the dulness is rarely triangular but rather is in- 
creased laterally, the shock-like impulse of the heart is more marked and 
often contrasts sharply with the weak radial pulse, compression of the 
lung is much less common, and the heart tones are more clear and 
"snappy". The .r-rays are often decisive. The very distinctive relation 
between the apex and the outer dulness to the left is rarely fallible (v. s.). 
If the pulse is strong and the apex weak, pericarditis is present; but com- 
pression or weakness of the heart in pericarditis necessitates a weak, rapid 
pulse. Leaning forward may clearly demonstrate the apex within the 
dulness of the exudate. When the patient lies on his right side the apex 
in pericardial effusion becomes visible, which does not obtain in extreme 
dilatation ; in children dulness of tener signifies dilatation than pericardial 
effusion. 

(e) When there is retraction of the left lung away from the heart, the 
diaphragm is high, the apex and outer cardiac dulness coincide, the spleen 
is high, the pulmonary artery is exposed, and the proper signs of pulmo- 
nary retraction are elicited. 

(/) In mediastinal tumor the dulness is irregular; there is no variation 
of dulness on postural change; and signs of increased conduction and 
bronchial breathing are noted. 

(g) From aneurysm the differentiation is usually possible, as well as 
from marginal infiltration of the lung; callous pleura, encapsulated 
pleurisy, and anterior mediastinitis (usually with friction, but with more 
vertically elongated dulness). 

Diagnosis of the Character of the Exudate. — The fluid is serofibrinous in 
rheumatism; ichorous in perforation from hollow viscera; hemorrhagic 
in scurvy, carcinoma, tuberculosis, hemorrhagic exanthemata and alco- 
holism; and purulent in sepsis and empyema. Paracentesis is the only 
certain test. Tuberculous pericarditis, even in clearly tuberculous cases, 
can be diagnosticated positively only by detection of tubercle bacilli in 
the aspirated exudate; a chronic pericarditis is probably tuberculous. 
In children 30 per cent, of pericarditides are suppurative and 17 per cent, 
tuberculous. 



388 DISEASES OF THE PERICARDIUM 

Course. — Exudation may follow the friction at once or only after many 
days. The exudate may be rapidly absorbed in a few days or endure 
for months. The average duration is one or two weeks. 

Prognosis. — The prognosis depends largely upon the causal disease and 
the character and quantity of the fluid; it is usually good in rheumatic 
and serofibrinous cases. Septic, purulent, putrid or hemorrhagic types 
are serious. The pneumococcic form is fatal in 62 per cent. Death may 
be rapid in hemorrhagic cases; it usually is due to cardiac exhaustion, 
especially in chronic cases, and results from myocarditis rather than from 
simple pressure. The prognosis is more favorable in men than in women, 
young children or aged subjects. Benign cases may result seriously from 
concretio cordis. 

Treatment. — 1. The hygienic treatment is managed as in any acute 
infection with cardiac involvement. Absolute rest in bed is indicated, 
even during convalescence, to spare the heart. The patient should 
never sit up to urinate or defecate, for fatal syncope may follow the 
effort. 

2. Laxatives should be given (sod. phosphate 5ss-ij), for constipa- 
tion per se may increase the heart action, and difficult bowel movements, 
with the attendant straining, may precipitate syncope. 

3. The diet should be light or fluid, avoiding tea and coffee, which excite 
the heart. Alcohol may be given in sepsis. 

4. Local Antiphlogistic Measures. — An ample ice-bag upon the pre- 
cordium quiets and regulates the heart-rate, relieves palpitation and 
pain and is often the best cardiant and sedative. No drug quiets the 
heart like opium. A Spanish-fly blister, as large as the hand, often 
not only relieves pain but stimulates resorption. 

5. Causal therapy, as salicylates, in the rheumatic form. 

6. Heart stimulation is indicated when the pulse is irregular, fast or 
small, due to early cardiac irritation or to later mechanical compression 
by the exudate. Strychnine, coffee and camphor operate more quickly 
than digitalis or may be used to follow up its action. Cardiac depressants 
are obviously injurious. 

7. In treatment of the fever, hydrotherapy is preferable. 

8. Compression symptoms, such as dyspnea and vomiting, are met by 
the judicious use of morphine hypodermically. When the face is 
pallid the heart is compressed by the exudate and tapping is indicated. 
Tardy resorption of large exudates or sudden or severe symptoms there- 
from necessitate tapping of the pericardial sac, under general aseptic 
precautions. The puncture is made in the fifth left (or right) interspace 
about an inch from the sternum, where the sac is not covered by the 
pleura. Gentleness in passing the trocar enables us to feel the giving way 
of the parietal pericardium and to avoid cardiac trauma. Removal of 
a small quantity frequently provokes absorption by relaxation of the 
vessels in the tense pericardium. The fluid is withdrawn very gradually 
by the gravity or siphon method (see Pleurisy). Sudden or extreme 
cardiac embarrassment may necessitate free venesection. 

9. Delayed absorption is treated by potassium iodide gr. x-xx, by 
diuretin 60 to 90 gr. per diem, and by small doses of calomel followed 



PERICARDITIS 389 

by salines. Hot packs, alcohol sweats and pilocarpine should be entirely 
avoided lest collapse occur. 

10. Early pericardiotomy is indicated in suppurative or putrid forms. 
About one-half of the cases recover. 

Adhesive Pericarditis. — Pericardial Concretion {Synechia)) Cicatricial 
{Callous) Mediastinopericarditis. — Pericarditic adhesions within the sac 
or more extensive bands to the chest wall, pleura or spine develop in 41 
per cent, of cases of pericarditis and are found in 6 per cent, of autopsies. 
In one group of cases, complete obliteration of the sac may occur with 
absolute clinical latency; the heart may beat itself loose from fresh or 
lax adhesions, especially about the apex. In a second group, there are 
undistinctive evidences of cardiac insufficiency. In a third series, dis- 
tinctive physical signs exist. Adhesions most frequently follow serofibrin- 
ous pericarditis. A clear history or the actual observation of a previous 
pericarditis is a strong point in the diagnosis. 

Symptoms. — 1. Cardiac insufficiency is caused more often by dila- 
tation or atrophy than by pressure on the coronary arteries or myocardial 
fibrosis. While severe heart symptoms without valvular disease in 
advanced life are indicative of myocardial degeneration, in the young 
they suggest pericardial adhesions (Wilks) . Failure of the right ventricle, 
without valvular, renal or pulmonary disease, or sudden decompensation 
in valvular lesions, directs attention to possible pericardial adhesions. 
Weiss and Pick described an isolated ascites, associated with enlarged 
liver; it is probably due to inflammatory extension along the vessels 
from the pericardium to the peritoneum. Sudden death is sometimes 
due to pericardial synechia?. 

2. Systolic Retraction of the Interspaces at the Apex. — This 
may occur even with slight basal adhesions which hinder the systolic 
descent of the heart, while diffuse adhesions other than basal often pro- 
duce no symptoms. It is especially significant when the normal systolic 
protrusion gradually is replaced after pericarditis by systolic retraction 
(for retraction of the apex also occurs in other conditions, and is merely 
an expression of impaired locomotion of the heart and lack of space at 
the apex). It is best seen on deep inspiration and disappears when the 
heart grows weak. 

3. Retraction of the sternum, epigastrium, diaphragm and lower 
chest wall may be observed when adhesions also exist outside of the peri- 
cardium as an indurative mediastinitis, which attaches the heart ante- 
riorly to the chest wall and posteriorly to the spine, and necessitates 
retraction, until cardiac weakness develops (Skoda). Broadbent's sign 
is a systolic retraction of the eleventh and twelfth ribs posteriorly. 

4. The diastolic recoil of the diaphragm and chest wall which are 
retracted in the systole, is recognized by palpation and by auscultation 
as a dull vibration. 

5. Diastolic collapse of the cervical veins is of great diag- 
nostic value, and is due to their aspiration by the heart; it may pro- 
duce diastolic pallor of the face. 

6. The Pulsus Paradoxus. — The pulsus paradoxus, a pulse inter- 
mitting with inspiration, strongly suggests cicatricial mediastinoperi- 



390 DISEASES OF THE PERICARDIUM 

carditis, particularly with the previously mentioned signs. In mediastino- 
pericarditis, inspiratory stretching of the great vessels by well-attached 
mediastinal adhesions, shuts off the pulse. Sometimes observed to a 
moderate degree physiologically, it is pathognomonic when (i) it appears 
without forced inspiration, (ii) when the pulse is completely suspended 
by inspiration, (iii) when the heart's action is strong and regular and 
(iv) when it is combined with inspiratory swelling of the cervical veins 
(v. i.). Slowing of the pulse during inspiration is explained as irritation 
of the vagus by the mediastinal connective tissue. 

7. Inspiratory swelling of the neck veins (Kussmaul), which 
normally collapse during inspiration, is due to mediastinal bands, which, 
on inspiration, interrupt the return venous flow. Cyanosis may occur 
with each inspiration. 

8. Other signs are fixation of the heart by adhesions, which gives 
no change of dulness by change of posture; absence of respiratory 
excursion over the heart; decrease of Traube's semilunar space by pleural 
adhesions; decreased movement of the left half of the epigastrium 
(diaphragmatic adhesion to heart) ; cyanosis and dyspnea due to adhe- 
sions with the diaphragm impeding respiration; expiratory weakening 




Fig. 27. — Pulsus paradoxus (Kussmaul) ; E, beginning of expiration, and J, of inspiration. 

of the apex by pleural adhesions; weak right heart with no accentuation 
of the second pulmonic tone; loud, even musical, murmurs, especially 
in the aged; systolic emptying of the veins of the thorax due to systolic 
dilatation of the internal mammary veins; a rumbling presystolic mur- 
mur at the apex, especially in children, without signs of mitral stenosis; 
precordial creaking when the patient moves the arm; and other mediastinal 
symptoms, e. g., left recurrent laryngeal paralysis, venous thrombosis in 
arm, etc. 

Diagnosis. — In the diagnosis, two groups of symptoms are observed; 
first, the myocardial (dilatation, hypertrophy, relative tricuspid insuf- 
ficiency); and second, the mediastinal (pulsus paradoxus, etc.). (See 
Pick's Pericardiac Pseudocirrhosis, under Diagnosis of Hepatic 
Cirrhosis.) 

Prognosis. — The prognosis depends upon the condition of the myo- 
cardium. Cardiac concretion is the usual cause of heart failure in juvenile 
rheumatic cardiopathies. 

Treatment. — The treatment is identical with that of valvular disease 
or myocardial insufficiency. Brauer advocates surgical solution of the 
adhesions (cardiolysis), conditional on the myocardium being strong; 
28 operations are reported (1910). 



HYDROPERICARDIUM 391 



PNEUMOPERICARDIUM. 



Gas or air in the pericardium. But 38 cases were collected in 1904 
by W. B. James, from whom the figures below were taken. 

Etiology. — It results from (a) trauma (18 cases), such as perforating 
wounds, crushing of the ribs or sternum; (6) perforating processes from 
cavities or viscera containing air or gas (15 cases); pulmonary cavities; 
gangrene, pneumothorax, esophageal or gastric ulcer, liver abscess or 
caseated bronchial glands. The attendant effusion may be ichorous, 
hemorrhagic, purulent (pyopneumopericardium), or more rarely serous 
(hydropneumopericardium) . (c) Exceptionally gas has been observed 
without solution of continuity, due to the Bacillus aerogenes encapsulatus. 

Diagnosis. — On inspection, there is precordial bulging and absence of 
the apex beat, though it may reappear upon leaning forward. On palpa- 
tion, the vocal fremitus about the heart and the apex beat are gone, fric- 
tion and occasionally splashing, churning, gurgling sounds may be felt. 
On percussion, when the patient is sitting, a tympanitic, cracked-pot, 
or even metallic note is obtained above or over the entire heart, especially 
when percussion is made with the plessimeter and the hard part of the 
percussion hammer. The tympanitic note varies during the systole and 
diastole; it becomes higher in the erect posture and varies with the 
amount of exudation. The change in note on change of posture and 
the condition of the apex depend upon hydrostatic laws, as is the case 
in pneumothorax. The lung is compressed. On auscultation, the heart 
tones vary with the fluid, being loud if there is no great effusion, and 
usually metallic or musical, like the sound from a zither. The same is 
true of the quality of the friction (for pericarditis is invariably present) . 
The tones, the metallic tinkling (in 63 per cent.) or splashing, the falling- 
drop sound, the mill-wheel churning (in 50 per cent.) and succussion may 
keep the patient awake and may be heard in an adjacent room, as in 
cases of Stokes, Laennec and Graves. 

Differentiation is required from cavities, encapsulated pyopneu- 
mothorax near the heart and distention of the stomach imparting a 
metallic note to the heart tones. Consideration of the heart dulness 
and apex beat renders the diagnosis easy; in James's series all but 6 were 
recognized. 

Prognosis. — Death occurs in 70 per cent, of the cases, usually within 
two weeks, from the inherently fatal causal disease and from cardiac 
insufficiency; traumatic cases are more favorable. 

Treatment. — Puncture to void the gas, and operation for putrid or 
purulent processes are indicated. (See Pericarditis.) 



HYDROPERICARDIUM (HYDROPS PERICARDII). 

Hydropericardium is secondary to circulatory disturbances, as heart or 
pulmonary lesions, or, infrequently, local obstruction in the pericardial 
veins; or cachectic conditions producing transudation, as Bright's disease 
or carcinoma. 



392 DISEASES OF THE ARTERIES 

Symptoms. — They are much the same as in pericarditis, except that 
friction is absent. The heart region is sometimes prominent, the apex 
beat is lost, the heart tones are distant, the fluid changes with change 
of posture and the dulness is clearly trapezoidal since no adhesions exist. 
In most autopsies a small amount of fluid is found which transudes 
during the death agony or after death. In hydropericardium, the fluid is 
yellowish-green, and is sometimes slightly tinged with blood. Evidences 
of inflammation are absent; the fluid is alkaline, contains some albumin, 
sugar and urea, and is of low specific gravity. Chyle-like effusions 
(chylopericardium) are very rarely seen. 

Diagnosis. — The signs of fluid are the same as in pericarditis, but 
there is no temperature, tenderness or friction. Dilatation of the heart 
causes the most frequent diagnostic confusion (q. v. for differentiation). 
The etiological diagnosis is important, as finding a cardiac or renal lesion. 

Prognosis and Treatment. — The prognosis and treatment depend 
wholly on the cause. Cardiac stimulants, blisters over the heart, laxa- 
tives, etc., are indicated. 

HEMOPERICARDIUM. 

Blood tinges the exudate in certain forms of pericarditis. A large 
quantity of blood may escape into the sac in trauma of the heart or of 
the sac, rupture of the heart (q. v.) or of aneurysms (q. v.). 

The symptoms and physical signs relate to (a) the acute anemia with 
pallor, syncope and rapid pulse, which usually ends, in a few hours or 
days, in death; (6) signs of fluid in the pericardial sac. The prognosis 
is favorable only in the traumatic cases; death may be postponed eleven 
days. The treatment is expectant; the heart should be stimulated and 
salt solution infused. 



DISEASES OF THE ARTERIES. 

ARTERIOSCLEROSIS. 

Synonyms. — Atheroma, arteriocapillary fibrosis (Gull and Sutton), 
endarteritis deformans (Virchow), angiosclerosis (Thoma). 

Definition. — A regressive change, evidenced first by malnutrition in 
the walls of the large or small vessels and later by compensatory thick- 
ening, either localized or diffuse. Morgagni recognized atheroma. 

Etiology. — 1. Age. — Arteriosclerosis is the essential element in senile 
involution, although some individuals attain their hundredth year with 
no arterial change. Cazalis said, " A man is as old as his arteries," and 
Peter spoke of "the vital rusting." Though usually found after the fiftieth 
year, hereditary influences, syphilis or the acute infections may develop 
hard arteries before the fortieth year, in adolescence or even in infancy. 
Chiari found it in 27 per cent, of those under twenty-five years, and 
Fremont Smith collected 144 cases in children. 



ARTERIOSCLEROSIS 393 

2. Sex. — Eighty per cent, of cases occur in men, from causes enu- 
merated below. In women it usually occurs a decade later. In factory 
women Jusserand found a larger percentage than in men. 

3. Artekial Poisons.- — Chronic alcoholism causes 25 per cent, of all 
cases; lead, coffee, tea and tobacco (affecting the coronary vessels and 
those of the legs) are causative factors. Angiosclerosis has been pro- 
duced experimentally by adrenalin. 

4. Overwork is second in importance only to alcohol. Physical 
exertion brings one-third of the blood to the muscles, thus lowering 
the tension in other vessels (v. i. Thoma's Theory). 

5. Poisons Produced by Perverted Metabolism. — Interstitial neph- 
ritis bears a threefold relation to arteriosclerosis: (a) It results from 
diffuse arterial hardening; (b) it raises arterial pressure mechanically 
(Traube) by increased peripheral resistance in the arterioles, or by 
alteration in the quality of the blood (Bright); (c) both processes are 
coordinate to a common cause. Gout, diabetes, high living, overeating and 
obesity come under this head. 

6. Specific Infections. — Syphilis causes but 12 per cent, of cases. 
Tuberculosis (in 16 per cent.), typhoid, rheumatism, influenza, scarlatina 
and other infections have a direct bearing on vascular sclerosis; Oppen- 
heimer described arteriosclerosis in children nine and ten years old, due 
to acute infections (v. s.). 

7. Other Causes. — Nervous factors, as worry, high tension and 
ambition are important. Excessive brain effort tends toward cerebral 
localization, precisely as digestive excesses may develop changes in the 
mesenteric vessels, as working with the arms, as in butchers, may develop 
changes in the brachials, and as excessive walking may produce arterio- 
sclerosis in the femorals. 

Pathogenesis and Pathology. — (A) Thoma considers angiosclerosis a 
compensatory process; to restore the caliber of widened vessels, the 
tunica media contracts, or when it cannot contract, the subendothelial 
connective tissue increases in thickness. Thus in the fetus there is no 
connective tissue in the tunica intima, but it appears when the fetal 
circulation changes at birth, new areas of circulation being opened up. 
All bloodvessels have a nervous supply ending in the Vater-Pacini bodies. 
They respond to persistent low pressure or dilatation, by increased pro- 
liferation of the connective tissue. (B) Others regard arteriosclerosis as 
due to inflammation in the nutrient vessels, the vasa vasorum, leading to 
growth of connective tissue, i. e., mesarteritis and periarteritis (Huchard, 
Koster). Arteriosclerosis in vessels with no vasa vasorum must be simply 
degenerative. 

Conceptions of its morbid anatomy differ widely, atheroma of the 
aorta and endarteritis or arteriocapillary fibrosis being sometimes de- 
scribed under separate headings, but the difference is rather anatomical 
than pathological. Large vessels, as the carotid, contain more elastic 
than muscular tissue, but the small vessels are largely muscular. Two 
main forms are distinguished, the diffuse and the nodular. Without dis- 
tinction as to form, Rokitansky found that arteriosclerosis occurred in 
the following order of frequency: ascending aorta, arch, thoracic, abdom- 



Diffuse form. 


Nodular 


variety 


89 


pei 


cent. 


2 per 


cent. 


88 




tt 


8 


a 


87 




tt 


8 


a 


64 




a 


25 


tt 


64 




n 


17 


a 


58 




tt 


14 


a 


53 




tt 


16 


a 


49 




a 


15 


a 


49 




a 


9 


it 


45 




a 


43 


a 


44 




it 


22 


a 


40 




a 


43 


a 


28 




a 


60 


a 


19 




tt 


56 


ti 


10 




ti 


69 


a 







a 


75 


tt 



394 DISEASES OF THE ARTERIES 

inal aorta, splenic, iliac, femoral, coronary (next after the aorta, accord- 
ing to Huchard and Sansom), cerebral, brachial and carotid arteries. It 
is rare in the gastric, mesenteric and hepatic vessels and least frequent 
in the pulmonary trunk. Bergmann found the two varieties as follows: 

Radial 

Ulnar 

Tibial 

Popliteal 

Splenic . 

Femoral 

Axillary 

External iliac 

Brachial 

Subclavian 

External carotid 

Cerebral 

Internal carotid 

Ascending aorta 

Common carotid ...:... 

Abdominal aorta 

(Both forms may coexist in the same vessels.) 

It will be noted that where the diffuse variety is most frequent the 
nodular form is least observed and that the converse is true. The diffuse 
form is most frequent in the extremities where arterial tension is most 
variable and more collateral circulation prevails; the nodose form is 
most common in the aorta, its primary branches and the circle of Willis, 
where arterial pressure varies greatly. 

To the naked eye the intima may be normal and smooth but most 
often is uneven and thickened. Small, gelatinous or yellowish, fatty 
areas are seen which though at first circumscribed, often fuse into large 
plaques; they occur where arterial pressure is greatest, as in the aortic 
arch (see Syphilis and Aneurysm), or where the vessel divides or gives 
off branches, as the subclavian or intercostal branches. The plaques 
of atheroma or nodular arteriosclerosis represent nature's effort to fill 
out areas of degeneration and dilatation and thus even the caliber of the 
vessel. Microscopically the intima may be increased three- or fourfold 
from swelling, increase of connective-tissue and round-cell infiltration. 
Granular detritus, fatty needles and cholesterin plates are seen in the 
atheroma plaques, a name indicating their pulpy, grumous appearance. 
An atheromatous area rupturing into the lumen produces the atheromatous 
ulcer, which may cause embolism, thrombosis or occlusion. Deposit of 
lime in these areas leads to calcification or produces rough areas in the 
aorta which break on manipulation or may cut the finger. The lumen of the 
smaller vessels is often decreased or obliterated (endarteritis obliterans) ; 
their middle and outer coats at times are thickened by hyaline degenera- 
tion and fibrous tissue; the muscular coat may waste and all elastic 
tissue may disappear; the essential changes are in the elastic tunic. 
In the larger vessels dilatation may develop where thickening of the 
intima fails to protect the vessel wall. 

The general results of arteriosclerosis are (1) vascidar inelasticity, 
deformity, tortuosity, obliteration, and high arterial tension, and (2) 
visceral alterations in the heart, brain, etc. (v. ?'.). 



A RTERIOSCLEROSIS 



395 



The rare sclerosis of the pulmonary artery occurs in mitral lesions and 
emphysema; pulmonary atheroma may occur alone, sometimes with 
aneurysmatic dilatation of its branches and with pulmonary regurgitation. 

Thoma's angiosclerosis includes phlebosclerosis, which frequently 
accompanies arteriosclerosis and sometimes occurs independently, in the 
lower extremities, lung and portal tributaries in cases of liver cirrhosis or 
pylephlebitis. 

Symptoms and Diagnosis. — In diffuse forms the process may be latent. 
The clinical picture is extremely variable. 

1. The peripheral arteries may be involved, with or without changes 
in the aorta, heart, brain and kidneys. The small arteries appear tortuous, 
pulsating and lengthened, as in the temporals or brachials when the 
elbow is flexed and the arm is rotated outward. With the finger, which 




Fig. 28. — Pulse tracing in arteriosclerosis. 

no instrument can totally replace, we distinguish between hardness of the 
vessel walls and increased arterial tension, although varying degrees of 
both conditions usually occur together. Normal blood-pressure does not 
mean a normal movement of the blood since accommodative vascular 
contraction may follow poor vascular filling; a large artery does not 
necessarily mean a strong pulse nor does a small artery always indicate 
a weak pulse. Pressing on the radial with one finger should obliterate 
the pulse beyond that point if the arteries are not sclerotic, unless there 
is an anastomotic or recurrent pulse from the ulnar to the radial vessel; 
this source of error is easily eliminated by simultaneous pressure on the 
ulnar vessel. The wall of the artery is hard, often uneven or nodular, 
and the serial atheromatous plaques sometimes feel like a rosary. In 



Fig. 29. — Pulse tracing in extreme arteriosclerosis (Sahli). 



extreme instances the vessel feels calcareous — the "pipe-stem artery." 
The Roentgen rays clearly show the arterial change. The pulse is hard 
{pulsus durus), retarded {pulsus tardus) or slow {pulsus rarus); it rises 
slowly and is long maintained {p. rotundus), the vessel is firm between 
the pulse beats, the elastic wave is lessened or absent, the tracing has a 
rounded or flat top, and the two radials may differ {pulsus different). 
In vessel obliteration or absolutely rigid walls the pulse cannot be felt. 
Slight pressure on the vessels often elicits a systolic murmur. The right 
radial is normally larger and more often shows changes than the left. 
Changes may occur in internal vessels without change in the radials (and 
conversely) . 

Increased arterial tension is a symptom only; barely one-half of the 
arteriosclerotics show hypertension. The normal tension ranges between 



396 DISEASES OF THE ARTERIES 

110 and 140 mm., any permanent register over 160 indicating hyperten- 
sion (excitement may raise the reading 10 to 20 points, temporarily). 
The causes of high tension are: (1) Toxins injuring the vessel walls 
(high living, sedentary life, intestinal putrefaction or tobacco); (2) 
causes raising blood-pressure without vascular injury (the toxemia of 
pregnancy); (3) local diseases, as nephritis, diseases of the brain, abdom- 
inal vessels or splanchnic circuit; (4) profound neurasthenia; and (5) 
arteriosclerosis. A pressure of over 160 indicates nephritis in 70 and 
of over 200 in 100 per cent, of cases. In few cases, hypertension — due to 
vascular spasm — is apparently independent of arteriosclerosis and 
nephritis. In determining blood-pressure instrumentally, we regard the 
systolic pressure (the maximum pressure, corresponding to the intra- 
ventricular pressure); the diastolic pressure (the minimal pressure, 
corresponding to the peripheral resistance in the arterioles); and the 
pulse pressure (the difference between the systolic and diastolic and 
normally 50 per cent, of the latter). Auscultatory estimation (Korotkow) 
gives the most accurate results. If the arm band is inflated to a point 
above the maximal pressure and the bell of a stethoscope is placed over 
the artery at the bend of the elbow, nothing is heard. As the pressure is 
slowly allowed to fall a systolic, knocking sound is heard over the artery 
as soon as the maximal pressure is reached. This sound (or first phase) 
is due to the sudden distention of the walls of the empty artery by the 
first jets of blood that pass below the occluding arm band. . As the 
pressure falls, this knocking sound grows louder, is then often replaced by 
a murmur (second phase), which again gives place to a clear, knocking 
sound (third phase) similar to the first. This last sound then suddenly 
becomes dull (fourth phase) and, after a further fall of a centimeter or 
so, ceases entirely ^ (fifth phase). The first and fourth phases are most 
important, indicating the systolic and diastolic pressure, respectively, 
and the mercury column is watched for the record at these phases. If 
the third phase is loud, long and clear, the heart is strong; if weak, 
there is decompensation. 

2. Heart Changes. — (a) Simple hypertrophy of the left ventricle may 
occur, with heaving apex, loud second aortic tone, tense pulse and thick- 
ening of the arteries. Some "consensual" right-heart hypertrophy is 
common because of anastomosis between the ventricular muscular fibers 
or because of pulmonary stasis. The heart is not hypertrophied in the 
majority of cases; it does not necessarily follow arteriosclerosis in the 
extremities or brain, but most often occurs when the splanchnic vessels 
or the aorta are sclerosed. The apex may sink downward and to the left 
from relaxation and lengthening of the aorta, (b) Hypertrophy plus 
dilatation, with heart insufficiency, dyspnea, scanty urine and hydro- 
thorax are common; a systolic murmur often leads to a wrong diagnosis 
of mitral insufficiency. Interstitial nephritis (v. s.) is the commonest 
cause of the hypertension, hypertrophy and dilatation; Cardiac weak- 
ness may accompany a blood-pressure of 200 to 300 mm. In high arterial 
tension a double impulse may be felt and seen at the apex, which precedes 
cardiac weakness. Edema is not frequent. Gallop-rhythm points to 
coronary or renal disease. The heart muscle shows various changes 



ARTERIOSCLEROSIS 397 

since arteriosclerosis is prone to starve the myocardium; they are atrophy, 
myocarditis, fatty heart, myofibrosis, myomalacia cordis, the cor renale, 
heart aneurysm, angina pectoris, heart-block, Adams-Stokes's syndrome, 
coronary embolism, cardiac asthma and arrhythmia; these lesions fall 
under the two forms of visceral sclerosis: (i) inflammatory, occurring 
about the vessels, and (ii) dystrophic sclerosis, often somewhat distant 
from the vessel involved. 

3. In the aorta, dilatation may give dulness in the second (and third) 
right intercostal spaces, confirmed by the fluoroscope; in the jugulum or 
abdomen may be felt the aorta, plaques or even crackling; the sub- 
clavian or innominate arteries may be felt even through their entire 
length. The normal aorta propels the blood onward after the aortic 
valves close; if the aorta loses its tone the peripheral vessels receive 
inadequate blood, depending wholly on the ventricular systole, giving 
perhaps a pulsus celer. A short systolic murmur over the aorta often 
results from atheroma or dilatation, and the second aortic tone is then 
accentuated and metallic. Its vibration may sometimes be felt; when 
emphysema is present it is best heard in the jugulum. The accentuation 
may be caused by increased tension, widening or rigidity of the aorta. 
The murmur and sharp tone are often heard in the neck and back, and 
the writer has heard the accentuation only in the neck. Atheroma may, 
by downward extension, cause aortic stenosis or regurgitation. 

4. Renal findings are next in frequency. The kidneys are often con- 
tracted (the senile arteriosclerotic and the genuine contracted kidney). 
The renal findings are probably most often primary (see Interstitial 
Nephritis). The urine may increase as a result of increased blood- 
pressure or decrease from asystole. 

5 . Brain symptoms rank next in importance. Syncope, vertigo, headache, 
tinnitus, neurasthenic symptoms, transient aphasia or hemiplegia result 
from transient ischemia. Brain hemorrhage and miliary aneurysms are 
frequent sequences; encephalomalacia results from cerebral embolism or 
thrombosis. Brain atrophy, depressive conditions, the lacunar sclerosis 
of Grasset and Marie, epileptic seizures and the Adams-Stokes's triad 
may be attributed to cerebral atheroma. Vascular brain lesions occur 
fairly often in cases which show arteriosclerosis in the extremities and 
temporal vessels, though sclerosis of the aorta, coronary or splanchnic 
vessels occurs more often without peripheral angiosclerosis. Most 
instances of myelitis, so-called, are not inflammation but arterial ischemia 
with myelomalacia. 

Charcot's claudication intermittente (Erb's dysbasia intermittens angio- 
sclerotica; intermittent limping; angina cruris) is chiefly due (a) to 
atheroma in the abdominal aorta and its branches in the limbs; it is 
seen in abdominal aneurysm in the horse. It appears also to result (b) 
from vessel spasm or (c) rarely atheroma in the spinal vessels. Erb, 
reviewing 159 cases found that 94 per cent, were in men over forty years 
of age; 33 per cent, were Jews; syphilis was causal in 23 per cent.; 
half were enormous, and half, moderate smokers; most cases developed 
in the upper classes. Pain, paresthesias and sometimes local cyanosis 
occur in the legs, which " give way" after moderate exertion. The dorsalis 



398 DISEASES OF THE ARTERIES 

pedis (sometimes also the tibial and femoral vessels) usually cannot be 
felt. Analogous changes occur in the arms, brain, heart, intestine, 
kidney and eye. Brooks reported an arteriosclerotic with the picture 
of myasthenia gravis. 

Some vasomotor neuroses — as erythromelalgia, Reynaud's disease, 
acroparesthesia — and some neuritides and neuralgias are occasionally 
associated with angiosclerosis; sclerotic vessels are prone to spasm. 

6. The g astro-intestinal symptoms rank next in frequency. Cases are 
described of dyspepsia, round ulcer, arteriosclerotic gastritis, gastro- 
intestinal hemorrhages, intestinal perforation and ulceration. Some 
cases resemble gastric cancer. Severe abdominal pain (angina abdominis) 
is due to local anemia (intermittent claudication of the abdominal vessels, 
intermittent dysperistalsis) ; Pal thinks spasm occurs in the mesenteric 
and gastric vessels; it develops in two or three hours after eating, and is 
often accompanied by distention and dyspnea. Proctitis, piles and blood 
in the stools are not uncommon. Abdominal angina is often associated 
with angina pectoris and angina cruris. 

7. The retinal vessels are not infrequently embolized, narrowed or 
aneurysmatic, which leads to softening, hemorrhage and exudation. 
As a rule, retinal is associated with cerebral atheroma. 

8. In the respiratory tract, emphysema and bronchitis are very com- 
monly coincident or consecutive. Hemoptysis is rarely referable to 
atheroma of the pulmonary arterioles. 

9. Peripheral vessels; gangrene results from obliterating endarteritis; 
44 out of 81 cases of gangrene of the legs in von Eiselsberg's Clinic were 
arteriosclerotic. Thrombosis or embolism may occur in the aorta, 
cerebral or other arteries. 

10. The general nutrition varies. Some writers distinguish between 
a plethoric and an anemic type. French writers speak of a cachexie arter- 
iole, in which the pallor is distinguished from the dusky anemia of cardiac 
disease, but the anemia is more apparent than real. 

Early Diagnosis. — Early symptoms are local disturbances in circulation 
and may only appear after exertion in cold weather, excitement, or mild 
infections as "bronchitis," which results from simple stasis, and responds 
only to cardiac therapy. The patient tires more easily and the arterial 
tension may rise; slight edema of ankles or epistaxis is suggestive. 
Early nervous symptoms are headache, irritability, emotivity, somnolence, 
difficulty in concentration or in undertaking new work, vertigo, neuralgias, 
insomnia, or neurasthenia appearing for the first time after forty years 
of age. Arteriosclerotic "rheumatoid" pains may be early symptoms. 
A slight albuminuria always should attract attention. Ocular and 
vasomotor disturbances may characterize the insidious onset. The 
above symptoms are important since successful therapy depends on the 
early recognition of what Huchard terms the " presclerotic" symptoms. 

Prognosis. — The process is frequently latent until it is far advanced. 
Its early stage may remain stationary for a long period, but there is 
constant danger of apoplexy, angina pectoris, myocardial paralysis or 
uremia. When a mitral murmur develops, there appears every sign of 
failing tonicity and contractility; when stasis predominates anginal at- 



ARTERIOSCLEROSIS 399 

tacks cease. Many deaths attributed to acute infections are deaths 
from arteriosclerosis. A patient may live years with a tension of 180 to 
200 mm., asthma or alternating pulse; he may work with great energy 
for years, until the end comes — often very suddenly. The writer observed 
a blood-pressure of 315, with which the patient worked a year. The 
prognosis is most favorable in angiosclerosis of the peripheral vessels. 
A slow pulse is less favorable than arrhythmia and moderate increase in 
rate ; the extra-systole is not unfavorable, whereas fibrillation is always 
menacing. 

Treatment. — I. Prophylaxis concerns the etiological factors and the 
patient's mode of life. Alcohol and tobacco should be forbidden, mercury 
and iodides given in syphilis, the diet regulated in diabetes, colchicum 
given in gout, etc. Overwork and excitement are to be avoided. In 
early cases the process may sometimes be arrested. 

II. Hygienic and dietetic measures are along lines recommended in 
chronic nephritis, though in general less strict. In some instances, 
mental rest or moderation, rest in bed and a low diet restore health, 
lower blood-pressure and revive the heart. To start with, the Karell 
diet is excellent, later carbohydrates, fats, fruits and vegetables are given, 
but the quantity of the intake is closely watched. Soups, gravies or 
meat rich in purin bodies are prohibited; later some meat, especially 
boiled, may be allowed. The salt-intake may require regulation. If the 
patient is able to resume work, exercise is adapted to his strength and 
to the effects upon the blood-pressure, but long hours of sleep, and keep- 
ing the patient abed longer than the sleeping hours, are most effective. 
Daily, prolonged warm baths and moderate sweats are excellent. Mas- 
sage, a warm climate, passive exercise and the Schott method of treatment 
may be employed (page 323). Skoda employed hot hand- and foot-baths 
to reduce peripheral resistance. Saline laxatives may reduce hypertension. 

III. Drugs. — Iodide of potash is generally advised — 15 to 30 grains 
daily for twenty days; then during a ten-day intermission, nitroglycerin 
is used (see pages 227 and 335). In a non-syphilitic series of personally 
observed cases the walls of the nodular, hard vessels distinctly improved 
with administration of iodides. Rhomberg thinks that iodides operate 
less by vasodilatation than by decreasing the viscosity of the blood, and 
others believe that they stimulate the thyroid gland and Krehl warns 
against the symptoms of hyperthyroidism which iodides may elicit, as loss 
of weight (even resembling cachexia), nervousness and fever. Iodides are 
particularly indicated in arteriosclerotics with bronchitis. 

Hypertension is pathological, yet clearly conservative; with some 
clinicians 200 mm. is an indication for drugs, yet here or with even higher 
figures, it is best to consider how the heart functionates. Vasodilators 
must not be used indiscriminately. Nitroglycerin gr. -^ is equivalent to 
Tfliij of spiritus gly eery lis nitratis, gr. j sodium nitrite or gr. iss erythrol 
tetranitrite. Nitroglycerin acts for thirty minutes, nitrite of amyl for 
seven, sod. nitrite for sixty and erythrol for one hundred and twenty 
minutes. The amyl pearls should be protected from the light, the spirits 
should not be diluted, as it thus deteriorates rapidly and the erythrol 
should be chocolate-coated. Nitroglycerin, if it initially reduces blood- 



400 DISEASES OF THE ARTERIES 

pressure, is not apt to maintain the lowered pressure, whereas sod. nitrite 
is more likely to maintain it, with repeated doses ; nitroglycerin operates 
very rapidly when simply placed under the tongue. Erythrol is prone to 
produce violent headache. Hewlett proved that amyl nitrite not only 
dilates the vessels but stimulates the heart. Vaquez employs spts. 
aetheris nitrosi, 5ss-j, over a protracted period. Lauder Brunton em- 
ploys pot. nitrate and bicarb., aa gr. x and sod. nitrite gr. j in a full 
glass of water. These remedies may produce a distinct fall of blood- 
pressure and yet they seem also to benefit in some other way, possibly 
by reducing pressure or spasm locally, e. g., in the coronary vessels. In 
considering their action, one must remember that spontaneous reduction 
of pressure may occur. 

Chloral hydrate, gr. v-x, often operates better than nitroglycerin, 
in pain, high tension, insomnia and nervousness (combined with bro- 
mides). Chloral operated very successfully in one case with pressure 
of 315 mm. in which nitroglycerin always induced delirium. Coffee 
may relieve anginal and abdominal pains. Venesection, iron and digitalis 
are indicated when the heart muscle weakens. Huchard advises the 
following pill: 

1$ — Sodii iodidi 5J 

Sparteinse sulphatis gr. xv 

Pulv. glycyrrhizse q. s. 

M. et fac in pil. no. xl. 

S. — One after meals. 

Rest is more efficacious than are cardiants. Morphine is a valuable 
nervous sedative, tonic and possibly a vasodepressant for severe cases of 
cardiac asthma, but must be used with great care. 

ANEURYSM, 

Definition. — A dilatation, usually localized and sac-like, of an artery. 
Aneurysm was described by Galen, Vesalius who made the first diagnosis, 
Pare, Lancisi and Morgagni. 

Etiology. — (a) Syphilis is the most important cause; it was estimated 
at 80 and 100 per cent. The Wassermann reaction proves that the 
relationship between syphilis and aneurysm is as well established as that 
between syphilis and locomotor ataxia. Lancisi, in 1728, first recognized 
"venereal aneurysm", (b) Trauma is an overestimated factor. Sudden 
effort with weakened aorta may induce partial rupture of the aorta with 
consecutive aneurysm, (c) Sex: aneurysm is from two to eight times as 
frequent in males as in females, (d) Age: the old statement is still 
valid that aneurysm occurs before and arteriosclerosis after the fiftieth 
year; 80 cases under twenty years of age were collected by Le Boutillier 
(1903). (e) Embolic and mycotic aneurysms are usually small and may be 
multiple in the small vessels. Lewis and Schrager collected 97 cases 
(1909). (/) The traction aneurysm at the ductus arteriosus Botalli is rare. 
(g) The arrosion aneurysm, in which the inner coats bulge out when 
the adventitia is eroded, occurs largely in tuberculous cavities. The 
"aneurysmal diathesis" is spoken of by older writers; Pelletier found 
63 in one case. Multiple aneurysms of the arch are clearly syphilitic. 



ANEURYSM 401 

Pathology. — The varieties are: (a) True aneurysm, in which the sac 
consists of one or more coats, very rarely all three arterial coats. The sac 
is usually (i) fusiform and diffuse, or (ii) sacculated and circumscribed. 
(b) False aneurysm, in which all the coats rupture, or in which one coat 
ruptures through the others, like a hernia. These are circumscribed or 
diffuse, especially in the transverse arch and abdominal aorta, (c) Dis- 
secting aneurysm, wherein the intima of the vessel ruptures and the blood 
channels down the vessel between the intima and media or between the 
layers of the latter; it is a partial rupture. The rupture back into the 
aorta is an attempt of nature toward recovery; the patient may live for 
years, (d) Varicose aneurysm, wherein the sac ruptures into, e. g., 
the innominate vein or cava; this form is also called arteriovenous, or 
aneurysmal varix when the main change is in the vein. 

Atheroma occurs very frequently in comparison with aneurysm; and 
the pathology of aneurysm is that of syphilitic mesaortitis; at the roof of 
the aorta, fleshy nodes develop in the media and adventitia; about the 
vasavasorum, cellular infiltration occurs which later necroses; cicatrization, 
shrinking or dilatation results ; that these lesions are luetic, is attested by 
the history, presence of spirochetes (Reuter, Benda) and by the positive 
Wassermann reaction in 66 to 85 per cent. (v. pages 208 and 219). In 
the sac, thrombi form from the roughened intima and slowed circula- 
tion and to a small extent guard against extension and rupture. Aneu- 
rysm occurs at those points in the aorta on which the blood stream 
impacts most strongly; 59 per cent, of thoracic aneurysms occur on the 
anterior surface of the ascending aorta, 29 per cent, on the convexity 
of the arch and 12 per cent, on the posterior surface of the descending 
segment. Aneurysm of the pulmonary artery occurs in but 0.4 per 
cent. 

Symptoms. — Bramwell distinguishes three classes of cases: (a) Those 
which are entirely latent, and become manifest only by rupture or at the 
autopsy, (b) Those presenting symptoms of intrathoracic pressure but 
without physical signs, (c) Those signalized by distinct physical signs, 
e. g., by pulsating expansile tumor. 

The Subjective Evidences of Aneurysm. — A disproportionate 
value attaches to the symptoms, because of its frequent latency or the 
variability or disappearance of its signs when the aneurysm changes the 
direction of its growth. 

1. Pain. — Pain is either' intrinsic, resulting from aortitis, localized, and 
dull or aching in character; or it is extrinsic, resulting from pressure on 
nerve trunks, especially in deep-seated tumors, or from the weight of the 
aneurysm, as illustrated by Stokes's case in which pain was relieved 
by the use of crutches. Pain in the majority of cases is the first, the most 
notable, and most enduring symptom. It is often alleviated by iodides, 
which is suggestive of aneurysm; it is usually paroxysmal, lancinating 
or boring in character (when, for instance, the spine is eroded); it is 
augmented by movement, but may cease when the part compressed is 
entirely eroded. The pain is local or is reflected into the brachial plexus, 
arm, neck or may cause numbness and paresis of the arm. Inter- 
costal neuralgia is always suggestive of aneurysm. Though more usual 
26 



402 DISEASES OF THE ARTERIES 

anteriorly, pain is sometimes felt in the interscapular region. Anginal 
pain follows involvement of the cardiac plexus. 

2. Dyspnea. — Dyspnea is frequently out of all proportion to the findings. 
It is due to compression by the aneurysm of the heart, vagus or phrenic 
nerve, trachea, bronchi, lungs or pulmonary artery; or to compression 
of the plexus cardiacus or pulmonicus, producing bronchial spasm, and 
laryngeal spasm or paralysis. Dyspnea may occur with change of posture; 
it is paroxysmal and may subside entirely. 

3. Cough. — Cough is one of its least distinctive features. It results 
from pressure on the air passages, vagus irritation, bronchitis or laryngeal 
involvement. It is often unproductive. Like all other eccentric pressure 
symptoms, it varies with the size and direction of the aneurysm, and it 
is paroxysmal (Morgagni). 

4. Difficult swallowing results from direct compression, from pressure 
on the recurrent laryngeal nerve, inducing esophageal spasm, or most 
often from adhesions between the aneurysm and esophagus. It occurs 
particularly in low aneurysms of the "recurrent type" (v. page 404). One 
of the earliest aneurysms reported by Stokes was the size of an egg, and 
produced pain, dysphagia and compression of the left bronchus, with 
rupture into the latter. Dysphagia may be intermittent or present only 
in one posture. Its infrequency is explained by the ready lateral luxation 
of the esophagus. The danger of sounding the esophagus is well known; 
lethal hemorrhages have occurred in the physician's consultation room. 

5. Compression of the vagus results in asthma, laryngeal spasm, vomit- 
ing, stenocardiac attacks, hiccough or dysphagia. 

The Physical Signs of Aneurysm. — 1. Inspection. — Stokes described 
two distinct areas of pulsation in the chest, "like two separate hearts," 
most significant when the cardiac impulse is the weaker. Inspection is 
most advantageously made with the eye just below the level of the 
shoulder and near the chest. The typical expansile pulsation is best 
detected in superficial thin-walled aneurysmata in the ascending arch, 
or those presenting in the jugulum; pulsation is less a question of size 
than location. Visible pulsation may be absent even in the largest 
varieties; deeply situated aneurysms give diffuse or no pulsation. Throb- 
bing over the aorta is least important when there is also marked arterial 
pulsation (aortic regurgitation). The pulsation must be expansile to 
establish a diagnosis ; the author saw one case with an expanding throb- 
bing aorta and dulness over the arch which was due to massive callous 
connective tissue involving the pleura and pericardium. Another in- 
stance was observed in pernicious anemia; the hands placed over the 
left side of the chest, as well as near the spine were lifted widely apart, 
and the expansile pulsation was seen at a distance of forty feet; the 
autopsy revealed no aneurysm. Pulsation lent to a tumor, a collapsed 
lung, the liver or a pleural exudate is readily distinguished. 

2. Palpation. — Pulsation felt slightly later than the heart shock, is 
more obvious the slower the heart rate becomes. The expansile pulsa- 
tion is more easily detected by the fingers than by the eye. Palpation may 
reveal remittent tension of the sac, tenderness on deeper pressure, resist- 
ance caused by lamellated thrombi and, in rare cases, fluctuation of the 



ANEURYSM 403 

tumor during diastole. Pulsation in a deeply situated aneurysm is best 
elicited by placing one hand anteriorly and the other posteriorly on the 
chest. A thrill may be felt which is most commonly systolic. A diastolic 
shock sometimes occurs over the jugulum and aortic area (Lancisi), due 
to retraction of the hypertrophic aorta near the heart. 

3. Percussion.— Dulness is significant only when it is present to one 
side of the sternum, but not when confined to the sternum. Dulness in 
the left interscapular region is less valuable, because of the thickness of 
the chest wall. The dulness may so merge with that of the spine, heart, 
liver or spleen that no certain statement can be made. Aneurysms are 
often obscured by an emphysema, or they may grow from a deep origin 
into the lung substance. Dulness ceasing or shifting to another place, 
almost certainly indicates aneurysm. It is inexplicable that aneurysms 
often press upon relatively unyielding structures, while the softer parts 
in their immediate vicinity, as the lungs, are less compressed. 

4. Auscultation is frequently negative, even in large sacs — explained 
by thrombi in the sac and weak heart action. Two clear tones are most 
frequently heard; the second circumscribed tone is pathognomonic of 
aneurysm especially of the ascending arch, and originates in the aneurysm 
itself (not in the closure of the aortic cusps). The frequent systolic mur- 
mur is blowing, roaring or scraping; it is due to vibrations in the aortic 
wall, to entrance or exit of blood from the sac, to blood currents, thrombi, 
or more rarely to pressure of the sac upon the aorta itself. 

The less frequent diastolic murmur is probably caused by (relative) 
aortic insufficiency, when the aneurysm lies in the first part of the aorta. 
It may be due to folds in the aorta or to dissection of the aneurysm into 
the sinus Valsalvae. A continuous murmur is rare. Of 132 cases only 12 
presented a systolic murmur, 25 gave systolic and diastolic murmurs, and 
in 6, diastolic murmurs alone were found (Sansom). Douglas Powell 
detected murmurs in about half of his cases of sacculated aneurysms. 

The Heart. — Its position varies with the size and location of the 
aneurysm, (a) Large aneurysms of the ascending aorta not only depress 
it, but cause such axial rotation that the left lies lower than the right 
ventricle; this type may cause pressure atrophy of the right ventricle. 
(b) Aneurysm of the undersurface of the arch may dislocate the heart to 
the median line, (c) Aneurysm of the descending segment may flatten the 
heart against the chest wall, simulating mitral regurgitation, (d) Second- 
ary aneurysmatic outgrowths from the chief aneurysm complicate the 
physical findings; and sometimes attain incredible proportions, (e) In un- 
complicated cases myocardial alteration is entirely accidental. The most 
violent aneurysmal pulsation Stokes ever witnessed occurred with marked 
myocardial atrophy. Failure of the heart to hypertrophy is explained by 
coronary disease or compression of the pulmonary artery, thereby decreas- 
ing the flow of blood to the left heart and coronary arteries ; compression 
of the pulmonary artery may cause relative tricuspid regurgitation or 
pulmonary insufficiency. Hypertrophy of the left ventricle bears an inti- 
mate relation to aortic leakage ; it may in rare cases result from aneurysm 
involving the entire periphery of the aorta. Stokes's early observations 
recount every symptom of aneurysm. 



404 DISEASES OF THE ARTERIES 

The Vessels. — The pulsus differens is frequently physiological, and 
the right radial is normally larger than the left, whence if the right 
radial pulse is smaller, it means more than if the left were slightly smaller. 
When the radials differ, it is advisable to compare the brachials. When 
one radial is small, its fellow ulnar is often vicariously larger. A pulse 
may grow smaller and later return to its normal size, due to change in 
the size and the direction of the aneurysm. Asymmetrical blood-pressures 
may be due to other causes than aneurysm, as atheroma, coagula, em- 
bolism or reduction of the lumen of a vessel by the dragging of the aneu- 
rysm or compression of the aorta by a sac between it and the spine. 
Changes are observed most often in the carotid and subclavian vessels. 
The pulsus paradoxus and capillary pulsation may occur with large 
aneurysm. Retardation of the pulse occurs especially in fusiform aneu- 
rysms. An aneurysm sometimes may be localized by regarding the 
vessels altered. If pressure is exerted upon the superior cava, dropsy of 
the upper portion of the body, of one or both arms, swelling of the face 
and of the tongue, sometimes exophthalmos and a "brawny" or "collar- 
like" distention of the neck occur. Obstruction above the azygos vein 
causes lividity and edema which are confined to the head and arms; when 
it occurs below that vessel the chest is also congested. The innominate 
and azygos veins or the venae cavse may be obliterated. Rupture into 
the superior cava is attended by cyanosis, and a continuous bruit (also 
heard in vascular sarcomata or aneurysms rupturing into the pulmonary 
artery or right ventricle.) In Ewart's case (not suspected during life) 
phlebotomy was performed, and bright-colored blood escaped in jets. 

The Respiratory Tract. — Tracheal tugging, described by Oliver 
and Cardarelli simultaneously, is elicited by lifting the larynx with 
the fingers; a tugging sensation in the trachea is then felt with each 
systole; this symptom occurs also in left ventricle hypertrophy and 
in tracheal adhesions. 

Tracheal pulsation may be demonstrated by the laryngoscope in many 
aneurysms. The examination should be made by direct sunlight, and 
the observer should sit before the standing patient. It also occurs 
in tumors which compress the trachea, and physiologically. A short 
systolic murmur can sometimes be heard over the trachea when the 
patient breathes quietly with the mouth open. 

Recurrent laryngeal paralysis was first described by Morgagni and 
Todd was the first to note laryngeal muscular atrophy. Unilateral 
paralysis with the cadaveric position of the vocal cords, in the absence 
of other causes, is indicative of intrathoracic aneurysm, neoplasm or 
mitral stenosis. The cough is hoarse, clanging or brazen. It is a par- 
alytic cough, i. e. f an imperfect expiration which lacks forcible closure 
of the glottis observed in ordinary coughing; it was called the bovine 
cough by Wyllie, from the fact that cattle have no false cords whose 
closure is an important mechanism in coughing. The right recurrent 
laryngeal nerve, curving around the subclavian artery, does not enter 
the thorax, and is therefore seldom involved; whereas the left recurrent 
nerve passes into the chest and curves between the aorta and left bronchus ; 
Dieulafoy described a "recurrent type of aneurysm," which is usually 



ANEURYSM 



405 



small, syphilitic in origin, often multiple, involves the left recurrent 
nerve, and causes spasm of the larynx, due to recurrent laryngeal irrita- 
tion contracting the posterior transverse arytenoid muscle and inducing 
dyspnea and inspiratory stridor. Irritation of other vagus branches 
induces spasmodic dysphagia, anginal pain, etc. 

Lung Symptoms. — Stenosis of the right bronchus is less frequent 
than that of the left, which lies nearer the aortic arch. The lung moves 
less freely than normal; it suffers inspiratory retraction, and the breath 

sounds and fremitus are dimin- 
ished; at times air may escape 
only during the diastole. A short 
note elicited over the left upper 
lobe may arouse suspicion of the 
"recurrent type." 

Rokitansky's dictum that large 
aneurysms are almost never asso- 




Fig. 30. — Dieulafoy's diagram of the region 
in which he describes his "recurrent type" 
of aneurysm; posterior view. A, aorta, in 
contact with the trachea and left bronchus; 
L, larynx (seen from behind) ; p, left and p', 
right vagus; r, left recurrent laryngeal nerve, 
passing under the aorta, and r' , right recur- 
rent, in relation to the subclavian artery. 




Fig. 31.— Dieulafoy— I- VI I, multiple 
syphilitic aneurysms. 



ciated with pulmonary tuberculosis, was disproved by Stokes ; tuberculosis 
results in 13 per cent, of cases of aneurysm from compression of the 
pulmonary artery or decreased lung excursion. 

Bronchiectasis, bronchorrhea and suppuration of the lung are well called 
"aneurysmal phthisis" by Osier and Ross. Pulmonary retraction is 
observed from compression or adhesions. Pleurisy with effusion may 
complicate and entirely obscure an aneurysm. Gangrene of the lung or 
bronchial mucosa occurs from compression of the nutrient artery of the 



406 DISEASES OF THE ARTERIES 

lung or stagnation of mucus; it may produce subcutaneous emphysema. 
Pulmonary hemorrhage may occur from gross rupture into a large tube, 
from mere granulations in a compressed tube, or from an aneurysm 
slowly leaking into the parenchyma of the lung. The hemorrhage 
may be continuous, premonitory or fatal; it may be seen as flecks in 
the sputum, as rusty sputum, as prune-juice expectoration, as pure blood 
or more frequently as partly coagulated blood. 

Sympathetic Symptoms. — The pupils are often involved; myosis 
results from sympathetic paralysis and high blood-pressure, and mydriasis 
from sympathetic stimulation and low blood-pressure. Irregular, im- 
mobile pupils, absence of the patellar reflexes and tabes compose the 
Babinski syndrome. 

Diagnosis. — The clinical signs and symptoms are most variable (Stokes). 
The presence of an aneurysm should be suspected when marked pain 
or paroxysmal dyspnea occurs. Variability of physical signs is suggestive 
of aneurysm. 

Early Diagnosis of Mesaortitis. — The sole therapeutic hope lies 
in the early recognition of aortitis. In the secondary stage of lues, 
its incipiency is marked substernal soreness, slight paroxysmal dyspnea 
and angina, pulsation of the cervical vessels, cardiac hypertrophy, 
substernal dulness and a positive Wassermann reaction in 85 per cent. 
(Longcope and Donath). 

Diagnosis of Location. — 1. Aneurysm of the ascending portion, 
called "aneurysm of physical signs," is most often observed in the first 
interspace to the right of the sternum, which is often eroded. Luxa- 
tion of the heart to the left, radial slowing, compression of the superior 
cava and pulmonary artery with hypertrophy of the right ventricle, 
dyspnea and phthisis occur. Anginal or other cardiac symptoms are 
frequent, and the aneurysm, however small, is usually rapidly fatal from 
rupture into the pericardium, pleura, upper cava or heart chambers. 
Aneurysms just above the valves tend to grow downward because of the 
reflux of blood from the aorta, whereas those located higher grow upward 
because of impact of blood from the left ventricle. Sympathetic involve- 
ment is common. 

2. In the arch, the "aneurysm of symptoms" is observed with left 
recurrent paralysis or spasm, stridor, pulsation in the jugulum, unusual 
prominence or luxation of the sternal ends of the clavicles, prominence 
of the subclavian arteries, dulness to the left of the sternum, myosis, 
slowing or lessening of the left radial pulse, compression of veins, par- 
ticularly the left innominate, the trachea, thoracic duct, sympathetic 
ganglia, bronchi and left upper lobe, and disturbance in the brain cir- 
culation (hemiplegia) when the carotid artery is occluded. These 
aneurysms usually grow backward. 

3. In the descending segment, the "aneurysm of latency" is most 
often encountered. If there are symptoms, pulsation in the left inter- 
scapular region, slowing of the femoral pulse, pressure on the azygos or 
hemiazygos, pressure on the spine with erosion and tenderness to touch , 
intercostal neuralgia (sometimes with recurrent attacks of herpes zoster) , 
stenosis of the left bronchus or esophagus, pressure upon the heart, 



ANEURYSM 407 

forcing it against the sternum, and increased heart rate from plexus 
pressure, are present. The arrays alone detect aneurysms lodged in the 
lung substance; pulsation is often observed, but not invariably. Letulle 
in three years detected 27 latent aneurysms by the x-rays alone. 

The Wassermann test was present in 74 per cent, of 182 cases (Long- 
cope), and in 92 per cent, in those under forty years of age (Harris). 
To illustrate the associations of aneurysm, Chiari found that 59 per 
cent, of luetics had mesa-ortitis syphilitica and Straub found 84 per cent, 
of paretics with mesa-ortitis. 

Differentiation. — Differentiation from solid tumors is determined 
by their propagated non-expansile pulsation, their more rapid develop- 
ment, leukocytosis, adenopathy and cachexia. In aneurysm the lymph 
glands are rarely enlarged. Pain, recurrent paralysis and dysphagia 
are common to all tumors, aneurysmatic and neoplastic. Venous 
ectasia is more common in tumor. A few rare instances of coincidence 
of tumor and aneurysm are observed. The pulsation in carcinoma is 
rarely associated with a diastolic "back stroke," which is frequent in 
aneurysm. An unequal pulse suggests aneurysm or atheroma. The 
bruit in tumor is usually systolic, but murmurs are frequently absent 
in aneurysm. Tugging is present in both but more common in the 
latter. Aneurysm runs a much more protracted course than tumors. 
Exploratory puncture, the x-rays and diagnosis ex juvantibus with 
mercury and iodides are of differential importance. 

Other causes for pulsation, such as a dynamic throbbing (aortic regur- 
gitation), throbbing in acute aortitis, pulsation in an aorta dislocated 
from kyphosis, and pulsation in pneumonia, anemias, or in vascular 
tumor of the lung or pleura, are usually differentiated when all symptoms 
and signs are carefully considered. In pulsating empyema the dulness 
is usually low in the chest and largely left-sided; puncture reveals pus 
and stops the pulsation. 

Prognosis. — Recovery is rare, though spontaneous cure is possible 
by compensatory thickening of the intima or by organization and calci- 
fication of thrombi in the sac; Adami collected 39 cures. The course is 
generally two years. The author watched for twelve years a blacksmith 
who worked, though he had an aneurysm of the ascending aorta, which 
was as large as his fist, and which protruded beyond the ribs. The size 
of the sac is of no. prognostic value. Those of the small "recurrent 
type" are most dangerous, and large ones may be protected by connective 
tissue. 

Mechanism of Death. — (a) Rupture occurs in 75 per cent, of cases: 
20 per cent, into the left and 13 per cent, into the right pleura; into 
the left bronchus 16; into the pericardium 12; into the left lung 9; 
externally 6; into the esophagus 5; into the trachea 4 per cent.; (6) 
suffocation; (c) marasmus; (d) intercurrent disease; (e) embolism; and 
(/) brain lesions. Hemorrhage usually shortens the course, but in one 
case rupture into the bronchus occurred five years before death. Another 
patient suffered external rupture of the sac; he collected the blood 
in a basin and, though he fainted from the hemorrhage, he lived four 
months, only to die of typhus fever. Stokes described an external 



408 DISEASES OF THE ARTERIES 

rupture in which the presence of mind of the nurse, in stuffing some 
cloth into the sac, kept the patient alive for a considerable time. 

Treatment. — 1. The Tufnell treatment dates from Morgagni, Albertini 
and Valsalva, without the venesection recommended by Valsalva, i. e., 
absolute mental and physical rest for several months, and food reduced 
to the minimum. The blood-pressure is greatly lessened. The treatment 
is of value only in cases of sacs with small necks. 

2. Iodides were given prominence by Balfour, though used first by 
Bouillaud. They increase the secretions but do not inspissate the blood. 
It is questionable whether arterial tension and dilatation of the sac are 
lessened; it is certain that pain is alleviated. Twenty grains are given 
at a dose (v. page 399). Aside from relief of pain, they are useless in fusi- 
form or large aneurysms with wide communications. 

3. Cold applications may relieve pain when the sac is superficial. 
Supports may relieve the pain and protect against rupture. Calcium 
chloride does not promote coagulation. 

4. Gelatin injections (1 per cent, solution) are recommended by Lan- 
cereaux to produce coagulation in the sac; the results are not convincing. 
There is danger of embolism and tetanus (q. v.). 

5. Electrolysis, introduction of fine wire, compression and surgical 
intervention have given discouraging results. A few recoveries are 
reported but one cannot help comparing their small number with the 
probably equal number of spontaneous recoveries (Borger, in 1906, 
compiled 19 cases of dissecting aneurysms of the aorta which recovered). 
Fatal thrombosis or total embolism of the aorta may occur. 

6. Dyspnea is treated as in cardiac disease. Venesection may afford 
temporary relief, and morphine is finally indicated. Tracheotomy may 
be necessary in laryngeal spasm (reflex recurrent irritation) but the actual 
compression by the sac is usually too low for operative interference. 
Digitalis is at all times contra-indicated. 

Abdominal Aneurysm. — Constituting 5 per cent, of aneurysms of the 
aorta, over two-thirds occur in the upper abdomen and 40 per cent, 
at or above the celiac axis. The average size is that of an orange and the 
tumor usually develops from the anterior surface of the vessel and grows 
downward. Most are false aneurysms. 

Symptoms and Signs. — Four per cent, of abdominal aneurysms are 
latent clinically; a good-sized sac may be hidden under the arch of the 
diaphragm. Pain is severe, boring and constant or paroxysmal; it 
may lessen after hemorrhage from rupture. Indefinite gastric symptoms 
are less frequent than duodenal, where obstruction and hemorrhage may 
occur. Inspection shows pulsation in 65, expansile pulsation in 15 and 
tumor in 57 per cent. Palpation may elicit the expansile pulsation and 
in some cases a thrill. Percussion may reveal dulness but its close 
relations give indefinite findings; the diaphragm bounds the aneurysm 
above ; the kidney to the left ; the liver, pancreas and kidney to the right ; 
and the stomach, pancreas and colon in front. The tissues about the sac 
thicken and produce adhesions. On auscultation, a systolic murmur 
obtains in 50 per cent, or two tones are heard; a diastolic murmur is 
sometimes heard. Rupture, diffusion by dissection, great thickening 



ANEURYSM 409 

of the sac and thrombus formation may easily obscure all auscultatory 
signs. 

Diagnosis. — In two-thirds of the cases an incorrect diagnosis is made. 

1. Compression symptoms, gastric and duodenal, may suggest ulcer or 
cancer. The spine, eroded in 10 per cent, of cases, may simulate lumbago, 
myelitis, Pott's disease and spinal tumor. Pulsation should be searched 
for along the spine. The affection may suggest renal colic, kidney tumor, 
perinephritis or psoas abscess (fluctuating blood from rupture). Press- 
ure on the splenic vein may provoke much splenic enlargement. The 
heart is rarely compressed. Retardation or absence of the femoral pulse 
and dyspnea may be of value in differentiation. • 

2. Abdominal Pulsation. — "Instead of being your first, it should 
be your last idea that abdominal pulsation is due to aneurysm" (Jenner). 
Epigastric pulsation may be confused with cardiac hypertrophy, liver 
pulsation, the dynamic pulsation of aortic regurgitation, the pulsation of 
acute hemorrhage, or especially neurasthenic pain and throbbing, with 
thrills, systolic and even diastolic murmurs — Rosenbach's "intermit- 
tent dilatation of the aorta." The pulsation must be distinctly expansile 
(even then occasional errors are made) and a definite sac must be felt. 

3. Communicated throbbing, lent to a tumor of the stomach lying 
on the aorta, may also be attended by a systolic murmur but the differ- 
entiation is usually made with ease, except in soft neoplasms. Tumors 
are often felt to better advantage in the genupectoral attitude; they 
are more movable, more often produce dilated veins and ascites. Ab- 
dominal aneurysms may, in exceptional cases, be movable. Stokes 
held that tumors developed upward and aneurysms downward. 

4. (a) Aneurysms of the celiac axis are difficult or impossible to dis- 
tinguish. Over 20 cases are recorded. They are often traumatic or 
embolic (mycotic), (b) Superior (20 cases, Baccelli, 1904) or inferior 
mesenteric aneurysms occur most frequently in children, from sepsis, 
(c) Over 20 cases of splenic aneurysm are recorded. The spleen is often 
enlarged, (d) In the hepatic artery (40 cases, Rolland, 1908) it is 
induced by acute infections (73 per cent.), trauma, embolism or gall- 
stones; 41 per cent, develop in the main trunk and 25 per cent, in its 
right branch; in but 1 case did it develop in the artery of the cystic 
duct. Pain (71 per cent.), hemorrhage (58 per cent.), icterus (63 per 
cent.), vomiting and large spleen have been noted; in 79 per cent, rupture 
occurred (in 10 cases into the peritoneum); they never pulsate; but once 
was there a systolic murmur; Kehr operated successfully, (e) Over 10 
aneurysms of the coronary artery of the stomach are recorded. (/) Renal 
aneurysm is rare (26 cases, Skillern, 1906; in 3 operation was successful). 

Prognosis. — The clinical course averages one to three years. Rupture 
occurs in 70 per cent. : 33 per cent, into the peritoneum; 16 per cent, into 
the pleura; 7 per cent, into the duodenum; and 7 per cent, into the retro- 
peritoneal tissue. Death does not necessarily nor at once follow rupture. 

Treatment. — Treatment is as in the thoracic type. From its acces- 
sibility, operative procedures are more common and somewhat more 
successful. Continued compression of the aorta has benefited cases 
of aneurysm located low in the abdomen. 



410 DISEASES OF THE ARTERIES 

ACUTE AORTITIS AND ARTERITIS. 

These are rare lesions, occurring in the aorta and associated with 
syphilis (v. page 208), aneurysm (v. page 401), sepsis, endocarditis, or 
in the peripheral vessels after influenza or other infections. 

Of periarteritis nodosa (Kussmaul and Maier, 1866), or "arteritis pro- 
liferans nodosa," only 26 cases have been published; it consists of local- 
ized proliferation and round-cell infiltration of the intima, with its 
rupture through the other coats, and leads to thrombosis or aneurysm. 
It is probably an infection. It occurs largely in men between twenty 
and thirty-five, years of age. The nodes are seen in the vessels of the 
muscles, heart, kidney, intestines and skin; they produce hydrops, 
muscular pains, nephritis, convulsions, paralysis, vomiting, diarrhea, 
alimentary hemorrhage, epigastric pain, low temperature and a rapid 
pulse. The affection is fatal within six to twelve weeks and is usually 
mistaken for typhoid or meningitis. In one-quarter of the cases syphilis 
was an antecedent and one patient recovered under mercury. 

RUPTURE OF THE AORTA. 

Rupture results from trauma, endarteritis or narrow aorta. But 6 
cases of rupture of a sound aorta are known and only 48 cases of spon- 
taneous rupture. All coats may be ruptured, usually transversely. If 
the rupture is partial, the resulting aneurysm may dissect even to the 
popliteal arteries. It most often occurs in the first segment when hemo- 
pericardium results, or into the lung, mediastinum or retroperitoneal 
connective tissue. The symptoms are sudden pain, a sense of "some- 
thing ruptured" and acute anemia; sudden death is usual, though 
patients with dissecting aneurysm may live eleven years or even recover. 

Embolism of the aorta is due to impaction of atheromatous plaques, 
tumor tissue, echinococcus cysts, endocarditic plugs or ordinary thrombi. 
It is very uncommon. Sudden death results if embolism occurs in the 
first part of the vessel. If it occurs near the iliacs, collateral circulation 
is possible. There are pain and stiffness in the legs, sensory disturbances, 
paresis and contractures from anemia of the spinal cord. The femoral 
pulsation is absent. The bladder and rectum are disturbed. Hemorrhage 
from the stomach, bowels and kidneys has been observed. The clot 
may back up toward the heart or it may resorb. The prognosis is bad 
and the treatment is symptomatic. Thrombosis results from infections, 
weak heart, aneurysm, atheroma or compression, mostly in the transverse 
arch or abdominal aorta at its division. Its pain, paraplegia or anes- 
thesia is sometimes confused with spinal cord disease. If gradual, 
collateral circulation may be established. 



SECTION III. 

DISEASES OF THE KESPIKATOKY 

TRACT. 



DISEASES OF THE NOSE. 

ACUTE RHINITIS, CORYZA. 

Definition. — An acute nasal infection. 

Etiology. — (a) It is an independent infection, sometimes epidemic 
in the spring and fall; cold is only a predisposing factor. The most 
common organisms are the Micrococcus catarrhalis, Micrococcus para- 
tetragenus, Bacillus septus, Bacillus Friedlander, and probably the 
Bacillus influenzas and pneumococcus; 80 per cent, of cultures are nega- 
tive. (6) It is a concomitant of various infections, notably of influenza, 
measles, pertussis, etc. (c) Toxic factors, as iodides, bromides, ipecac dust, 
dust, etc., may cause coryza. (d) Local disease, as chronic catarrh, polyps 
and ulceration are predisposing factors. 

Symptoms. — The initial symptoms are depression, chilliness, fever of 
101° to 102°, pains in the limbs and sometimes, in the young, delirium. 
The mucosa is dry, reddened, painful and swollen. There is repeated 
sneezing and anosmia. Herpes is common. There follows a clear, watery, 
nasal discharge (coryza) for one or two days, which subsides at night and 
recurs in the morning; within two days it becomes thickened and purulent. 
Extension may occur to the eyes, frontal sinus, antrum of Highmore, 
ear, by the Eustachian tube, or to the pharynx or larynx. In infants 
nasal occlusion prevents nursing and may cause dyspnea, because the 
tongue lies so near the palate. Acute rhinitis lasts one-half to one week 
and is seldom confused except with incipient measles. 

Treatment. — At the very onset lavage with simple hot water is often 
sufficient; Dobell's solution (sod. borat. and sod. bicarb, aa 5ij> phenol 
3 ss to water 5 x), diluted freely to avoid irritation, is beneficial; adrenalin 
solution 1 to 1000 is excellent, but excessive application may induce 
edema of the throat and epiglottis. A cocaine solution (the plain alkaloid 
gr. j to albolene 5 j) relieves turgescence and frontal pain, but is a danger- 
ous remedy to give into the patient's hands. Dover's powder gr. x, 
a saline aperient and a hot bath at the onset, usually give relief, especially 
when followed by: 



412 DISEASES OF THE NOSE 

1$ — Extr. belladonrise gr. iiss 

Fluidextr. aconiti TH,x 

Acetphenetidini gr. xv 

Camphorse monobromatse gr. xv 

M. et ft. capsulae x. 

S. — One capsule every hour for five or six doses. 

1$ — Phenolis gr. iij 

Mentholis gr. iv 

Olei theobromatis q. s. 

M. et. fac suppositoria no. x. 

S. — One locally in nose every two hours. 
Menthol in infants may cause cyanosis and asphyxia. 

Drugs are futile unless the patient remains in bed. Salicylates mitigate 
the frontal pain. Cool baths may avert recurrence. 

HAY FEVER. 

Gatarrhus sestivus or summer catarrh, was first described by Bostock 
(1819). Morill Wyman described the "June" or "rose cold." 

Etiology. — The disease has long been attributed to the pollen of timothy, 
rag weed and golden rod. Dunbar demonstrated that pollen contains 
toxalbumins. It prevails especially in the United States and England, 
develops in persons between fifteen and thirty years of age, and twice 
as frequently in males as in females. It is more common in the educated 
classes, and is most prevalent in the warm months and in cities. Three 
special factors are noted: (a) A predisposition in the form of nervous 
instability, (b) A nasal irritability or turgescence, to dust, odors, etc., 
hyperesthesia of the inferior turbinates, polyps or septal irregularities; 
Austin Flint became asthmatic from sleeping on feather pillows, (c) 
The exciting irritant, as pollen, dust, sudden change of temperature and 
apparently in some cases, mental excitement. Local anaphylaxis is the 
most recent theory. 

Symptoms. — The onset is that of the vulgar coryza, but with greater 
constitutional depression. Injection of the eyes with lachrymation and 
photophobia accompanies or precedes the coryza. The throat, larynx 
and bronchi are dry and burning. Fever, 100° to 101°, is fairly common. 
There is pain over the frontal sinuses, sometimes over the temporal and 
occipital regions. The nasal vessels are congested and the nose itself 
becomes sivollen and injected, resembling closely the alcoholic facies. 
In many cases cough develops, frequently with asthmatic seizures like 
bronchial asthma {q. v.). Recurrences are usual and attacks of coryza 
may alternate with asthmatic paroxysms. With the first frost the 
affection stops, as if by magic. The outlook is good as to life, for death 
from asthma is rare; as to recovery, the outlook is much less favorable. 

Treatment. — (a) Prophylactic cauterization of irritable, congested or 
hypertrophic areas, and correction of polypoid or other abnormalities 
cure some cases and alleviate others, (b) Nasal treatment; much 
relief may be given by irrigating the nose with 1 to 1000 adrenalin or 
other astringent solutions; suprarenal extract in doses of gr. ij to v has 
been used internally, (c) The general physiological resistance is increased 
by fresh air, cool rubs, tonics and nervines, (d) Change of climate is 



RHINITIS FIBRINOSA 413 

advisable before the date on which, with certain regularity, hay fever 
appears; a sojourn at the seaside, in northern Michigan, Canada and in 
a high altitude, as the Adirondacks or White Mountains, greatly relieves 
or checks the symptoms, (e) Asthma (v. Bronchial Asthma). (/) 
Dunbar's serum, patented as pollantin, is used in the nose every morning, 
as a powder. In 1240 cases Dunbar claims that 56 per cent, were greatly 
helped, and 31 per cent, benefited. Vaccines are being tested. 

CHRONIC RHINITIS. 

Minor cases of chronic nasal catarrh are often treated by the prac- 
titioner; some are due to syphilis, anemia or to other constitutional 
causes. Chronic catarrh may develop from repeated acute attacks, 
or may be chronic from the onset. 

The Hypertrophic Form. — The nasal mucosa is red, swollen and 
covered with secretion which may desiccate and sometimes form rhino- 
liths; the vessels are wide and surrounded by round cells, and the sub- 
mucosa is thickened. The nasal obstruction necessitates oral breathing, 
partially nasal speech, obtunded taste and smell, and produces an 
elevation of the hard palate and a peculiar facial expression — often 
associated with adenoids and follicular hyperplasia in the pharynx. 
The secretion is usually thick, yellow and purulent, rarely thin and 
abundant. The lachrymal duct may be obstructed, and Eustachian 
occlusion may induce deafness; laryngitis, bronchitis, bronchial asthma, 
polyps and sinus disease are not infrequent complications. Nasal disease 
may be the cause of facial spasm, limitation of the field of vision, vertigo, 
mental depression and dysmenorrhea. In its treatment possible con- 
stitutional factors, as anemia, syphilis or scrofula are to be considered. 
Douches of carbolic acid, insufflations of equal parts of alum and calomel, 
and the cautery or chromic acid are indicated. Douches should be given 
under low pressure, lest fluid reach the middle ear. 

The atrophic form may begin as an atrophic process or result from 
hypertrophic disease. It usually begins early in life. The mucosa is 
pale, dry and metaplastic, the erectile tissue wastes, the nasal passages 
are unduly roomy and the secretion emits a most offensive odor {ozena). 
Its actual cause is not determined; it may originate in sinus troubles. 
Various microorganisms have been found, as the Bacillus fcetidus, mucosus 
and fluorescens liquefaciens. It is associated with a widening of the 
face in 33 per cent, of cases. Its sequences are those of the hypertrophic 
variety. The treatment is not satisfactory. Douches of a 1 per cent, 
permanganate of potash solution, iodoform insufflations, massage with 
iodine 1 part, potas. iodide 10 and glycerin 100 parts, and packing with 
gauze soaked in balsam of Peru are employed. Paraffin injections beneath 
the mucous membrane are recommended to restore the normal lumen of 
the nasal passages, 

RHINITIS FIBRINOSA. 

Rhinitis fibrinosa has been considered under nasal diphtheria, to which 
it is most often due. It may result from streptococcus and staphylo- 



414 DISEASES OF THE LARYNX 

coccus infection; it occurs in measles, scarlatina, pneumonia, typhoid 
and also as an independent lesion. Irrigation with 1 per cent, carbolic 
acid or 1 to 1000 sublimate solution is efficacious. 

EPISTAXIS. 

Epistaxis is a symptom only. Its causes are: (a) Local nasal lesions, 
trauma, catarrh, picking of the nose, foreign bodies, ulceration (simple, 
tuberculous, syphilitic, carcinomatous) and telangiectases of the skin 
and nasal mucosa, (b) Hyperemia, either venous, as in cardiac and 
respiratory lesions, or arterial, as in cardiac hypertrophy, interstitial 
nephritis, atheroma, etc. Some cases are seemingly vicarious to sup- 
pressed menstruation, (c) Acute infections, principally typhoid, (d) 
Hemorrhagic diseases, as pernicious anemia, chlorosis, leukemia, pseudo- 
leukemia, scurvy, hemophilia and cachexias, (e) Liver cirrhosis, icterus, 
and high altitudes are also causative. 

The most frequent point of hemorrhage is the lower anterior part 
of the cartilaginous septum. The symptoms are local hemorrhage from 
the anterior nares, but occasionally trickling into the pharynx may 
simulate hemorrhage from the stomach when vomited, from the intestine 
when passed with the stool, or from the lung when coughed up. Occasion- 
ally acute anemia or death may occur, especially in blood diseases. 

Treatment. — The Datient should be kept quiet, in the semi-erect 
posture. After douching the nose with hot or ice-cold water to which 
adrenalin 1 to 1000 has been added, the nose should be tamponed by 
Bellocq's catheter, or in less serious cases the patient enjoined not to 
blow the nose, for this only dislodges the forming clot. Gelatin may be 
injected into the nose. Horse serum excels internal remedies, as ergotin. 
Erosions or ulcers may be cauterized later. 



DISEASES OF THE LARYNX. 

ACUTE CATARRHAL LARYNGITIS. 

Etiology. — Acute catarrhal laryngitis is observed largely in males 
between twenty and forty, and in cold, windy, changeable weather, (a) 
Cold operates only by lessening the resistance, particularly in delicate 
subjects; the bacteriology of these " rheumatic cases" is unknown, (b) 
Acute laryngitis may complicate acute or chronic affections such as 
measles, pertussis, typhoid, hay fever and tuberculosis, (c) Extension 
may be caused per contiguitatem from the nose, pharynx or bronchi. 
(d) Chemical, thermal or mechanical agents, as dust, trauma, overuse 
of the voice, alcoholism, inhalation of tobacco smoke and internal use 
of iodides are etiological factors, (e) Stasis from thoracic lesions or 
enlarged thyroid, local ulcerations in the larynx, nephritis, liver disease 
and rhachitis are also causes. 



ACUTE CATARRHAL LARYNGITIS 415 

Symptoms. — Sudden fever or chill is seldom observed. The local 
symptoms are rawness or tickling, dry, even spasmodic cough, and moder- 
ate pain on breathing; external tenderness or dysphagia usually indicates 
coincident pharyngitis. After a day a thin, transparent sputum appears, 
which later becomes purulent, yellow or in very rare cases, hemorrhagic. 
Some cases void no sputum (laryngitis sicca). The voice becomes hoarse 
or is wholly lost. The laryngoscope reveals redness, viscid mucus, swelling 
and occasionally epithelial erosions. The false cords are often swollen. 
The true cords lose their smooth, glistening appearance and become 
uneven, so that their even coaptation is hindered. The swollen mucosa 
may get between the cords, and their infiltrated muscles are often paretic. 
The acute symptoms last for a day or two and the catarrh remains about 
a week longer. 

Diagnosis. — Nervous aphonia and cordal paralysis are distinguished 
by means of the mirror. (See Vagus Disease.) 

Treatment. — Alcohol and tobacco are forbidden. The general resist- 
ance is increased by cold rubbings, douches or baths; mufflers should 
be avoided and cold compresses should be applied over the larynx. The 
voice mu&t be used carefully and the nose, uvula and pharynx should 
be examined for predisposing lesions. 

At the onset sweating should be induced by hot drinks and a hot bath; 
Dover's powder gr. x or aconite, is indicated as in coryza; rest in bed 
is necessary. The voice must not be used. An ice-bag should be applied 
locally; codeine or morphine with bromides, and inhalations of moist 
air or steam should be given (v. Acute Bronchitis). Painting the 
larynx with a 3 per cent, silver nitrate solution may induce submucous 
extension and is not to be recommended. 

R- — Heroin, hydrochloridi gr. j 

Terpini hydratis gr. xl 

Ammonii chloridi 5ss 

Extr. glycyrrhizse 5j 

M. et ft. capsular xxx. 

S. — Two after meals. 

In children acute laryngitis is attended by great swelling above and 
below the cords and by stenosis of the small, infantile larynx, resembling- 
genuine croup (laryngeal diphtheria), from which it is distinguished 
as false croup, faux croup or laryngite striduleuse. After an attack of 
mild laryngitis, coryza or sore throat, the child becomes restless and 
anxious, usually during the night when the secretion accumulates. 
Inspiratory dyspnea develops, there is inspiratory retraction of the inter- 
spaces and epigastrium, the accessory muscles of respiration come into 
play, cyanosis appears and asphyxia seems imminent. The paroxysm 
subsides, spontaneously or after an emetic has been given, to recur on 
the next two or three nights. Trousseau remarked that there is rarely 
that complete aphonia observed in laryngeal diphtheria. The diagnosis 
is made from the history of coryza; the absence of diphtheritic patches 
in the pharynx and of diphtheria bacilli, found in diphtheria even when 
the throat seems normal; and the absence of severe constitutional 
reaction. Laryngismus stridulus (v. Vagus Nerve) is not attended by 



416 DISEASES OF THE LARYNX 

fever, laryngitis or aphonia. Laryngoscopic examination is notoriously 
difficult m easily frightened children. Treatment is the same as in adults; 
hot drinks, inhalation of steaming water and ipecac should be given to 
induce vomiting and evacuation of laryngeal secretion; the patient is 
awakened at intervals and given a hot drink to evacuate the mucus. 

Other acute forms are (a) laryngitis acuta nodosa, observed in rheu- 
matism and yielding to salicylates. (b) Laryngitis fibrinosa, which is 
usually diphtheritic, but may be streptococcic, in measles, scarlatina or 
other infections, (c) Laryngitis submucosa acuta invades the submucous 
tissues. This rare affection may develop as an independent lesion, may 
follow a similar process in the pharynx or may represent a septic local- 
ization. The invasion symptoms are severe, with fever, rigor and other 
septic phenomena. The laryngoscope shows injection and yellowish- 
white, bulging areas of submucous suppuration which, without operation, 
almost invariably cause death by edema of the larynx or by sepsis, 
for spontaneous rupture is exceptional. For treatment (a) an ice-bag 
should be placed over the larynx, morphine given for pain and whisky 
for the sepsis; (b) incision of the foci is indicated; and (c) if necessary, 
intubation or tracheotomy should be performed. 



CHRONIC CATARRHAL LARYNGITIS. 

Etiology. — The etiology is identical with that of the acute form, of 
which it frequently follows repeated attacks; it is often associated with, 
or is dependent on, pharyngitis or rhinitis. 

Symptoms. — The symptoms are those of the acute form. Hoarseness 
alternates with fairly normal phonation. By the mirror there may be 
seen injection, darker than in the acute form, swelling, secretion and 
sometimes hemorrhages. There are forms with no secretion (laryngitis 
sicca chronica). In some forms granules appear, from proliferation of 
connective tissue (laryngitis granulosa). Erosions and rhagades may 
develop on the edges of the cords. 

Treatment. — Prophylaxis is the same as in the acute form. Inhalations 
of 1 per cent, tannic acid or of 1 per cent, turpentine and sod. bicarbonate 
solution; insufflations of tannic acid, lead acetate and alum aa gr. j; 
and painting the larynx every third day with a 2 to 10 per cent, solution 
of silver nitrate with the aid of the laryngoscope, are valuable. Terpin 
hydrate gr. iij t. i. d. is often helpful. Sea air may be beneficial. 

Other Chronic Forms. — Chorditis tuber osa occurs as small, grayish 
nodes on the cordal edges at the junction of their anterior and middle 
thirds, especially in singers and in alcoholics; they are composed of 
fibrous and epithelial hypertrophy. Scarification and lactic acid are 
indicated (v. Tuberculosis). 

Pachydermia laryngis is an increase of the submucous tissue and 
transformed epithelium into which connective tissue grows. Warty 
excrescences are common between the arytenoids, and the thick mucosa 
may resemble cancer. Topical application of salicylic or lactic acid, 
iodine in glycerin, electrolysis and the cautery are indicated. 



PERICHONDRITIS LARYNGIS 417 

Laryngitis hypertrophica inferior is a hyperplasia of the tissues below 
the cords, and is identical with rhinoscleroma, due to the downward 
extension of the rhinoscleroma bacillus from the nose. It may stenose 
the larynx. It is treated by scarification, dilatation, prolonged intubation, 
iodides, or, when extreme, by tracheotomy. 

EDEMA OF THE LARYNX. 

Edema laryngis is a better designation than edema of the glottis, as the 
vocal cords are seldom involved. It is most marked in the submucous 
tissue, about the epiglottis and aryepiglottidean folds; 70 per cent, of 
cases occur in males and 89 per cent, in those over fifteen years. 

Etiology. — There are three etiological forms: (a) Inflammatory edema 
results from inflammatory diseases of the larynx, submucous suppuration 
or perichondritis; from typhoid, syphilitic, tuberculous or cancerous 
ulceration; from iodides, trauma, surgical measures, thermic, chemical 
and allied causes; extension from pharyngitis, parotitis or cervical 
cellulitis; and from infections, (b) Congestive and hydremic forms result 
from chronic heart and lung disease, tumors and nephritis, in which it 
may antedate edema elsewhere, or from cachectic conditions, (c) Angio- 
neurotic edema, as in R. S. Morris's fatal case, is the last type. 

Symptoms. — Symptoms appear with varying acuity, sometimes 
suddenly, as in Bright's disease, at other times gradually but progres- 
sively. Hoarseness or aphonia, and a metallic cough are common. The 
chief sign is inspiratory dyspnea, which characterizes nearly all forms of 
laryngeal stenosis. It is usually stridulous, and is attended by retraction 
of the interspaces, cyanosis, up-and-down excursion of the larynx and 
ultimate suffocation. The mirror shows a pallid swelling on incision of 
which a clear serum escapes. Edema of the epiglottis and aryepiglotti- 
dean folds may be felt with the finger if the tongue is drawn forward, or it 
may be seen without the mirror if the larynx is pushed up and the tongue 
depressed. 

Treatment. — Treatment is urgent, irrespective of the cause, for the 
75 per cent, mortality is due to delay until the patient's strength 
is exhausted. Ice over the larynx, purgatives and painting the larynx 
with a 10 per cent, silver solution are at best palliative. The edematous 
tissue should be fully incised, and in case this should fail, intubation or 
tracheotomy should be performed. 

PERICHONDRITIS LARYNGIS. 

Purulent perichondritis of the larynx nearly always results secondarily 
to various inflammations or ulcerations. Pus accumulates most fre- 
quently under the arytenoid or cricoid perichondrium. The cartilage 
may necrose secondarily. Perichondritis laryngis most often develops 
in males between twenty and forty years of age. 

Symptoms. — Its symptoms are commonly obscured by the causal 
disease. The rare primary cases are the most acute. Well-localized 
pain and tenderness are peculiarly significant. Dysphagia, especially 
27 



418 DISEASES OF THE TRACHEA AND BRONCHI 

from arytenoid involvement, is frequent, and even aphagia may result. 
Phonation is impaired by the fundamental disease, cordal paresis and 
muscular infiltration. The cervical glands sometimes tumefy. Stenosis 
and dyspnea are present. The mirror discloses focal accumulation of pus, 
swelling, redness, edema and perhaps fistulae from intralaryngeal rupture. 
The probe may scrape on eroded cartilage. Differentiation from laryngitis 
and edema is impossible, unless definite pus pockets are seen. The 
outcome may be suddenly fatal from rapid edema; pus and cartilage 
fragments may rupture, thus giving relief or perhaps occluding the larynx; 
fistulas may remain, and may burrow to the mediastinum; sepsis and 
aspiration pneumonia are not uncommon, and if recovery ensues, a 
distorted or stenosed larynx may remain. 

Treatment. — Pain should be relieved by opiates, but early incision 
under cocaine, or tracheotomy or intubation is necessary. 

ULCERATIONS AND NEOPLASMS OF THE LARYNX. 

The tuberculous, leprous and syphilitic ulcers and glanders have been 
considered. Superficial erosions may follow catarrh; deep ulcers result 
from submucous suppuration, perichondritis, pressure by foreign bodies 
or laryngeal " bed-sores" analogous to intestinal ulceration in typhoid, etc. 

Tumors include the benign singer's nodes (v. s.), fibromata, cysts, 
enchondromata, lipomata and the malignant tumors of which carcinoma 
is far more frequent than sarcoma. Primary cancer develops as an ex- 
crescence which assumes a cauliflower appearance; the basis of the later 
ulceration is nodular (v. page 209); hoarseness is an early symptom; 
incipient tumors are easily mistaken for laryngitis. Pain radiating to 
the ears or temples, cough and dysphagia are constant in the advanced 
stage. Early operation alone affords relief; inoperable cases must be 
narcotized. 

Nervous aphonia, the paralyses and spasms of the larynx are considered 
under Affections of the Vagus Nerve. 



DISEASES OF THE TRACHEA AND BRONCHI. 

Tracheitis is frequent with laryngitis and bronchitis. Hemorrhage 
may result from ruptured varices. Tuberculosis, syphilis and tumors 
are very infrequent. 

ACUTE BRONCHITIS. 

Acute bronchitis in some localities constitutes 10 to 15 per cent, of all 
diseases. Three-fourths of all cases occur in cold, dusty or variable 
weather, between December and April. Its forms are (a) inflammation 
of the larger air tubes, bronchitis or tracheobronchitis, and (b) inflamma- 
tion of the smaller tubules, known as bronchiolitis or capillary bronchitis, 
which in children is identical with bronchopneumonia (q. v.). Badham 



ACUTE BRONCHITIS 419 

(1819) coined the term bronchitis but it was first described by Laennec, 
who described every essential up to its bacteriology. 

Etiology. — (a) It is a symptom of various infections, as measles, pertussis, 
influenza and typhoid; or frequently also in pneumonia, tuberculosis, 
sepsis, etc. In these maladies bronchitis is secondary and toxemic. 
(b) Cold and bacteria. It is disputed whether cold alone is an adequate 
factor without bacterial cooperation, but it at least plays a potent pre- 
disposing part. Even in cases of primary bronchitis the pneumococcus, 
pyogenic cocci, Friedlander's pneumobacillus and rarely fungi, yeasts, 
streptothrix or Vincent's organisms (t\ s.) are detected. PfeifTer's Micro- 
coccus catarrhalis is found in 59 per cent, of cases (Ghon, Pfeiffer) ; it is 
larger than the staphylococcus and often occurs in pairs, (c) It may re- 
sult from the toxic effects of potassium iodide or.bromide, tobacco, mercury 
and alcohol which acts locally on the air passages, (d) Mechanical irritants 
are dust and particles of wool, stone, etc., which exist in many factories. 
(e) Constitutional conditions, as nephritis, rhachitis, obesity, diabetes and 
various cachexias, such as cancer or syphilis, are important etiologically. 
(/) Venous stasis in the pulmonary veins favors bronchitis; mitral lesions 
are far more important than other valvular diseases, arteriosclerosis, 
scoliosis, etc. (g) Respiratory diseases, as pneumonia, tuberculosis, 
abscess of the lung, asthma and bronchiectasis are associated with 
bronchitis, (h) Age: Acute bronchitis is peculiarly frequent in the aged 
and in children between six and thirty months old. 

Symptoms. — 1. Acute bronchitis of the larger tubes (macrobronchitis 
or tracheobronchitis) begins (a) with some depression, sometimes with 
fever and chilliness, or in children with marked toxemia. It often follows 
acute coryza or pharyngitis, (b) The local symptoms are substernal 
rawness or tickling ; actual or intense pain or tenderness over the sternum 
is mostly tracheal, for the bronchi possess no pain nerves. On inspection 
of the trachea there is visible inflammation, diffuse or circumscribed 
injection, submucous ecchymosis, swelling and laxness of the mucosa, 
and dryness, which is followed by a transparent, glairy mucous secretion; 
the mucous glands are often distended by globules of mucin which slightly 
resemble young tubercles; these findings are also noted in the bronchi 
in the rare cases which come to autopsy, but injection and redness 
largely disappear after death. Microscopically we observe inflammatory 
paresis of the vessels, round-cell emigration and desquamation of the 
ciliated epithelium, (c) The cough is at first dry and unproductive and 
may remain so. Later a viscid, transparent sputum is raised, consisting 
of mucin and very few white cells (sputum crudum) . A day or two later 
the coughing becomes less severe as the sputum grows more abundant 
and mucopurulent (sputum coctum); it contains polymorphonuclear 
and sometimes abundant eosinophilic leukocytes and epithelial cells 
showing myeloid degeneration. Localized inflammation at the tracheal 
bifurcation causes special irritation, (d) The symptoms resulting from 
cough are disturbed sleep; hoarseness from forcible closure of the glottis in 
coughing; pain in the side or at the diaphragmatic insertion, from unusual 
strain on the expiratory muscles; venous stasis which induces head- 
ache, vertigo, swollen cervical veins, cyanosis and epistaxis; mechanical 



420 DISEASES OF THE TRACHEA AND BRONCHI 

sequences, as vomiting, involuntary urination, especially in females, 
weak and old subjects; and in women, even abortion or uterine prolapse. 
(e) Physical findings are usually bilateral; unilateral signs suggest other 
lesions, especially tuberculosis. Auscultation reveals rhonchi, which 
result from swelling of the bronchial mucosa, slight stenosis by bronchial 
secretion and air passing through or dislodging the secretion; they at 
first are dry (r. sicci), and later moist (r. humidi). Over the large tubes 
these rales are sonorous, in the smaller tubules they are sibilant. They 
may be heard simultaneously over the large and small passages, or over 
the large and then by extension over the small tubules. These rales, 
large and small, may be felt with the hand (mucous fremitus) or may be 
heard without the stethoscope. The breathing may be "cog-wheel," 
lengthened or slowed, but in quality it is only exaggerated or puerile, 
never bronchial. Thoracic breathing develops in men when the tubes in 
the lower lobes are invaded. Percussion is wholly negative. Macrobron- 
chitis lasts a few days, possibly longer than a week. 

2. Microbronchitis or capillary bronchitis will be considered under 
bronchopneumonia, because of its great tendency toward pulmonary 
inflammation. 

Treatment. — In the early stage a full hot bath may be given, followed 
by a hot alcoholic drink. A hot Turkish bath is dangerous from the 
exposure afterward. Hot fomentations, a hot water-bag or large poultice 
may be applied over the sternum, but cold packs over the neck and chest 
are even more efficacious. But few patients recover promptly unless 
they are kept in bed. With the initial symptoms, gr. x of Dover's powder 
should be given; it relieves pain, muscular soreness and coughing and 
modifies the inflammation; in children it should be given with caution 
because of the frequently unequal mixture of its constituents, and the 
peculiar susceptibility of the youthful nervous system to narcotics; 
in the aged it should likewise be administered with care, because the 
kidneys in old persons excrete slowly, and in cerebral atheroma may 
induce psychical disturbance and Cheyne-Stokes's breathing. Opiates 
are followed by some saline aperient. Other treatment is frequently 
superfluous, but if the cough persists or the initial symptoms are severe, 
we administer: 

1$ — Vini antimonii . . 5iv 

Heroin hydrochloridi gr. is 

Vini ipecacuanha? 5v 

Syr. tolutani q. s. ad. gij 

M. et S. — One teaspoonful every three or four hours. The physician should watch lest 
gastric symptoms appear. 

Brown mixture may be given (see Chronic Bronchitis). 

1$ — Potassii citratis 5hss 5j 

Codeinse sulphatis gr. iv gr. j 

Syrupi ipecacuanhse 3iv 3iss 

Succi limonis oj 5ss 

Aquae . . . .' q. s. ad. * gij gij 

M. et S. — One teaspoonful every two hours. The first column is the dosage for adults, 
the second for children, 



CHRONIC BRONCHITIS 421 

For high fever aconite and belladonna may be given, as in coryza, but 
tepid sponging is more beneficial. A kettle of water (with co. tr. benzoin 
3j-Oj) kept boiling in the room moistens the atmosphere, or a steam 
tent may be advisable, as in croup (see page 89). See formulae under 
Chronic Bronchitis. 

CHRONIC BRONCHITIS. 

Etiology. — The etiology is that of the acute type. Chronic bronchitis, 
common in advanced life, may develop as a chronic process, or, more 
often, follows repeated acute attacks. It most often develops on change 
of weather or as the "winter cough." 

Pathology. — The larger bronchi are most involved. Their color is a 
grayish-red or brown; the bloodvessels are thickened, and the bronchi 
become thicker from extravasation of leukocytes and proliferation of the 
peribronchial connective tissue; the mucous membrane sometimes hyper- 
trophies and even protrudes in papillary excrescences, or is atrophied, 
and appears thin and pale like a serous membrane. Erosions are 
sometimes seen at the tracheal bifurcation. Stagnation of secretion is 
common. The inner surface of the bronchi is at times reticular, due to 
the prominence and hyperplasia of some elastic fibers and the wasting 
and sinking of other elastic or muscular fibers. Emphysema is frequently 
found at autopsy. 

Symptoms. — Fever and pain are absent, except in the frequent acute 
exacerbations. The usual physical findings in chronic macrobronchitis 
are large sonorous rales, and sibilant rales when acute exacerbations 
cause invasion of the finer tubules. The cough varies with the intensity 
of the inflammation, the amount and character of the secretion, or 
changes in the weather. The sputum varies greatly, and upon its char- 
acter is based the division into the following forms: (a) Dry bronchitis, 
the bronchitis sicca of Laennec, which is seen in the aged, associated with 
emphysema; the sputum is absent or very scant and viscid, (b) Bron- 
chorrhea, in which the excessive bronchial secretion may be mucous, serous 
or purulent; in the serous form the secretion is thin and transparent, 
as in Laennec's case, in which two quarts were raised daily for twelve 
years; serous bronchorrhea may result from enlarged peribronchial 
glands; the purulent form may be confused with bronchiectasis, lung 
abscess or rupture of an empyema into the bronchi, (c) Putrid bronchitis, 
which complicates chronic bronchitis but occurs more often with bron- 
chiectasis, foreign intrabronchial bodies and tuberculosis; in this form 
the sputum stinks, particularly when first voided. It consists of three 
layers: an upper foamy, a middle serous and a lower one of granular, 
grayish-green sediment, in which are the mycotic plugs of Dittrich (1850) ; 
these plugs contain various bacteria, leptothrix, strepto- and staphylo- 
cocci, etc., and " acid-fast" bacilli which closely resemble tubercle bacilli, 
though narrower and more pointed at their ends. Fat and myelin drop- 
lets, fatty needles, leucin and tyrosin are also present. Fever is common; 
"drumstick" fingers may develop, and complications may follow, as 
lung induration, gangrene, pleurisy, hemoptysis, abscess, cerebrospinal 
meningitis or pseudorheumatism. (d) Blood-stained sputum occurs 



422 DISEASES OF THE TRACHEA AND BRONCHI 

particularly in the brown induration of the lungs, due to stasis (see page 
368). 

Chronic emphysema (v. i.) is an almost regular complication. 

Diagnosis. — Determination of its relation to tuberculosis, chronic 
nephritis and other causal factors is most important. 

Prognosis. — The prognosis depends on the etiological factors. Ab- 
solute recovery is most unlikely. 

Treatment. — 1. Prophylaxis. Causal affections require treatment. 
Woolen underwear protects against sudden changes of temperature. 
In obstinate cases restriction of fluids may benefit. 

2. Climate. — A dry, warm, even climate is beneficial, as Florida, 
California, New Mexico, Egypt and the Riviera. 

3. Cough. — Codeine, morphine, creosote, cod-liver oil and other 
remedies are employed as in tuberculosis (q. v.). Ammon. carb. (v. 
Pneumonia) gr. iij can be given with syr. senegse 3j; syr. scillee 3j is 
incompatible with ammon. carb. but may be combined with ammon. 
chlor. gr. v-x. 

1$ — Ammonii chloridi 3iss 

Misturse glycyrrhizse composite §iv 

M. et S. — One teaspoonful after meals. 

The mistura glycyrrhizse composita (Brown mixture; paregoric 12 
parts, antimonial wine 6 and sweet spirits of nitre 3) may be given, 
3j-iv. If the heart is weak, it is contra-indicated because of the anti- 
mony. The stomach may become deranged by the ammonium, syrups, 
etc. Chloroform is valuable in paroxysmal, unproductive coughs, which 
opiates may not alleviate. 

1$ — Ammonii carbonatis 3J 

Spiritus chloroformi §iss 

Syrupi senegae q. s. ad. 5 iij 

M. et S. — One teaspoonful in hot water as indicated. 

1$ — Apomorphinae hydrochloridi gr. ss 

Heroin hydrochloridi gr. j 

Spiritus chloroformi 3j 

Aquae q. s. ad. 34J 

M. et S. — One teaspoonful two or three times a day. 

Syr. scillge compositus (Hive Syrup) gtt. xx-xl, also contains senega, 
tartar emetic and antimony. Terpini hydras is excellent, gr. iij, t. i. d., 
given in capsules with an equal amount of benzoic acid. The balsams are 
even more efficacious, as emulsum ol. terebinthinw 3j i n milk, though 
ol. santali Tfl,x-xx in emulsion is less likely to disturb the kidneys; 
balsamum Peruvianum 3 ss ranks with the best. The balsams and creosote 
are directly indicated in fetid bronchitis. Retention of secretion may be 
treated by rhythmical compression of the chest during expiration. Potas. 
iodide gr. v-x, t. i. d., is excellent in bronchitis, asthma and emphysema. 

4. Cardiac Weakness. — Cardiac weakness is relieved more effica- 
ciously by strychnine than by digitalis. 



BRONCHIAL DILATATION— BRONCHIECTASIS 423 

FIBRINOUS BRONCHITIS. 

Etiology. — There are three types of fibrinous or croupous bronchitis: 
(a) The infrequent primary form, of which McPhedran collected 204 
cases (1907); it occurs in males (66 per cent.), between ten and thirty 
years of age, and in weakly subjects; it results from the Bacillus diph- 
therias, pneumo-, strepto- and staphylococcus, aspergillus fungus, and 
protozoa, or from their toxins. (6) The secondary type develops by ex- 
tension from laryngeal and pulmonary disease, or in infections, as diph- 
theria, pneumonia, etc.; tuberculosis causes 50 per cent, of this group, 
(c) Mechanical, thermal and chemical agents, valvular heart disease 
and exophthalmic goitre are causative factors in a few cases. Fibrinous 
bronchitis was first clearly described by Clark, in 1697, though Hippo- 
crates and Galen mentioned the condition. 

Symptoms. — The early symptoms of bronchitis, sometimes with fever, 
chills and hemoptysis (in 33 per cent.), are ambiguous until bronchial 
casts of fibrin or mucin are expectorated, after a severe coughing 
paroxysm. The casts may be eight inches long, and as thick as a finger; 
their upper, larger parts are circular or oval, solid or hollow, but the 
lower, small portions are branched, solid, spiral and often beaded with 
air and clubbed at their tips. Though usually fibrinous or croupous, 
many casts are mucous (bronchitis mucinosa) . Their microscopic appear- 
ance is hyaline, their texture fibrillar, and their surface covered with 
blood disks, hematoidin or Charcot-Leyden crystals. Smaller casts may 
not be seen until the sputum is washed of the adherent blood, pus or 
mucus. Pending their evacuation, there are signs of unilateral bronchial 
stenosis, e. g., dyspnea, cyanosis and inspiratory retraction, and absence 
of breath sounds in the corresponding lung. Slipping of the casts in the 
bronchus may cause peculiar flapping rales. Niemeyer observed the 
daily shedding of a complete cast of a bronchus and its divisions. 

Diagnosis. — In some cases casts are not voided during life, and are 
found first at autopsv. Asthma and bronchitis fibrinosa have certain 
common symptoms, as paroxysmal occurrence, eosinophilia, crystals and 
spirals, but are usually differentiated with ease. 

Course and Prognosis. — In the acute form, which lasts two weeks or 
less, there is a death-rate of 75 per cent, in the young and 50 per cent, 
in adults from asphyxia during evacuation of the casts. In chronic 
forms the process lasts for months, years or decades. 

Treatment. — Treatment is unsatisfactory if not futile. Inhalation of 
steam and alkaline vapors and pilocarpin are given to loosen the casts, 
emetics to facilitate evacuation and iodides and mercurial inunctions 
to inhibit reformation. 



BRONCHIAL DILATATION, BRONCHIECTASIS. 

Etiology and Pathology. — Laennec first described bronchiectasis in 
1819. It is found in 2 per cent, of autopsies and is always secondary 
(a) to bronchial disease, stenosis preeminently, and influenza, pertussis, 



424 DISEASES OF THE TRACHEA AND BRONCHI 

foreign bodies or pressure by aneurysm; (b) to lung disease, tuberculosis, 
interstitial or bronchopneumonia or atelectasis; coughing increases the 
expiratory pressure, even fortyfold; (c) to pleural disease, such as ad- 
hesions pulling on the bronchi. Nearlv all cases are acquired and 77 
per cent, occur in middle-aged males. The rare congenital cases may be 
divided into (i) the unilateral, universal or diffuse form, (ii) those due to 
congenital atelectasis and (iii) those resulting from bronchial (syphilitic) 
stenosis. 

There are two forms of bronchiectasis: (a) The cylindrical or fusi- 
form, multiple or pater noster form, which develops from the atrophy 
of the muscular and elastic fibers induced by protracted coughing and 
stagnation of secretion, e. g., in catarrhal pneumonia, whooping-cough or 
emphysema, (b) The rarer sacculated form, in which the bronchus, reach- 
ing a diameter of even 3 inches, might be called a bronchial aneurysm. 
The connective tissue wastes, the ciliated are replaced by flat epithelia, 
and the mucosa is thin, red, sometimes villous. The sacs close at their 
necks, particularly when caused by aneurysm, syphilis or tuberculosis, 
and are filled with gelatinous or cheesy contents. Lung stones of calcium 
carbonate and phosphate may develop; they sometimes cause "bronchial 
colic," or symptoms like phthisis. 

In multiple bronchiectasis the lung sometimes resembles a sponge or 
porous cheese. It occurs principally in the lower lobes, in bronchi of 
the third and fourth order, and is bilateral in 60 per cent. Adhesions 
are very common when the cavity reaches the pleura. 

Symptoms. — Weil stated that most cavities escape detection and most 
diagnoses of cavities are incorrect. Sacculated give more symptoms and 
signs than cvlindrical forms, which are almost always impossible to 
recognize. 

1. The sputum and cough are paroxysmal. On change of posture 
or when secretion fills the sac and flows over onto the normal sensitive 
mucous membrane beyond it, cough develops and quantities of mucopus 
are voided in the "mouthful" fashion described by Wintrich. The 
largest amount is raised in the morning and frequently evokes vomiting. 
The daily quantitv may amount to a quart. Its odor is acid, sweat-like, 
but less offensive than the fetor of putrid bronchitis or the foulness 
of gangrene. When collected it forms in three layers; the upper one is 
foamy, the middle serous and the lower purulent. A nummular sputum 
may be noted, as in tuberculosis, but if put in water it is more flocculent, 
more granular and airless; and microscopically it contains altered 
leukocytes and fatty needles, occasionally red cells, hematoidin crystals 
and very rarely, when the bronchial wall is ulcerated, elastic fibers. 

2. Physical Examination. — (a) Inspection may reveal diminished 
respiratory movement, inspiratory retraction over the cavity or flattening 
of the chest wall. The patient generally leans toward the diseased side 
to lessen the trickling out of the secretion. In the rare bronchiectasis 
of an upper lobe the constant escape of the secretion results in exhausting 
coughing. The x-rays may locate the cavity. In rare cases the cavity 
may bulge through the interspaces, (b) Palpation and (c) percussion: 
Dulness prevails when the cavity is full; when it is empty there is 



BRONCHIAL DILATATION— BRONCHIECTASIS 425 

tympany. A higher note on opening the mouth, on inspiration or change 
of posture has the same value as in tuberculous cavities (q. v.). (d) 
On auscultation, bronchial or metallic breathing may be heard when the 
cavities are superficial but it is absent in dilatations which are small, 
deep or full of secretion. Metamorphosing breathing is a certain sign of a 
cavity. Skoda's superficial, "veiled-puff" sound is frequent. Large and 
small rales, heard persistently in the same locality, are suggestive of a 
deep bronchiectasis. The sound tissue over the cavity imparts a metallic 
consonance. 

3. Complications. — Emaciation, putrid bronchitis, slight cyanosis 
and anemia are frequent. Hectic fever is often absent, but death may 
result with symptoms resembling phthisis. Hemoptysis from ulceration 
of varices occurs in 40 per cent, of cases; pneumothorax, pleurisy, 
empyema, lung induration or gangrene, emphysema, lobular pneumonia, 
amyloidosis and hypertrophy and dilatation of the right ventricle are 
fairly common. Marie's osteo-arthropathie hypertrophiante pneumonique, 
rheumatoid affections, suppurative meningitis and brain abscess are 
occasional. 

Diagnosis. — Diagnosis depends upon the character of the sputum, 
its paroxysmal voidance and the signs of cavity. Differentiation is 
required (a) from tuberculous cavities; this is made by elastic fibers and 
tubercle bacilli (definitelv determined by inoculation); tuberculous 
cavities are most often apical, but frequently bilateral; they void less 
sputum and suffer less rapid variation in their physical signs. Bronchiec- 
tatic cavities occur mostly in the lower lobes, void more sputum, less often 
induce hemorrhage and more frequently cause right-heart changes; 
(b) from perforating empyema, in which cholesterin and hematoidin 
crystals are far more frequent than in bronchiectasis; (c) from abscess; 
(d) from gangrene of the lung (v. i.) ; (e) from putrid bronchitis, in which 
there is no sudden volume of evacuated sputum or signs of cavity; (/) 
from encapsulated pyopneumothorax, which may be very difficult of 
differentiation; and (g) aneurysm or tumor causing bronchiectasis. 

Prognosis. — Ultimate recovery is exceptional, except in acute cases, 
e. g., postinfluenzal; patients have lived half a century. The complica- 
tions require consideration (v. s.). 

Treatment. — The therapeutic indications are {a) evacuation of the 
secretion, for which expectorants, raising the foot of the bed, and ex- 
piratory compression of the chest, as in bronchitis, are somewhat useful ; 
sedatives should never be given lest gangrene develop ; (b) modification 
of putrescence by balsamic remedies, as in fetid bronchitis; a dram of 
creosote is slowly vaporized over a flame, and the patient, in a closed 
room, inhales the fumes with the eyes closed and the anterior nares 
plugged; the procedure may be gradually lengthened from a few minutes 
to half an hour; the irritation evacuates the residual secretion; (c) surgical 
drainage; an accessible cavity may be incised and drained, though 
accurate diagnosis of its location is difficult, the mortality high and the 
affection multiple. In Garre's 57 cases, 63 per cent, recovered and 37 
per cent, died; (d) change of climate (v. Tuberculosis). 



426 DISEASES OF THE TRACHEA AND BRONCHI 

TRACHEAL AND BRONCHIAL STENOSIS. 

I. Tracheal Stenosis. — Etiology. — Tracheal causes are rhinoscleroma, 
syphilis (q. v.), tumors (cancer, polyp, fibroma, enchondroma, sarcoma 
or aberrant thyroid), foreign bodies and in rare cases perichondritis. 
Causes outside the trachea are more frequent, as retrosternal, cystic 
and circular goitre, or struma in which hemorrhage or inflammation 
has occurred. Aneurysm, adenopathies, mediastinal tumors, vertebral 
tumors or caries and thymus hyperplasia are other factors. Thiesen 
collated 135 cases of tracheal tumor, of which 89 were benignant and 46 
malignant; 24 were fibromata and 10 intratracheal struma (penetrating 
the rings of the trachea, when sudden death may result, Paltauf ) . 

Symptoms. — The symptoms develop three stages: (a) no symptoms 
or symptoms only on exertion; (b) constant dyspnea, and (c) suffocative 
attacks and final asphyxia. Dyspnea is mixed, i. e., inspiratory and 
expiratory; respiration is slowed, there is inspiratory stridor and inter- 
costal retraction, all tjie accessory muscles come into play and the head 
is held well forward. The pulse is tense. Tracheoscopy may reveal the 
location of the lesion; the patient should stand with his back to the 
strong sunlight, with the head bent forward, and the observer seated on 
a low seat before him. In 25 per cent, of tracheal stenoses, due to tumor 
or aneurysm, there is coincident paralysis of the vocal cords. 

II. Bronchial Stenosis. — Etiology. — Intrabronchial causes are most 
common and consist of pus, mucus, blood, fibrin and foreign bodies; 
obstruction due to the latter is laryngeal in 33, tracheal in 26 and bronchial 
in 41 per cent, of the cases. Extrabronchial factors are next in frequency; 
aneurysm, mediastinal lymphosarcoma and perilymphadenitis leading 
to fibrosis occur most often; less common are pericarditis with effusion, 
dilatation of the left auricle, cancer of the esophagus, tumor of the lung 
and thyroid or thymic strumas. Twenty cases have been reported in 
which lymph glands ruptured into the trachea or bronchi, causing suffoca- 
tion; only three were saved by tracheotomy. Interbronchial causes 
(i. e., in the bronchial wall) are the least common, as syphilis, rhino- 
scleroma and tumors. Thirty-six cases of primary cancer are recorded. 
The right is stenosed nearly twice as often as the left bronchus. 

Symptoms. — Occlusion of a bronchus lessens the amount of air entering 
the lung which it supplies, whence the vocal fremitus and breath sounds 
are weakened or suspended and the respiratory excursion and Litten's 
diaphragmatic sign are decreased. There is inspiratory retraction of the 
intercostal spaces on the affected side. Inspiratory dyspnea occurs, 
particularly in acute cases. The head is thrown forward. Absence of 
dulness excludes many causes of dyspnea, as pneumonia, etc.; after a 
time a somewhat tympanitic note may result from relaxation of the lung 
or acute emphysema. A local stenotic murmur over the bronchus is present 
in a few cases. Paroxysmal dyspnea may result from stagnating secretion. 
Coughing is usual and may resemble that of pertussis. The pulse is more 
tense. The arrays and bronchoscopy may locate the obstruction. Death 
results from (a) the original disease, as aneurysm or tumor; (6) failure 
of the right heart; (c) asphyxia, with delirium, cyanosis or Cheyne- 



BRONCHIAL ASTHMA 427 

Stokes's breathing, or (d) pulmonary edema, gangrene, tuberculosis, 
lobular pneumonia or hemorrhage. 

Diagnosis. — (a) Of the location: In laryngeal obstruction there are 
local findings and free up-and-down laryngeal excursion; the subject 
holds the head well back, and the ingress of air to both lungs is equally 
impaired; tracheoscopy, bilateral lung involvement, absence of laryngeal 
excursion and the holding of the head forward are proof of tracheal 
obstruction; in bronchial stenosis but one lung suffers for air, the larynx 
is nearly immobile and the head is thrown forward, (b) Of the nature 
of stenosis, certainty is impossible without physical signs, as aneurysm, 
history of foreign bodies, etc. 

Treatment. — Treatment is that of the cause, as syphilis, tuberculosis; 
thyroid extract in struma; or rest, mercury iodides and venesection 
in aneurysm. To dislodge foreign bodies the patient should be inverted, 
sharply struck on the back and shaken; the physician should have long 
forceps and tracheotomy instruments in readiness; the mortality is 
52 per cent, without, and 23 per cent, with, operation. 

Bronchial and lung stones (v.s.) result from tuberculosis of the bronchial 
glands, bronchiectasis, petrification of the bronchi, calcification and 
ossification of the lungs, and foreign bodies. Boerhaave described the 
case of the botanist, Vaillant, who expectorated 400 calculi. Symptoms 
are frequently absent or are those of the primary disease; purulent 
bronchitis, asthma ("bronchial colic"), hectic fever and hemoptysis mark 
some cases. 

Stenosis may result from bronchiolitis fibrinosa obliterans. 

BRONCHIAL ASTHMA. 

Definition. — A paroxysmal dyspnea, due to nervous or reflex stenosis 
or spasm of the smaller bronchioles, and characterized by expiratory 
dyspnea, slowing of respiration, congestion of the bronchioles, a peculiar 
mucous exudation and acute emphysema. It is also known as asthma 
spasmodicum or nervosum, to distinguish it from other so-called asthmas, 
as the cardiac and renal types. 

Etiology. — When due to no obvious cause, asthma is termed essential 
or primary, and when due to a clear cause it is called symptomatic asthma, 
reflex through the vagus: (a) Nasopharyngeal disease often initiates 
reflex asthma, e. g., rhinitis, tonsillar hypertrophy, adenoids or pharyn- 
gitis granulosa; the nose may be so hypersensitive that the odor of flowers, 
dust, feathers or smoke precipitates an attack, (b) Asthma may be 
induced by pressure on the vagus trunk, by thyroid tumors or enlarged 
bronchial glands, following tuberculosis, measles, pertussis or rickets. 
(c) Abdominal diseases are not frequent causes, e. g., asthma dyspepticum, 
uterinum, etc. (d) Asthma toxicum occurs in lead and mercurial poisoning, 
uremia and gout, (e) It occurs especially in weakly, anemic, nervous, 
scrofulous and rhachitic subjects, in the upper classes, and in males 
(66 per cent.) between the ages of twenty and forty (it has recently 
been claimed that 33 per cent, of the asthma cases develop under ten 
years). 



428 



DISEASES OF THE TRACHEA AND BRONCHI 



The mechanism of the asthmatic paroxysm is explained as: (a) A 
spasm of the bronchial muscles; Trousseau spoke of asthma as "an epi- 
lepsy of the lungs." (6) Like the exudative diatheses, e. g., urticaria, 
angioneurotic edema, intermittent hydrops of the joints, eczema, colica 
mucosa, etc. (c) An acute exudative bronchitis, causing bronchial spasm. 
(d) Meltzer suggests that it is an anaphylaxis. Its pathology is uncertain, 
as but half a dozen autopsies are recorded; the ciliated epithelium is 
desquamated, the bronchioles are congested and there is eosinophilic 
exudation. 

Symptoms. — The attack begins very suddenly, often at night and 
with or without such causes as fright, cold, heat, change of residence, 
etc. Sometimes there are prodromes, as conjunctivitis, coryza or flat- 
ulence and sometimes the attack coincides with the menses, (a) Dysp- 
nea is the first and the essential symptom; at first slight, it soon becomes 
urgent; the patient opens the windows, sits upright, grasps the arms of 





Fig. 32. 



1 ^^m^ 



-Spirals and crystals in bronchial asthma, b, Charcot-Leyden crystals; a, Leyden 
and Curschmann spirals magnified, and c, their natural size. , 



the chair to brace the accessory respiratory muscles and exhibits extreme 
distress, anxiousness and pallor, followed by cyanosis; the dyspnea is 
expiratory and the abdominal muscles are board-like during expiration; 
inspiration is somewhat, and expiration is greatly, prolonged, wheezing 
and whistling; respiration is generally slow, (b) There is extreme cyanosis, 
the cervical veins bulge out like cords, the skin is clammy, and the pulse 
indicates poor oxygenation by its tenseness, smallness and frequency, 
as also do the far rarer headache, delirium, twitchings, convulsions 
and coma, (c) The cough is dry and unproductive, (d) Other physical 
signs are as follows : On palpation, the vocal fremitus is found decreased 
by the bronchial spasm or secretion; rales are often felt. The normal 
percussion note is replaced by a tympanitic note, due to acute pulmonary 
emphysema; the voluminous lungs distend the thorax, cover the heart 
and depress the diaphragm, whose excursion is thus minimal. On 
auscultation, the vesicular murmur is usually faint or absent (Laennec) 
because of secretion in the bronchioles, and loud whistling, piping or 
sibilant rales are heard often without the stethoscope, largely during 



PLATE XII 









»t- 






■•.$*. 



9* *W&-- 



'"". : .V. . •'• 



■ »:'. .)&•• 






tyfi 



01 



rt »i^f 



' r to 






Sputum from a Case of Bronchial Asthma, sho^ving large 
numbers of Eosinophilic Leukocytes and Free Granules. 
(Simon.) 



It will be noted that the leukocytes are all mononuclear. 
(Eye-piece 1, objective 1-8, Bausch & Lomb.) 



BRONCHIAL ASTHMA 429 

expiration and due to bronchiole stenosis, (e) Sputum is first voided 
toward the end of the attack, as a species of crisis to the threatening, 
but very seldom fatal, asphyxia. A few drams of tenacious mucus, 
resembling egg albumen, and minute gray balls are seen. The latter are 
the "perles" of Laennec; when unrolled the "pearls" are seen to contain 
the spirals, best detected with the naked eye, and on a black background ; 
they measure 2 or 3 to 10 x \ to 1 mm. and are mucin casts of the bron- 
chioles, to which may cling leukocytes, epithelia, fat or myelin droplets; 
some show a central band of mucin; it is thought that they occur from 
the passage of mucin through the contracted bronchioles; they disappear 
within a day or two; spirals are also present in catarrhal or fibrinous 
bronchitis and pneumonia. The Charcot-Leyden crystals may be seen 
as yellow dots in the sputum; they are pointed and hexagonal (not 
octahedral) , consist of an organic basis with phosphoric acid, and originate 
from the eosinophile leukocytes which are increased in the sputum and 
blood, constituting a quarter to more than half of the white cells; W. W. 
Herrick's case had 11 per cent, polynuclears, 15 per cent, lymphocytes 
and 72 per cent, eosinophiles. The crystals, spirals and the occasional 
fibrinous casts are a result, not a cause of the asthma. (Plate XII.) 

The attacks last an hour or two, to be repeated at long or short intervals. 
In the hebdomadal form, attacks recur every Sunday or Monday, due to 
change in routine or to digestive excesses. 

Diagnosis. — The diagnosis is made by its paroxysmal occurrence, the 
expiratory dyspnea and the transient emphysema. 

Differentiation. — (a) All diseases causing inspiratory dyspnea can 
be at once excluded, such as edema or spasm of the glottis, paralysis 
of the post, cricoarytenoid muscles, tracheal or bronchial stenosis. 
In glottis spasm the spasm is inspiratory and short, the larynx moves 
up and down, and the epigastrium retracts during inspiration; there 
is no emphysema and no spirals are found. Spasm of the diaphragm 
is very rare (v. Phrenic Nerve); it lasts a much shorter time, the 
epigastrium bulges during inspiration, there is spasm of all the inspiratory 
muscles, hysterical stigmata are often observed and the lungs are normal. 
(b) Expiratory dyspnea may also occur in (i) chronic bronchitis with 
emphysema, in which the emphysema and rales are constant and eosino- 
philia is absent, (ii) It also occurs in movable tumors below the vocal 
cords which may turn upward during expiration, as shown by the laryngo- 
scope, (c) Asthma cardiale is inspiratory and expiratory, and therefore 
readily differentiated; the "lungenstarr" or lung distention, due to 
engorged vessels, may simulate the emphysema of bronchial asthma 
(see page 368). Cardiac asthma may occur either with high or low 
arterial tension. Eosinophilia is absent. 

Prognosis. — The prognosis is uncertain and depends on the etiological 
accessibility of the asthma. It is more favorable in young individuals 
than in those of advanced years. Cases which recurred for sixty-four 
years are recorded. Chronic bronchitis and emphysema are likely to 
develop. Death in an attack is very rare. 

Treatment. — 1. Of the Attack. — A hypodermic injection of mor- 
phine gr. J, with atropine gr. -£$■ and spt. glycerylis nitratis TTlij, gives 



430 DISEASES OF THE LUNG 

the most prompt and reliable results. Chloral is useless, for the condi- 
tion requires single doses of gr. xxx-xl, which are too large for safety. 
Adrenalin solution (1 to 1000) TTlx hypodermically, usually gives instant 
relief ; it is not without danger, and the author saw edema of the lungs and 
doubling of the blood-pressure follow its use. It also may be sprayed into 
the larynx. Strong coffee, whisky, a cigar or cigarette, the application of 
cocaine to the nose, nitrite of amyl pearls, or a few whiffs of chloroform, 
sometimes give relief. The vexing question arises as to leaving morphine 
in the hands of the patient whose attacks often come and go without 
medical aid; as a rule it is dangerous. Inhalation powders, burned like 
incense, are very generally used. (Lobelia, powdered black tea and 
powdered stramonium leaves, each one ounce; soak well in two ounces 
of a saturated solution of potassium nitrate; dry.) The Cigarettes d'Espic 
contain the following: 

Belladonna leaves . 5 \ parts 

Hyoscyamus leaves ............. 2f parts 

Stramonium leaves 2| parts 

Phellandrium aquaticum 1 part 

Extract of opium \ part 

Cherry-laurel water a sufficiency 

All these drugs depress the peripheral filaments of the vagus. 

2. Of the Tendency. — Etiological therapy helps over half the cases; 
cauterization of sensitive areas in the nose, even without gross lesions, is 
imperative. Strumpell effected 11 cures by sweating with strong lamps. 
The evening meal should be light, and carbohydrates and tea should 
be restricted; an emetic may abort an attack of the gastric type. Ner- 
vines (valerian, arsenic, bromides) may be used. The best remedy 
between attacks is potassium iodide, continued for months ; it is com- 
bined to advantage with Fowler's solution and belladonna, not only 
to correct its action on the skin and secretory glands, but also for their 
antispasmodic effects : 

1$ — Liq. potassii arsenitis 5J 

Tr. belladonnas 5J 

Potassii iodidi . 5ij 

Fluidextr. grindelise (U. S. P.) . . . . 3vj 

Aquae q. s. ad. 5iv 

M. et S. — One teaspoonful in water after meals. 

A low level near the sea, in a semitropical climate, helps the bronchitis, 
emphysema and dilated right heart. General hygiene and the hardening 
by fresh air and cold rubs are important. 



DISEASES OF THE LUNG. 

EMPHYSEMA. 

Definition. — A pulmonary disease, characterized pathologically by 
alveolar atrophy and distention, and clinically by a large chest of the 
inspiratory type, distended lungs, and hypertrophy and dilatation of 



EMPHYSEMA 431 

the right ventricle. Emphysema means a "blowing up" of the lungs. 
It was first described by Laennec (1826). 

Etiology. — Substantive or alveolar emphysema occurs mostly in indi- 
viduals over 30 or 40 years of age, in men more than in women, and 
in cold climates. The immediate cause is chronic bronchitis and bron- 
chiolitis (Laennec), catarrhe sec; it may follow bronchial asthma, etc.; its 
infrequency (0.7 per cent, of autopsies) is not understood, whence a 
congenital hypoplasia of the elastic tissue of the lung is sometimes 
assumed. Coughing, blowing, as on wind instruments, straining during 
parturition or physical toil, artificial respiration in the newborn, and 
alcoholism are possibly causative. 

Pathology. — On opening the chest at autopsy, the lungs are found 
distended (volumen pulmonum auctum, Traube); they overlap the 
heart, depress the diaphragm and narrow the mediastinum. Their 
surface is pale rose-colored and presents numerous small vesicles, \ to 
4 mm. in diameter, or some large bullous areas representing the fusion 
of several alveoli. The lungs crepitate slightly to the fingers, under 
which they feel, as Laennec put it, "like a pillow of down." The lungs 
collapse but little on section. In some places the pigment deposit is 
lessened — albinism. Emphysema is most marked on the surface of the 
lung, particularly over the upper lobes, anteriorly and near the spine. 
The normally thin edges of the lung are greatly rounded. Histologically, 
two findings are characteristic: (a) There is atrophy of the inter 'alveolar 
elastic tissue, so that the alveoli fuse, corresponding to the vesicles seen 
on the surface; these changes account for nearly all the clinical findings 
in the lung, (b) The capillaries are obliterated by thrombosis, which 
explains the clinical hypertrophy, dilatation and ultimate failure of 
the right heart. The bronchi are frequently inflamed, thickened and 
shortened. 

Pathogenesis. — The changes may be brought about (a) mechanically 
by forced inspiration or forced expiration, a theory favored by clinicians; 
or according to the pathologist, (b) by nutritive alterations, as vascular 
changes or atrophy of elastic or muscular tissue; calcification of the 
costal cartilages is probably more sequential than causal. 

Symptoms. — Symptoms fall under two headings: (1) Expiratory in- 
sufficiency of the lungs, due to their distention (from the loss of elastic 
tissue); and (2) cardiac insufficiency, resulting from obliteration of the 
vessels in the lesser circuit. 

1. Expiratory Pulmonary Insufficiency. — Normally expiration is 
wholly passive, resulting from the elasticity of the lungs and collapse 
of the chest. Expiration in emphysema is incomplete, as shown by 
the cyrtometer (showing the chest more circular) ; the spirometer, showing 
a decrease of 20 to 60 per cent, in the normal vital capacity (2000 to 4000 
c.c.) ; and mensuration giving a reduction of the normal expansion of 2 
to 3 inches. Upon inspection, dyspnea is the most conspicuous finding; 
it is expiratory and is due to the loss of lung elasticity and consequent 
impairment of lung circulation and oxygenation ; it is enhanced by exer- 
tion, bronchial catarrh, accessions of true asthma and by cardiac insuf- 
ficiency. The respiration-rate is increased to twenty-five or thirty and 



432 DISEASES OF THE LUNG 

the type is costal. The fades and habitus are most characteristic; the 
eyes are somewhat prominent, the nose is bluish and thickened, the head 
is thrown back and the chest forward to give play to the accessory 
muscles of respiration, and the skin is cyanotic. A network of dilated 
veins is often seen over the lower chest, resulting from venous obstruction. 
The jugular veins fill enormously on expiration and often pulsate during 
the diastole. The neck is short, and the hypertrophied sternomastoids, 
scaleni and trapezii protrude rigidly. The back and abdominal muscles 
are rigid, and thus supplement the inadequate action of the diaphragm. 
The shoulders are elevated, though stooped ; the chest is of the permanent 
inspiratory type and is usually barrel-shaped (from the elastic atrophy), 
rarely of the paralytic type; the anteroposterior, oblique and sometimes 
the transverse dimensions of the chest are increased. The raised clavicles 
accentuate the supraclavicular spaces in which the apices sometimes 
protrude, on coughing, as hernial tumors. The angle of Louis is prominent 
and the interspaces are wider in the upper, and narrower in the lower, 
parts of the chest, and retract with each inspiration. The lower thorax 
shows a groove indicating the attachment of the expiratory muscles. 
The play of the diaphragm is limited, as shown by the arrays and by the 
absence of Litten's sign. Palpation detects the rigidity and dilatation 
of the thorax, its poor excursion, the hard muscles, the calcified costal 
cartilages and decreased vocal fremitus. The edge of the liver may be 
found depressed and tender but the spleen is seldom palpable. Per- 
cussion, absolutely essential to a diagnosis, gives a note which is loud and 
deep — hyperresonant — or on the sides and back is actually "box-like" 
or tympanitic, also described as wooden and in extreme cases as dull 
(Skoda). The voluminous lungs narrow or wholly cover the cardiac 
dulness, depress the upper level of the splenic and hepatic dulness, 
invade Traube's space, and show little respiratory excursion. At the 
back the lungs may reach the twelfth dorsal or second lumbar vertebra. 
Upon auscultation, expiration is found greatly lengthened so that it is to 
inspiration as 2 or 4 to 1, the converse of normal. Vesicular breathing 
is absent, or the breathing is indeterminate, even when the stethoscope 
rises and falls. Rales result from bronchitis or stasis; a pearly mucin 
with few cells may be evacuated after coughing. 

2. Cardiac Insufficiency. — The work of the right ventricle is 
increased because the pulmonary arterioles are in part occluded, and 
the imperfect expiration allows neither free aspiration of venous blood 
into the auricles nor adequate filling of the aorta. The right ventricle 
therefore hypertrophies, mostly about the conus, causing the accentuated 
second pulmonic tone. The diaphragm is low, whence the hypertrophied 
and more horizontal heart beats in the epigastrium. Dilatation soon 
follows and is accompanied, in advanced cases, by tricuspid leakage, 
nutmeg liver, congested kidneys, and other signs of cardiac insufficiency. 
The cardiac alteration, so marked at autopsy, is obscured during life, as 
the lungs cover the heart and muffle its tones. Functional heart murmurs, 
mostly systolic, result from myocardial degeneration or relaxation. 

The clinical course often covers decades. Patients may acquire emphy- 
sema in childhood and live to 60 or 70 years of age. 



EMPHYSEMA 433 

Diagnosis. — Developed types are easily recognized by the barrel-chest, 
its hyperresonance, the low borders of the lungs, their lack of excursion, 
the obscuration of cardiac dulness, the expiratory dyspnea and cardiac 
stasis. 

Differentiation.— (a) Acute distention of the lung or acute emphysema, 
as after asthma or pertussis, cannot be distinguished by one examination. 
It is seen repeatedly in bronchial stenosis due to aneurysm. It regresses 
rapidly even after months, when its cause is removed. (6) Vicarious or 
compensatory emphysema often develops in one lung when contralateral 
pleurisy or cirrhosis of the lung exists; it may occur on the same side 
with the lesion; marked apical emphysema almost certainly indicates 
some deeper induration, (c) Emphysema senile, Jenner's "small-lunged" 
emphysema, is merely atrophy of the connective tissue; the lungs are 
not enlarged, but smaller, the diaphragm stands higher, the cardiac 
dulness is increased, the chest flattened, the ribs oblique, the respiratory 
muscles wasted, the right heart is not hypertrophied and respiratory 
excursion is retained, (d) From inter alveolar interstitial emphysema the 
first differential point is the etiologyj (i) trauma, external or internal 
(in tracheotomies), and frequently with pneumothorax, (ii) Foreign 
bodies, (iii) Ulceration of the air passages, gangrene, abscess or tuber- 
culosis and less often gastric ulcer or cancer. Other etiological factors 
are (iv) forced entrance of air, as in resuscitation of the newborn; (v) 
severe coughing efforts, as in whooping-cough; (vi) severe pressure 
efforts, as in parturition; and (vii) spasm of the glottis. The second 
point is a series of symptoms often present, as creaking in the medi- 
astinum, sometimes systolic; emphysema and crepitation of the cervical 
cellular tissue, bulging of the interspaces, creaking and tympany at the 
edge of the ribs; absence of the vesicular murmur; and obliteration of the 
heart dulness. It is usually fatal, (e) In congenital hypertrophy of the 
lung (pulmo excessimis) the lungs are very voluminous, but their ex- 
cursion, auscultation and percussion-note are normal. (/) Pneumothorax 
(q. v.) is unilateral, has a more tympanitic note and is associated with 
succussion, tinkling rales and other pathognomonic signs. 

Prognosis. — Recovery is unknown in the genuine substantive form. 
Transient forms often or usually regress completely. Life, even relative 
comfort, may be sustained for years or decades. Much depends on 
associated conditions, as frequent severe bronchitis, chronic nephritis, 
arteriosclerosis or myocarditis. Extreme forms impede the flow of chyle 
which, with dyspnea and fatigue, impair nutrition. The most grave 
complication is failure of the right heart upon which compensation 
devolves. 

Subjects of emphysema show no predisposition to pulmonary inflam- 
mation. The doctrine that tuberculosis (Rokitansky) or valvular disease 
(Bouillaud) excludes emphysema is incorrect. 

Treatment. — (a) Prophylaxis concerns chiefly the concomitant or causal 
bronchitis. Severe exercise is to be avoided, (b) Coincident gastric, 
renal or gouty disease must be treated, (c) Climate is as important a 
factor as in chronic bronchitis, the inseparable associate of emphysema ; 
high altitudes are avoided, as they directly promote emphysema, {d) 
28 



434 DISEASES OF THE LUNG 

Pneumotherapy is sometimes beneficial. It includes inhalation of thinned 
air, or, where there is marked catarrh, of compressed air. Two or three 
treatments of ten minutes should be given daily, and the time should 
soon be extended to half an hour, (e) Chronic bronchitis (q. v.), and (/) 
asthma (q. v.) are important considerations in treatment, (g) Rhythmic 
compression of the chest, three or four times daily, should be practised 
during 20 to 30 expirations; it increases the circulation in the lung. 
(h) Cardiac insufficiency is treated as in valvular or myocardial disease 
(q. v.) and strychnine, venesection and other measures may be used. 
(i) Freund's operation for calcification of the first chondrocostal joints, 
has been done in over 50 instances; in some cases, striking benefit is 
at once apparent but. chondrotomy has narrow indications. The therapy 
is discussed briefly, as no measure can restore lost elastic tissue or 
patency to obliterated vessels. 

BRONCHOPNEUMONIA. 

This affection was first well described in 1840, by Rilliet and Barthez, 
who separated it from lobar pneumonia and recognized it as a secondary 
disease. It might be well classed among the infections, except that unlike 
fibrinous pneumonia, it is not due to a specific microorganism. 

Definition. — Bronchopneumonia is defined with difficulty; (a) etio- 
logically due to various microbes, it is generally secondary to the bron- 
chiolitis of some specific infection, chiefly in children; (b) pathologically 
it develops about the bronchioles (bronchopneumonia) and in a few 
lobules (p. lobularis), rather than throughout a lobe; its exudate is 
rather catarrhal (p. catarrhalis) than fibrinous, and. its distribution is 
multiple or disseminated (p. disseminata) ; (c) clinically it is identical 
with capillary bronchitis, which, in the first years of life, almost never 
spares the lung tissue; it is marked by fever, cough, dyspnea and cyanosis, 
often without signs of hepatization. 

Etiology. — (a) Some cases, especially in children under two years, are 
primary; these are estimated by Holt and Connor at 35 per cent., Jby 
others at a much lower figure; (b) most cases are secondary to infections 
affecting the upper air passages; 32 per cent, follow measles; 24 per cent, 
pertussis; 16, diphtheria; 15, macrobronchitis; 7, ileocolitis; 3, scarlatina; 
2, influenza; 0.5 per cent, each varicella and erysipelas, (c) Predisposing 
causes in the young are poor sanitation, malnutrition, syphilis, tuberculosis 
and rickets. Bronchopneumonia causes 9 per cent, of deaths in foundling 
asylums, (d) Age. Most cases are observed in children two or three 
years old. Seventy-five per cent, of cases of pneumonia in children under 
five years of age are lobular (Holt). Less frequently in weak, cachectic, 
nephritic and aged persons it may cause death, (e) In some cases microbes 
may act directly on the lungs, as in the primary cases in children, in the 
influenza of adults, and in aspiration or inhalation pneumonia. " Schluck 
pneumonie" is prone to develop in diseases in which the laryngeal 
sensibility is decreased, as in diphtheritic or bulbar palsies; in ether 
anesthesia in which the germ-laden saliva is drawn into the lungs; in 
comatose states, as apoplexy or uremia; in mental diseases; in the new- 



BRONCHOPNE UMONIA 435 

born; in partial drowning; in operations on the throat; or when there is 
persistent vomiting. (/) It is probable that infection may occur by the 
lymph or blood stream. 

Bacteriology. — Bronchopneumonia has no specific bacteriology. In 
adults one-third of the cases show more than one organism, the pneu- 
mococcus ranking first and the streptococcus second; and two-thirds 
show one germ, of which the pneumococcus constitutes 39, the strepto- 
coccus 31, Friedlander's bacillus 23, and the staphylococcus 7 per cent.; 
in children mixed infection is present in half the cases, the streptococcus 
predominating, while in the other half there is but one organism, the 
pneumococcus being the most common. Other germs found are the 
influenza, typhoid, tubercle and colon bacilli, Pfeiffer's Micrococcus 
catarrhalis, tetragenus and the meningococcus. The tubercle bacillus is 
often associated with the pneumococcus. 

Pathology. — The foci of consolidation are usually diffused in the 
lower and sometimes in the upper lobes, posteriorly and usually bi- 
laterally. They vary in size from a pin-head to a walnut or larger; 
most foci lie near the pleura, through which they may be seen and felt; 
the pleura is often granular or fibrinous. On section the consolidated 
nodes appear reddish-brown and later yellowish from fatty degeneration 
of the cells; they are firm, airless, whence they sink in water, and on 
section are generally smooth and glistening, though some pneumococcus 
infections show the granulation and viscid secretion of genuine fibrinous 
pneumonia. The bronchioles supplying the consolidated nodes are 
plugged with mucopus, so that air cannot be forced through them; the 
bronchioles are reddened, swollen or ecchymotic. Though atelectasis is 
frequent its importance has been overestimated. In fortunately made 
sections a dendritic or grape-like arrangement may be seen in which 
the bronchioles correspond to the stems and the alveoli to the leaves 
or grapes. Microscopically the bronchioles show dilated vessels and 
leukocyte emigration, the alveoli show epithelial desquamation, serous 
exudation, leukocyte outpouring and a scattering of red cells; the 
alveolar walls show interstitial inflammation. Though influenza pneu- 
monia is strictly cellular (catarrhal) , aspiration, pneumococcic and other 
forms not infrequently show a fibrin network, though decidedly less than 
in lobar types. Near the foci and in the upper lobes compensatory 
emphysema appears. Extension occurs from alveolus to alveolus or 
along the peribronchial tissues. In some forms numerous lobular foci 
fuse so that the greater part of a lobe consolidates; this pseudolobar 
form is often due to the pneumococcus, is seen in measles and diph- 
theria and clinically may closely simulate lobar pneumonia, though 
pathologically areas of collapsed, vascular or sound tissue lie between 
the bronchopneumonic patches. 

Symptoms. — The clinical picture varies considerably. In the primary 
form, most often pneumococcic, the onset is brusque, with chill, vomiting 
or pain in the side. The fever rises suddenly, and often falls by crisis. 
Capillary bronchitis is absent, consolidation is often marked, the course 
short and the death-rate low. In adults this form is frequently unilat- 
eral. The more common secondary form begins insidiously, if it follows 



436 DISEASES OF THE LUNG 

a microbronchitis ; it is often obscured by the disease it complicates. 
The fever gradually rises to 103° or 104°, and is irregular or remittent, 
rising with each new focus; fever in bronchitis seldom exceeds 102° 
and higher registrations suggest pneumonia; it may be low or absent 
in marantic subjects. There may be no physical findings, or they are 
frequently indeterminate. If recovery ensues, lysis is the usual solution. 

Subjective and General Manifestations. — These are often more 
obvious than the objective pulmonary symptoms. The pulse rises to 
120 or even 180 and in convalescence is more tardy in reaching normal 
than the fever. The respiration is often 60 to 80, the expiration is fre- 
quently catchy or grunting, and the respiration-pulse ratio, normally 1 to 4, 
becomes 1 to 3 or 2; dyspnea, restlessness and irritability develop early. 
Cyanosis arises from impaired flow of blood due to continued coughing 
and stagnant secretion. Pain is not as common as in lobar pneumonia. 
The cough becomes drier and more distressing; the sputum is usually 
swallowed in patients under seven years of age, but if obtained shows 
nothing characteristic. Meteorism is not uncommon in severe or mori- 
bund cases. 

Lung Findings. — On inspection, irregular excursion is sometimes 
seen. The accessory muscles of the nose, neck, chest and abdomen 
are in full play. The interspaces, ribs, sternum and epigastrium in 
young plastic chests retract greatly with each inspiration. Palpation 
may show increased fremitus in a focus near the surface and measuring 
2x5 cm. Stagnant secretion in the air tubes may temporarily suspend 
fremitus. Percussion is often negative for a few days or even through- 
out the course, as deep, isolated foci cannot produce dulness. In the 
thin, infantile thorax, special importance should be attached to light 
palpatory percussion. Dulness obtains over a focus having an area of 
2x5 cm. It is most often found along the spine over the lower lobes. 
Dulness is most marked in the pseudolobar (confluent) forms. Atelec- 
tasis may cause dulness but not bronchial breathing. A hyperresonant 
note in front indicates emphysema; behind it shows relaxation. Auscul- 
tation reveals subcrepitant or crepitant rales, often heard over an area 
not exceeding the bell of the stethoscope. Bronchial breathing and 
bronchophony are fairly frequent, and occur especially when the child 
cries. In other cases the breathing may be rude or puerile. 

Special Types. — Special types have been considered under measles, 
pertussis, etc. The following classification gives the clearest under- 
standing of the physical findings: (a) In capillary bronchitis there is 
no sign of consolidation. Sibilant rales, coarse and fine crepitant rales 
are spread over one or both lungs. Sibilant rales are due to swelling 
of the mucosa of the larger and smaller tubes. A feeble respiratory 
murmur indicates areas of congestion, (b) In disseminated broncho- 
pneumonia, characterized by small areas of consolidation, percussion 
usually gives negative results, or very slight dulness, and the fremitus 
is not altered, since the consolidated areas are deep in the lung, or too 
small to alter the percussion-note. Auscultation reveals crepitant rales 
and bronchovesicular breathing over, the consolidated areas. Vocal 
and crying resonance is exaggerated, (c) In acute generalized broncho- 



BRONCHOPNE UMONIA 437 

pneumonia, the percussion-note is dull over a large area, even an entire 
lobe, with increased vocal fremitus, bronchial breathing and fine moist 
rales, while the rest of the lung shows bronchitis. 

Issues. — Death may occur from carbonic acid narcosis, irritability 
passing into apathy, the harassing cough becoming less marked and 
allowing stagnation of bronchial secretion ("suffocative catarrh"), 
eventuating in heart failure. Complete resolution is the rule in cases 
which recover. Delayed resolution with remissions and exacerbations 
may occur. Complications may develop; (a) pleurisy is the most fre- 
quent; (b) gangrene; (c) abscess, especially in aspiration and influenzal 
forms; (d) pulmonary induration; (e) bronchiectasis; and (/) tuber- 
culosis, less often a sequel than awakened by the new infection. 

Diagnosis. — Reliance on physical signs alone leads to many errors and 
a diagnosis is often determined only by the symptoms, sudden high 
fever, mild fever suddenly rising during bronchitis, dyspnea, rapid res- 
piration, cyanosis, etc. In the very young or marantic and aged the 
symptoms may be very atypical. Lobar pneumonia (q.v., variations in 
children) occurs mostly in sound children over three years of age, runs 
a cyclical course, ends by crisis, is unilateral and involves one or more 
lobes; while bronchopneumonia occurs more often in younger weakly 
children, often after bronchiolitis, runs a longer, more atypical, unfavor- 
able and relapsing course, resolves by lysis, is bilateral and is less marked 
by definite pulmonary findings. Tuberculosis is often distinguished only 
by the course; it invades the upper lobes more and bacilli-laden sputum 
may be recovered by washing the stomach or swabbing the throat after 
the child coughs. Pleurisy (q. v.) is diagnosticated by the aspirating 
needle. 

Course and Prognosis. — The acute course lasts a week, of which the 
measles pneumonia is the prototype; the subacute, lasts two to eight 
weeks, exemplified by pertussis pneumonia, and the chronic, covering 
months, as tuberculous bronchopneumonia. 

The prognosis depends on the patient's social situation, age, the disease 
which the pneumonia complicates and its extent. The outlook is serious, 
especially in the secondary forms (measles and pertussis); in the very 
young it is almost as fatal as infantile diarrhea; aspiration forms are 
very grave, as are those in marantic and aged subjects. In private 
practice the death-rate ranges from 10 to 33 per cent., in hospitals 33 
to 50 per cent., and in asylums even 50 to 100 per cent. 

Treatment. — 1. Prophylaxis — (a) In nasal or pharyngeal infections 
the nose and throat should be frequently cleaned with alkaline anti- 
septics. (6) In laryngeal or bronchial inflammation, congestion and 
atelectasis are avoided by frequent and regular change of posture. It is a 
great advantage to avert influenza, pertussis and measles, in the first 
three years of life, (c) Deep breathing is enforced by affusions of cold 
water on the neck and thorax, (d) Exposure should be avoided by 
firmly fastening the nightgown to the foot of the bed. 

2. Therapy. — Actual treatment is symptomatic, (a) The tempera- 
ture of the room is maintained at 67° to 70° with constant moderated 
ventilation, (b) The diet should be fluid, diluted or predigested; egg 



438 DISEASES OF THE LUNG 

albumen, milk and plenty of water are indicated. At the onset calomel 
gr. y 1 ^ every hour for five doses, is followed by castor oil. (c) Expec- 
torants, as ammonium carbonate, tartar emetic or ipecac, derange the 
digestion, which is of greatest importance. Aromatic spirits of ammo- 
nia, lUv-xx every three or four hours, is the least deranging, and 
stimulates, (d) Pain rarely indicates opiates, which induce stagnation 
of secretion, notably in young, old or weak subjects; dyspnea, pain, 
restlessness, cough, cyanosis and rapid pulse may be relieved by pare- 
goric, which is preferable to Dover's powder or morphine. Fresh air 
is better than drugs, (e) Local applications, as poultices or pneumonia 
jackets and blisters, are useless. (/) In the treatment of fever, anti- 
pyretics, aconite, antimony and other cardiac depressants must be 
avoided; cool applications are equally efficacious; they also lessen 
tympany and carbon dioxide narcosis, stimulate the heart and brain 
centres and deepen respiration, but they must be used with care in very 
young and marantic subjects; in such cases a warm sponge or bath 
may be given, with cold affusions to the neck (v. s.). (g) For cardiac 
stimulants, brandy in daily doses of 5ss-iij, very well diluted in 
water or peptonized milk, aromatic spirits, digitalis, saline infusions 
or enemata, camphor or strychnine may be used. (See page 269 for 
dosage.) (h) Respiratory stimulants include tr. belladonna, oxygen, 
thoracic faradization and mechanical compression of the chest, (i) 
Emetics are unreliable; ipecac has no effect in carbon dioxide intoxica- 
tion, whence it is given with coffee, camphor or cognac. Phlebotomy 
is inadvisable, (j) Inhalations of steam (v. Diphtheria and Croup). 
(k) During convalescence a sojourn in the country or in a warm climate 
is advisable. 



INDURATIVE PNEUMONIA, LUNG CIRRHOSIS, FIBROID PHTHISIS. 

Definition. — An overgrowth of the pulmonary connective tissue. 

Etiology. — 1. Diseases of the Lung. — These may induce local, 
lobular or lobar, unilateral or bilateral fibrous induration. Local indura- 
tion frequently occurs about tumors, tubercles, gummata, abscess, gan- 
grene, etc., and is of no importance, except as it demarks dangerous foci 
of disease. Diffuse induration is important, (a) Fibrinous pneumonia 
sometimes results in lobar induration (0.7 per cent.), notably in marantic 
subjects from delayed resolution; the lung becomes airless and dense 
from fibrous tissue within the alveoli whence it involves contiguous 
structures; on section its surface is smooth, and the connective tissue 
is strikingly translucent. (b) Bronchopneumonia in measles, pertussis or 
influenza, sometimes leads to induration, beginning from an alveolitis or 
peribronchitis, (c) Foreign bodies and aspiration pneumonia; (d) chronic 
tuberculosis; and (e) syphilis, gangrene, etc., are etiological factors. 

2. Bronchial Affections. — (a) Bronchiectasis, noted by Corrigan, 
who first used the term lung cirrhosis; (b) bronchial stenosis, as by 
aneurysm or gumma; and (c) pneumohmiosis and putrid and chronic 
bronchitis may cause indurative pneumonia. 



INDURATIVE PNEUMONIA 439 

3. Pleural Affections. — In Charcot's " pleurogenous" interstitial 
pneumonia, strands of connective tissue invade and cirrhose the lung, 
converging toward the hilum. 

Pathology. — The pathology of an affection with such numerous causes 
can scarcely be described. The early induration is reddish, and the older 
connective tissue is darker, slate-colored or gray. The new connective 
tissue may be formed in the bronchi, septa, alveoli, bloodvessels or 
pleurae. The lung is airless and dense; is cut with difficulty and on sec- 
tion presents either a granulated or a smooth surface, the latter in cases 
following lobar or aspiration pneumonia and sometimes gangrene. The 
lung shrinkage produces changes in the mediastinum, heart, diaphragm 
and sound lung (v. i.). 

Symptoms. — Symptoms in incipient or localized lesions may be insepar- 
able from the causal affection (tuberculosis, bronchiectasis) or may follow 
closely upon it (pneumonia, pleurisy). There may be a low fever, cough, 
dyspnea on exertion, pain in the side, rapid pulse, cyanosis, anemia, 
malnutrition and night sweats. 

Physical findings in the typical chronic case are as follows: (a) On 
inspection the interspaces are narrowed on the affected side, the nipple 
and scapula are nearer to the median line, the shoulder is lower, the spine 
is convex toward the sound side and the measurement is unilaterally 
decreased. In left-sided induration the lung retracts from the heart, 
increasing its pulsation and disclosing the pulmonary artery, over which 
may be seen and felt its systolic filling and the strong diastolic closure 
of the pulmonary valves; in right-sided induration the heart beat may 
appear to the right of the sternum or may be covered up by the compen- 
satory emphysema of the left lung, (b) Palpation corroborates these 
findings, and, as a rule, shows increased vocal fremitus. The second 
pulmonic tone is much accentuated, corresponding to the routine hyper- 
trophy of the right ventricle and the occasional atheroma of the pul- 
monary artery, (c) Percussion elicits dulness below, and sometimes a 
slightly hyperresonant note above, the indurated area; the apex of the 
upper lobe is on a lower level and the diaphragm stands higher (the 
liver rising or Traube's space increasing); there is no respiratory excur- 
sion, (d) Auscultation brings out the absence of breath sounds below, 
and bronchial breathing and subcrepitant, crepitant and bubbling rales 
above. Additional signs result from the right heart hypertrophy and 
dilatation, from coincident bronchiectasis or cavity formation on the 
same side, and compensatory emphysema on the opposite side. There 
is nearly always some sputum. 

Diagnosis. — Diagnosis is more easily made in chronic than in the 
subacute postinfluenzal or postpneumonic induration which may sug- 
gest tuberculosis or interlobular suppuration. Slow-growing tumors of 
the lung may cause confusion. The x-rays are helpful. 

Prognosis. — The prognosis varies with the etiology. Ulcers from arte- 
rial occlusion or infected bronchial secretion, explain the frequent lung 
^morrhage (in 50 per cent.) and its occasional role as a cause of death. 
Amyloidosis sometimes results but death is usually caused by right 
he r t failure. 



440 DISEASES OF THE LUNG 

Treatment. — Life may be prolonged for decades under proper hygiene. 
Exercises with the arms may check the early shrinking, but nothing can 
remove an established induration. Warm climates at the sea level or 
at slight elevation are beneficial. Some writers hold that turpentine 
checks induration. 

PNEUMOKONIOSIS. 

Zenker employed the term to include various indurative diseases of 
the lungs due to "dust" inhalation. 

Etiology and Pathology. — 1. Anthracosis is due to inhalation of carbon, 
coal dust, soot, charcoal or graphite, and is known as "coal miner's 
disease" or phthisis melanotica. (a) Moderate amounts of carbon 
inhaled into the bronchi are absorbed by the leukocytes, worked upward 
by the ciliated epithelial cells and expectorated, (b) Larger amounts 
penetrate the bronchial mucosa to the connective tissue, or enter the 
lymph stream whence they reach the small lymph nodes around the 
vessels and bronchi or mediastinal lymph glands. A moderate pigmen- 
tation occurs in all city inhabitants, while the lungs of countrymen 
are pink, (c) Very large amounts reach the alveoli, when the lungs are 
ink-black; connective tissue proliferation develops in insular foci (endo- 
perialveolitis nodosa and endoperilymphangitis fibrosa); the foci occa- 
sionally measure 5 x 15 cm., on section are hard and exude an inky 
fluid. Induration involves the mediastinal lymph glands, and often 
extends beyond them (perilymphadenitis) ; by this latter process the 
glands may become adherent to, and rupture into, the pulmonary veins, 
whence pigment-metastases into the liver, spleen, kidneys and mesenteric 
glands are not infrequent. Bronchial perilymphadenitis may also lead 
to diffuse induration, mediastinopericarditis, stenosis of the trachea, 
bronchi, esophagus, cava, vena azygos and pulmonary artery, to esopha- 
geal diverticulum, fatal hemorrhage into the pericardium or bronchi 
when the aorta is also eroded, to aspiration pneumonia by intrabronchial 
rupture or to recurrent laryngeal paralysis by pressure. Lehmann holds 
that the great bulk of dust and similar bodies find their way into the 
system by absorption from the digestive tract. 

2. Siderosis pulmonum (Zenker) is a similar change, due to inhalation 
of metallic dusts, as iron, brass or bronze; there are the same interstitial 
deposit, lung induration, bronchial gland cirrhosis and metastases. The 
irritation is greater, nodes are more frequent and induration is more 
intense than in anthracosis. 

3. Chalicosis pulmonum (Peacock) is due to inhalation of alumina, 
quartz or sandstone, known as "stone-cutter's or millstone-maker's 
phthisis," "grinder's rot" or "potter's asthma." Calcium is less irritating 
than silica or quartz. Of all forms, the most nodules and induration 
occur in chalicosis. 

4. Similar changes are observed from inhalation of wool, flax, cotton, 
grain, tobacco, glass, porcelain, pepper, cinnamon, bone, lead, mercury, 
phosphorus, zinc, arsenic and horn. 

Symptoms. — After many years, the symptoms of chronic bronchitis 
asthma, emphysema and finally of lung cirrhosis appear. The sputy 1 



ATELECTASIS 441 

contains coal dust, soot, charcoal particles, as in Traube's celebrated 
case, and yellow oxide or dark phosphate of iron, quartz and silica. 
Cavities may form from bronchiectasis, softening of the nodose indura- 
tions or tuberculous complications; in some cases lung stones, set free 
by ulceration, may be raised. Tuberculosis occurs in 13 per cent, of 
anthracosis and in 44 per cent, of chalicosis. Scissor-grinders rarely 
live beyond forty years of age and blasters in mines usually succumb in 
four years. 

Treatment. — Treatment is largely prophylactic and that of the con- 
comitant bronchitis and emphysema. 

ATELECTASIS. 

Apneumatosis is a congenital or acquired "absence of air." 

I. Congenital atelectasis was first described by Jorg (1834). 
Etiology and Pathology. — This variety is due to deficient inspiratory 

efforts from weak muscles, insufficient stimulation of the bulbar centres 
and aspiration of mucus or meconium. The base, anterior margin and 
lingual lobe are most involved and the distribution is lobular. If the 
subject lives, the atelectatic portions do not become pigmented. These 
airless areas are sunken, bluish, lax, do not crepitate and sink when put 
in water. Bronchiectasis may result; the ductus Botalli and foramen 
ovale are usually patent, the right heart is dilated and thrombosis is 
frequent in the brain sinuses, kidney and right heart. 

Symptoms. — The newborn with atelectasis breathe superficially and 
cry but little. Inspiration is marked by retraction of the epigastrium, 
subclavicular and intercostal spaces, for the lungs cannot follow the 
inspiratory distention of the thorax. If the undistended area measures 
2 by 5 cm. it may be dull and increased fremitus with bronchial breathing 
may be detected, but more often the breathing is weak or entirely absent. 
Carbon dioxide narcosis develops, the pulse becomes small, the sensorium 
becomes dulled and, without active intervention, asphyxia causes death. 
If the patient lives, the chest is peculiarly deformed, its lower parts 
being sunken, so as to show the ribs. 

Treatment. — Removal of meconium and mucus by swabbing or aspira- 
tion, artificial respiration, swinging, and warm baths with cold affusions 
to the neck and chest are indicated. 

II. Acquired Atelectasis. — Acquired atelectasis was first described by 
Legendre, Bailly and Traube. 

Etiology. — The lungs, already distended and ventilated, collapse and 
the air is absorbed, (a) The marantic form occurs in bed-ridden indi- 
viduals reduced by typhoid, infantile diarrhea or cachectic conditions. 
(b) Obstructive collapse develops most frequently in bronchopneumonia, 
as the bronchioles in the young are narrow, or in any stenosis, bronchial, 
etc. (c) Compressive apneumatosis follows compression by aneurysm, 
dilated heart, tumors, exudates, pneumothorax, abdominal tumors, 
kyphoscoliosis, etc. 

Pathology. — Pathologically the same general findings obtain as in 
the congenital type. The lung is reddish-brown or bluish. Hyperemia 



442 DISEASES OF THE LUNG 

may cause a flesh-like appearance (carnification) , or serous transudation 
may cause a spleen-like aspect (splenization) . There may be coincident 
inflammation or vicarious emphysema. Long-standing atelectasis 
results in bronchiectasis, fatty degeneration of the alveolar epithelium 
and hyperplasia of the interalveolar connective tissue, known as collapse 
induration. 

Symptoms. — Symptoms are easily obscured by the causal pleural 
effusion or bronchopneumonia, with whose foci it may be confused. 
Inspiratory retraction, lessened vesicular breathing, a slightly tympanitic 
note from relaxation of the collapsed lung and crepitant rales are com- 
mon. Increased vocal fremitus and bronchial breathing are uncommon. 
Dilatation of the right heart is usual. In recent cases the physical signs 
disappear after a few hours of change of posture, or after deep breathing, 
which, with absence of fever, pain and cough, effectually differentiates 
from infarct, pneumonia or effusive pleurisy. After sleep for some hours 
on the back, a few crepitant rales may be heard physiologically over the 
lower posterior parts for three or four inspirations. 

Prognosis and Treatment. — The prognosis and treatment vary accord- 
ing to the cause. In all fevers and all respiratory inflammations the 
posture must be changed frequently; orders to this effect should be 
written, and the change should be recorded on the history sheet. Cold 
affusions, hydrotherapy and cardiants are indicated. 



ABSCESS OF THE LUNG. 

Suppuration may occur in a sound or diseased lung. 

Etiology. — (a) Lobar pneumonia causes 62 percent.; upper lobe localiza- 
tion, alcoholism, pneumonia complicating emphysema and lung indura- 
tion and hemorrhagic types are the predisposing factors, (b) Lobular 
pneumonia, especially the influenzal type, may suppurate, (c) Aspira- 
tion pneumonia is causal in 18 per cent., particularly in insane or delirious 
subjects; foreign bodies, food, saliva or pus from lesions in the upper 
respiratory tract, vomiting, esophageal cancer rupturing into a bronchus, 
are its usual causes, (d) Embolic suppuration produces 17 per cent. 
(e) Trauma is another factor, (f) Abscess may. complicate tuberculosis, 
bronchiectasis, echinococcus, etc. (g) Rupture into the lung of contiguous 
suppuration, such as empyema, suppurating peribronchial glands, sub- 
phrenic abscess, spinal caries and gastric ulcer, causes 3 per cent, of lung 
abscesses. Most cases occur in middle-aged males. 

Bacteriology. — The staphylococcus is most frequently the causative 
microorganism; the streptococcus, pneumococcus, pneumobacillus, 
influenza bacillus, colon bacillus and leptothrix are also found. 

Pathology. — The cavity varies from the size of a hazel-nut to an orange ; 
it may occupy even an entire lobe or lung. The abscess is usually single, 
except in the embolic form. Its shape is irregular and it is sometimes 
multilocular. Its inner surface is irregular with floccular mural shreds, 
and is walled with pus-secreting granulations, which in some cases fill 
and obliterate the cavity. Fibrous tissue develops about the cavity, and 



ABSCESS OF THE LUNG 443 

in chronic abscess becomes dense and scar-like. The cavity is usually 
near the lung's surface, whence the frequency of complicating pleurisy; 
80 per cent, of lung abscesses are in a lower lobe (Tuffier). 

Symptoms.— The symptoms vary with the causal lesion; in lobar pneu- 
monia the crisis is delayed and resolution is incomplete; in influenza 
the respiratory symptoms and fever persist; in sepsis, multiple lung 
involvement perpetuates the septic process, (a) The sputum is purulent, 
offensive or rancid without putridity, alkaline and may measure a pint 
to a quart daily. It separates, on standing, into two layers, a granular 
sediment and a serous upper layer, sometimes with frothy surface. In 
metapneumonic cases the sputum is sometimes grass-green. The sedi- 
ment reveals shreds of lung tissue (Traube and Leyden) and yellowish- 
green or gray flocculi ; these are absolutely essential to diagnosis and 
consist of elastic fibers to which alveolar epithelium adheres. Hematoidin 
crystals or platelets, short sheaths of fatty crystals, bacteria (v. s.) and in 
chronic cases cholesterin and scar-like connective tissue are also found. 
The "mouthful expectoration" is voided periodically, as from cavities 
of other causation, (b) The decubitus varies with the location of the 
cavity; the patient assumes the erect posture if the cavity is in a lower 
lobe, to prevent leaking of the secretion into the bronchi, (c) Signs 
of cavity are found if the exulceration is large and superficial, and in 80 
per cent, occur in the lower lobes. They are essentially those of tuberculous 
or bronchiectatic cavities (q. v.) and vary with the stagnation or evacua- 
tion of the pus; thus a tympanitic note, bronchial or amphoric breathing 
and increased vocal fremitus are found when the vomica is empty, and 
dulness, weakened breath sounds and decreased fremitus obtain when it 
is full. The arrays also serve to localize, but when the findings differ 
the physical signs are more trustworthy, (d) Hectic fever, sweats, rigors 
and leukocytosis occur from resorption. 

Diagnosis. — The etiology and cavity formation are often, and the 
sputum always, characteristic, (a) Abscess breaking into the lung from 
the spine or the subphrenic or pleural spaces is sudden, sometimes 
suffocative in onset, and the hematoidin crystals and shreds of pul- 
monary tissue are absent, (b) Gangrene (v. i.). (c) Tuberculosis usually 
occurs in an upper lobe; abscess in a lower one; elastic fibers and hema- 
toidin crystals are more abundant in abscess, and tubercle bacilli are 
found in tuberculosis, (d) In bronchiectasis elastic fibers are seldom 
voided. 

Prognosis. — Spontaneous recovery may follow granulation and cica- 
trization, especially in lobar pneumonia, where recovery is the rule. 
In influenzal or aspiration pneumonia or in sepsis the outlook is far 
less favorable; marasmus, hectic fever, amyloidosis, lung induration, 
empyema, pneumothorax and pericarditis are frequent issues. 

Treatment. — (a) The general strength should be maintained by a full 
diet, tonics and alcohol, (b) Decomposition, if present, should be modi- 
fied as in bronchiectasis or gangrene, by administration of creosote or 
turpentine internally, (c) Surgical intervention is indicated (i) when the 
abscess is large, shows no tendency toward spontaneous cure and the 
contents decompose; (ii) when rupture into the pleura occurs; and 



444 DISEASES OF THE LUNG 

(iii) when the abscess results from the breaking into the lung of a 
contiguous focus of suppuration. The mortality is 25 per cent, under 
surgical, and 54 per cent, under expectant, treatment. 

GANGRENE OF THE LUNG. 

Definition. — A necrosis and mortification of lung tissue. Gangrene, 
though more common than abscess, is found in 0.1 per cent, of clinical 
cases only and in 1.6 per cent, of autopsies. 

Etiology. — Reduced physiological resistance, e. g., from diabetes, is 
a necessary factor. Lobar pneumonia may terminate in gangrene when, 
as in abscess, the patient is weakly, diabetic, addicted to alcohol or 
suffering from putrid bronchitis; though its frequency is but 0.4 per 
cent., pneumonia causes 23 per cent, of lung gangrene. Lobular pneumonia 
is less frequently causal, though grippe pneumonia may terminate in gan- 
grene. In Coupland and Hensel's combined cases, 14 per cent, were due to 
pulmonary tuberculosis and 10 per cent, to tumor of the lung. Aspiration 
pneumonia resulting in gangrene occurs particularly in insane, delirious, 
paralyzed or emaciated subjects; foreign bodies, necrotic diseases of the 
throat, larynx or bronchi, bronchiectasis, putrid bronchitis and bronchial 
stenosis promote gangrene. Embolic gangrene, a cause of 19 per cent, 
of lung gangrene, may result from suppurative gangrenous lesions in 
the appendix, uterus or extremities. Rupture into the lung, as of esopha- 
geal cancer or diverticulum, putrid pleurisy, subphrenic abscess or 
gastric ulcer may cause gangrene. Gangrene usually occurs within 
the second to fourth decades of life and in males. 

Bacteriology. — Some maintain that certain germs produce the necrosis 
and other germs the gangrene, but probably one microorganism pro- 
duces both changes. The staphylococcus is found, also the strepto- 
coccus, colon bacillus and " acid-fast" pseudotubercle bacillus; the B. 
pyocyaneus, Micrococcus tetragenus, a micrococcus which produces 
skatol and indol, and causes a putrid odor in the cultures, and a bacillus 
resembling that of malignant edema, are enumerated. 

Pathology. — Genuine gangrene must not be confused with softening 
of the lung, due to regurgitation of the gastric juice into the lung during 
the death agony or after death. There is a rare non-putrid pneumo- 
malacia, analogous to myomalacia cordis. Lung gangrene occurs in 
the right lung in 45 per cent., in the left in 37 and in both lungs in 18 
per cent, of the cases. Laennec, who first described pulmonary gangrene, 
distinguished two types, the circumscribed and the diffuse, (a) Cir- 
cumscribed gangrene occurs chiefly in the lower lobes near the surface, 
and oftener on the right than on the left side. The focus may attain the 
size of an orange. Laennec distinguished three stages: (i) The forma- 
tion of a yellow, green or brown slough, which may be expectorated 
entire; (ii) liquefaction, or moist gangrene; and (iii) formation of a 
cavity which is irregular in shape, has ragged walls and contains a stink- 
ing liquid resembling the sputum of gangrene (v. i.). The cavity is 
limited by granulations and later by connective tissue, or gradually 
spreads, corroding more and more lung tissue, or extension may follow 



GANGRENE OF THE LUNG 445 

aspiration of the septic matter into other lung areas. Recovery may 
follow localization, organization of granulations and contraction of con- 
nective tissue. Microscopically there is (i) an inner zone of offensive 
fluid or necrotic tissue, bacteria and emigrated leukocytes; (ii) outside 
of this is a zone of granulations, beyond which is (iii) congested or edema- 
tous lung, (b) The rarer diffuse gangrene has no demarkation, and a 
large area, an entire lobe, or even the whole lung may be discolored, 
stinking and macerated. The diffuse form occurs more often in the 
upper lobes, and on the right side. In both forms the sputum irritates 
and injects the bronchial mucosa, the bronchial glands are tumefied 
and degeneration or metastasis may occur in various viscera. 

Symptoms. — 1. Sputum. — The sputum is characteristic, essential to 
diagnosis, and absent only when the putrid focus has no bronchial con- 
nection. It is extremely offensive, fecal, stinking or garlicky. It is 
most offensive at the moment of evacuation, and on standing may 
gradually lessen. The sputum, voided periodically and sometimes in 
mouthfuls, is usually abundant (a pint to a quart), and on standing 
separates into three layers, an upper layer of foam, a middle of green 
or gray serum, and a lower of green or brownish granular sediment. In 
the sediment there are flocculi of lung tissue, best seen against a dark 
background, varying in size from small particles to pieces as large as 
the thumb and showing alveolar arrangement; elastic fibers are much 
less common than in abscess of the lung, for a trypsin-like ferment rapidly 
digests the fibers; DittricJis plugs are found, consisting of detritus and 
bacteria, and emitting a most fetid odor (v. pages 421 and 422); long 
fatty needles, lung pigment, pus cells, red corpuscles, hematoidin crystals, 
bacteria, infusoria, leucin, tyrosin, phenol, indol, skatol, ammonia and 
sulphuretted hydrogen are also found. 

2. Chest Findings.— Besides bronchitis caused by the offensive 
sputum, signs of infiltration or cavity formation are obtained if the focus 
is superficial and measures two and one-half inches. In the common cir- 
cumscribed form the signs of cavity are identical with those in tuber- 
culosis, bronchiectasis or abscess, i. e., a tympanitic note, increased 
vocal fremitus, bronchial or amphoric breathing and metallic rales are 
obtained when the cavity is empty, or dulness, decreased fremitus and 
weak breathing when it is full. In the rare diffuse form there are signs 
of infiltration, as in pneumonia, which signs are also found in the initial 
stage of the circumscribed gangrene. The .r-rays are valuable in localiza- 
tion of the gangrene. The patient lies so that the cavity is dependent, 
to avoid constant trickling of the secretion into the bronchi, i. e., on his 
back when it is posterior or on his face when it is anterior or in an upper 
lobe. 

3. General symptoms result from the causal disease or sepsis. Remit- 
tent fever, chills, sweats, emaciation, pallor, rapid pulse, vomiting, 
diarrhea, leukocytosis, albuminuria and in severe cases a profound 
typhoid state mark the degree of intoxication. 

4. Complications may dominate the clinical picture, (a) Pleurisy, 
usually purulent or putrid, may be the chief symptom, and operation 
may evacuate offensive fluid with fragments of necrotic lung, (b) Hemop- 



446 DISEASES OF THE LUNG 

tysis is seldom fatal, though frequently profuse, (c) Pyopneumothorax, 
or (d) rupture into the esophagus, aorta, mediastinum, etc., may occur. 
(e) There may be metastatic deposits in the brain, liver, joints or muscles. 
(/) Clubbed fingers or amyloid degeneration occasionally result from 
septic absorption. 

Course and Prognosis. — The course is usually fatal within a week in 
diffuse, and is more chronic in circumscribed, forms. The prognosis 
depends on the etiology, resistance of the patient, degree of toxemia, 
localization and surgical accessibility. 

Diagnosis. — Exploratory puncture is dangerous, for it favors diffusion. 
(a) In fcetor ex ore the breath is fetid but the sputum, if any, shows no 
findings characteristic of gangrene. (6) In putrid bronchitis the sputum 
shows Dittrich's plugs and fetor, but no fatty crystals or pulmonary 
tissue, (c) In abscess elastic fibers and pus are more abundant, the 
fatty crystals are oftener in sheaths than in long needles and hematoidin 
crystals are more common; bronchial plugs and fetor are absent, (d) 
In bronchiectasis elastic fibers are very rare and lung tissue has never 
been found, (e) In tuberculosis coincidence of the two affections and the 
pseudotubercle bacillus may alone cause confusion (v. Tuberculosis). 

Treatment. — 1. Surgical. — Expectant treatment results in a mor- 
tality of 90 per cent. With operative treatment the death-rate is 45 
per cent. (In 20 personal cases, 66 per cent, recovered under medical 
treatment.) The surgical indications are (a) the vital indication when 
acute gangrene assumes the foudroyant type, or (b) when, in chronic 
forms, there is no tendency toward spontaneous healing. Accurate 
localization by physical findings or by the arrays was possible in 65 
per cent, of Tuffier's series. 

2. Expectant treatment is indicated in deep-seated gangrene, 
hopeless metastases or apparent demarkation. The patient is kept on 
his back to avoid leakage into sound bronchi. The diet should support 
the strength and include full alcoholic stimulation. Carbolic acid, 
balsam of Peru, creosote, or turpentine (when there is a complicating 
hemorrhage) may be given internally. 



TUMORS OF THE LUNG. 

I. Carcinoma. — Cancer of the lung may be primary (17 per cent.), 
metastatic (73 per cent.) and extension by contiguity (10 per cent.). 
It occurs in 0.17 per cent, of autopsies or in 1.8 per cent, of cancer autop- 
sies (Passler). Most primary cases develop between forty and sixty 
years of age. In primary forms Passler found 73 per cent, in males; 
the secondary forms are more frequent in women, following cancer of 
the mamma or the digestive or genital organs. 

Etiology and Pathology. — Cancer usually develops in the bronchi, 
in which previous ulceration, syphilis or adherent rupturing lymph 
glands are predisposing, factors. It probably may develop from the 
bronchial mucous glands or even from the alveolar epithelium. His- 
tologically the cylindrical type is by far the most frequent, though 






TUMORS OF THE LUNG 447 

medullary, scirrhous and other forms are encountered. Cancer usually 
begins at the hilum, and may extend toward the pleura, either by 
contiguity along the bronchi or by the lymph spaces. The upper lobes 
are more often involved than the lower and the right twice as frequently 
as the left. Primary disease is generally unilateral. Secondary cancer is 
generally bilateral; the lungs are strewn with miliary nodules resembling 
miliary tubercles, or present many larger nodules. Calcification and 
ossification may occur. Krieg collected 201 primary tracheal tumors 
(40 carcinomas and 21 sarcomas, most of the balance being benign). 

Symptoms. — With a primary tumor in another part of the body, 
cyanosis, dyspnea, blood-stained sputum and signs of lung infiltration 
or of cavity, facilitate a diagnosis of lung metastasis. When there is a 
hidden primary focus or a primary lung tumor, diagnosis is for a long 
time difficult or impossible. 

1. Early General Symptoms. — These are usually ambiguous or 
suggestive of tuberculosis, pleurisy or bronchitis. Thoracic oppression, 
coughing, stridor and dyspnea result from pressure on the trachea and 
vagus or wide substitution of tumor for lung tissue. Cyanosis, dyspnea, 
rapid breathing, emaciation and sweats may suggest miliary tubercu- 
losis; this resemblance may also be noted at autopsy in miliary carcinosis; 
fever develops in over half the cases. Rokitansky's contention that 
pulmonary cancer and tuberculosis do not coexist is disproved by Wolff's 
31 cases of cancer of the lung of which 23 had tuberculosis. 

2. Sputum. — The sputum in over half the cases is rather characteristic. 
Altered blood gives it a reddish-brown color or it resembles raspberry 
jelly in hue and in consistency; it is sometimes grass-green or prune- 
juice in color. Occasionally macro- and microscopic bits of cancer tissue 
in characteristic nest-like arrangement are seen. 

3. Physical Signs. — (a) Inspection: The patient usually lies on the 
affected side to give freer play to the sound lung. Marked ectasia is 
common; sometimes the diseased side is shrunken from lung cirrhosis 
or bronchial stenosis, (b) Palpatio)! elicits increased fremitus if the tumor 
partially occludes the bronchi, (c) Percussion gives increased resistance 
and irregular dulness, increasing to absolute flatness, most often over an 
upper lobe or substernally. Flatness persisting after tapping, and 
blood-stained sputum without tubercle bacilli in a patient over fifty 
years, at once suggest pulmonary neoplasm, (d) Auscultation varies 
with the patency of the bronchus, giving bronchial breathing when it is 
open and weak or absent breathing when occluded. 

4. Compression Symptoms.- — Besides the early dyspnea and cough, 
(a) the heart is often luxated or its yielding auricles are crowded, (b) 
The venous trunks suffer compression, with cyanosis and edema of the 
face, neck and arms and with collateral dilatation of other veins of the 
thorax, (c) Other symptoms of compression are rapid or slow heart 
(vagus compression), recurrent laryngeal compression with phonic changes, 
dysphagia, intercostal neuralgia, brachial neuralgia or paralysis, and 
bronchial stenosis. 

5. Metastasis.- — This occurs in 85 per cent, of cases; there may also 
be extension, by contiguity, to the axillary or cervical glands. 



448 DISEASES OF THE LUNG 

6. Complications include hemoptysis from necrosis and cavity forma- 
tion; gangrene and bronchiectasis; and pleurisy, which is usually serous 
(hemorrhagic in 12 per cent., even like venous blood, or rarely adipose 
or chyliform effusions); hydropic, fatty and granular cells or flocculi 
of tumor tissue, may be obtained by puncture. Carcinomatous nodes 
may develop at the site of puncture. The course is indicated by 
Marfan 's types; the acute or galloping pleuropulmonary cancer, and the 
chronic type (the typical, bronchopulmonary, the mediastinal, and the 
pleuritic with or without effusion). 

II. Sarcoma and Lymphosarcoma. — Sarcoma and lymphosarcoma 
are more frequent than cancer. They probably begin chiefly in the 
lymph nodes of the bronchi, and oftener on the left than on the right 
side. Extension in all directions occurs along the peribronchial tissues 
from the hilum. A primary, very malignant lymphosarcoma develops 
in cobalt miners of Saxony; 150 cases among less than 700 miners were 
described by Anke in 1884. Ulceration is less common than in cancer, 
but the symptoms are, in the main, identical. Sarcomatous tissue is 
occasionally voided in the sputum or aspirated by the exploring needle. 
The differentiation of malignant lung tumors must be made chiefly 
from aneurysm (q. v.) and pleurisy (q. v.). The arrays may be of value. 
There are three main clinical groups, (a) in which a neoplasm, perhaps 
its exact type, can be diagnosticated; (b) in which some growth is 
present but differentiation from aneurysm is uncertain; and (c) in which 
the disease escapes detection or is only suspected. 

Prognosis. — Death generally occurs in less than a year with cachexia 
or suffocation, but sometimes within a few weeks. 

III. Other Tumors of the Lung. — Fibroma, lipoma, osteoma, hyper- 
nephroma and enchondroma are of solely anatomical interest. 

Treatment. — It is only palliative — morphine for extreme dyspnea and 
cough. The ^-rays and arsenic offer little encouragement. 

CIRCULATORY AFFECTIONS OF THE LUNG. 

I. Active Congestion. — As a secondary lesion acute hyperemia occurs 
commonly with tuberculosis, pneumonia, influenza, pleurisy or cardiac 
strain. French writers describe an acute primary congestion (Maladie 
de Woillez); some cases are apparently abortive pneumonia; perhaps 
it is due to attenuated pneumococci, which Carriere has demonstrated 
by puncture of the lung It develops like pneumonia, with chill, fever 
of 101° to 103°, pain in the side, dyspnea, cough and an abundant, viscid 
but not blood-stained sputum. Physical examination is said to elicit 
somewhat impaired resonance and weak or occasionally bronchial 
breathing. 

II. Passive Congestion; Hypostasis. — In broken compensation, par- 
ticularly in mitral stenosis, the lungs are distended, heavy; indurated, 
and pigmented a brownish-red; this is brown induration (indnratio 
pulmonum fusca). The capillaries are turgid, the connective tissue is 
increased, the lungs are tinged with blood pigment and the sputum con- 
tains the so-called heart disease cells (see page 368).. 



CIRCULATORY AFFECTIONS OF THE LUNG 449 

Hypostasis is a passive congestion from weak heart, in typhoid and 
other fevers, old age, cachexias, in opium and other narcoses and in 
apoplectic or other comas; it rarely occurs if the patient's position is 
changed every few hours. The lung is dark red, engorged with blood and 
serum, and may also show aspiration pneumonia and atelectasis; the 
latter conditions are incorrectly called hypostatic pneumonia. There 
is moderate dulness over the lower lobes posteriorly, in apoplexy perhaps 
only on the paralyzed side; the breathing is more often weak than 
bronchial, and moist or crepitant rales are heard. Fever is no part of 
hypostasis. 

Treatment. — Treatment of the fundamental lesion, phlebotomy, stimu- 
lation and frequent change of posture are indicated. 

III. Infarct; Embolism. — Etiology. — Embolism, first observed by 
Laennec, is most frequently caused by (a) fibrinous coagula from the 
right heart, the frequency and mechanism of which have been discussed 
under Acute and Chronic Endocarditis and Septic Infections. 
Clots may also reach the lung from peripheral thromboses or rarer causes 
are (b) tumor or hepatic tissue, fat embolism after fractures and liver 
injury, air embolism or echinococcus cysts. 

Pathology. — The embolus may obstruct a main branch of the pul- 
monary artery, straddle one of its bifurcations or lodge in a smaller 
vessel. Not every embolism produces an infarct, for the occlusion may 
be incomplete or collateral circulation possible. Occlusion of an end- 
vessel results in the hemorrhagic infarct, which is often wedge-shaped 
with its base toward the pleura, is airless, on section projects above the 
cut surface, and is attended by extravasation of blood into the lung, 
though the lung is not torn. This is known as a fibrinous or simple 
infarct. If the embolus contains pus or putrefactive microorganisms, 
it initiates abscess or gangrene. Infarcts occur in the right lower lobe 
in 46 per cent., right upper in 21, left lower in 15, left upper in 12 and 
right middle lobe in 6 per cent. They are often multiple. Small infarcts 
may be absorbed, but larger ones leave pigmented cicatrices. 

Symptoms. — (a) Infarction of the main pulmonary trunk may result 
in immediate death, as from sitting up after childbirth (two-thirds of 
these cases die) . In other cases death occurs in a short time from cerebral 
anemia and cardiac failure. The infarct may cover the greater part of 
the lobe involved, and a systolic murmur may develop over the pul- 
monary artery. (6) Infarction of a smaller vessel is often ushered in 
with chill, vomiting, dyspnea, cyanosis and fever, even with bland 
embolism. The sputum contains dark blood and a "stitch in the side" 
denotes pleuritic participation. Physical examination frequently elicits 
a pleural rub and later, in some cases, slight dulness, especially behind, 
between the spine and scapular line; crepitant rales and bronchial 
breathing are frequently present. Pyogenic or putrid clots cause abscess, 
gangrene, empyema or pneumothorax. 

Diagnosis. — Sudden cardiac failure is very difficult to differentiate 
from embolic occlusion of the pulmonary trunk, especially when death 
occurs without hemoptysis. The etiology, sudden onset and circum- 
scribed chest signs are of diagnostic importance.' Treatment lies in 
29 



450 DISEASES OF THE LUNG 

cardiac stimulation and prophylaxis — rest during endocarditis, cardiac 
insufficiency or phlebitis. 

IV. Edema of the Lungs. — Etiology. — Pulmonary edema was described 
by Laennec (1819). In the etiology of this secondary, common, fre- 
quently terminal or agonal affection, three important causes stand in the 
foreground, viz., heart, kidney and lung disease. Edema is a serous trans- 
udation into the air cells and interstitial tissue. Classification of its 
mechanism is difficult: (a) Stasis due to heart weakness is its most 
frequent mechanism. Cohnheim and Welch demonstrated experimen- 
tally that it may result from failure of the left ventricle, with continued 
activity of the right ventricle (this explanation is not entirely satisfac- 
tory, for cases in which the pulse is strong; however, general cardiac 
anasarca may occur when the radial pulse is strong, though it is known 
that the heart must be weak). Weak heart may result from any disease 
of the endo-, myo- or pericardium. Sahli explains certain cases by (b) 
paralysis of the pulmonary vessels. Under (a) or (6) nephritic or toxic 
edema, edema from pleural paracentesis, the iodides, ether, adrenalin or 
pilocarpine may be included, (c) Inflammatory edema, e. g., around 
fibrinous pneumonia and other pulmonary disease, is an exudation, not 
a transudation; the pulse is usually strong and there is often fever. 
It is possible that (d) angioneurotic edema or (e) occult changes in the 
blood and bloodvessels are causal factors. These varied mechanisms, 
most common in cardiac, renal and pulmonary lesions, may also operate 
in cachexia, anemia, cerebral disease, old age or innumerable other 
conditions. 

Pathology. — Edema may be circumscribed or oftener diffuse. The 
lungs are large, heavy and spongy; they pit and on section, especially 
of the bases, a frothy serosanguineous fluid exudes. 

Symptoms. — Symptoms usually come on precipitately , with dyspnea 
and cyanosis. The sputum is copious, foamy, somewhat resembling 
soapsuds or at times tinged with blood; it is rich in albumin and poor 
in mucus and cells. The bubbling breathing indicates serum in the 
alveoli. The second pulmonic sound is accentuated, the pulse is weak, 
the lung note is slightly tympanitic from relaxation and coarse and 
fine rales are heard everywhere. If the lower lobes are filled, the physical 
signs may closely resemble those of consolidation. Recurrent attacks are 
described. The diagnosis is determined from the sputum and lung findings. 

Treatment. — Too often edema is the death agony itself, (a) Prophyl- 
axis concerns, e. g., the causal, cardiac weakness or anasarca in nephritis. 
(b) Diffusive stimulants are indicated hypodermically, as camphor, 
strophanthus and strychnine, and by mouth, coffee or champagne, (c) 
Morphine is almost specific, (d) Venesection relieves the right heart 
and is particularly indicated in hypertension, (e) Stimulating expec- 
torants and rapid purgation by croton oil, TTliij, on the tongue and 
artificial respiration are rarely of value. The author has obtained no 
results from the acetate of lead. Atropine and adrenalin are dangerous, 
adrenalin not infrequently inducing edema. 

V. Hemoptysis. — Hemoptysis or hemoptoe refers to "spitting of 
blood," while profuse hemorrhage is known as pneumorrhagia. 



CIRCULATORY AFFECTIONS OF THE LUNG 451 

Etiology. — (a) Laryngeal ulceration or inflammation; (b) tracheal 
ulceration or aneurysm bursting into the trachea; (c) severe inflamma- 
tion or ulceration of the bronchi, cardiac stasis, bronchiectasis, putrid 
and fibrinous bronchitis, rupture into the air passages of aneurysm or 
anthracotic lymph glands; hemoptysis may also occur in the acute 
exanthemata, in blood affections as hemophilia, scurvy, purpura and 
leukemia, and in renal disease and cholemia; hemoptysis occurring as 
vicarious menstruation, mentioned by Hippocrates, is an established, 
though rare, variety ; hemoptysis vicarious to suppression of hemorrhoidal 
bleeding must be regarded with scepticism, (d) Lung disease is its 
most important etiology, notably (i) tuberculosis (q. v.), which explains 
80 to 90 per cent, of blood-spitting. It very rarely occurs under six 
years of age, as children seldom develop cavities. It occurs as capillary 
or profuse hemorrhage. Hemoptysis sometimes occurs epidemically 
among tuberculous subjects, referable to the pneumococcus. (ii) Infarcts 
are characterized by hemoptysis, (iii) Pneumonia, abscess and gangrene; 
(iv) tumors; (v) parasites of the lung, trauma; and (vi) syphilis and 
leprosy are more uncommon causes, (e) Hemoptysis nervosa is most 
rare, though authentic cases have occurred in cerebral traumatism, 
hysteria (where it has caused death) and epilepsy. (/) Toxic hemoptoe 
from mercury or iodides is very rare. 

Symptoms. — Symptoms follow those of the causal tuberculosis, mitral 
stenosis or aneurysm, or develop in apparent health. Blood poured out 
into a cavity or into the lung substance may not be voided, in weak or mori- 
bund persons. Prodromes are unusual; without warning, a salty taste in 
the mouth, substernal warmth, a sense of something rising from the chest 
and coughing are followed at once by a few spoonfuls or more of blood, 
which also may be accidentally noted in a previously mucous sputum. 
The blood varies from the merest stain to 5 quarts; it may appear but 
once or repeatedly. It is generally bright red and well mixed with air. 
If the blood has clotted, the clot is mixed with air and perhaps with 
mucus. Casts of the bronchioles may be voided. In gangrene or abscess, 
the blood may be brown or buff-colored and the red cells disintegrated. 
Brown hemosiderin granules or, if the blood has remained as a clot two 
weeks, hematin crystals may occur. 

Physical findings, other than those of the causal condition, are fre- 
quently lacking; if blood stagnates in a large bronchus, there may be 
bronchial breathing, bronchophony or dulness if the affected area measure 
2 by 5' cm. In the bronchioles, blood gives rise to small rales, in the 
bronchi to coarser rales. 

Complications. — Fever, aside from the causal disease, may result from 
resorption (ferment fever). Urobilin icterus, functional heart murmur, 
relaxation of the right heart, albuminuria and puffiness of the ankles 
are possible complications. 

Diagnosis. — Examination of the nose, gums, throat and larynx excludes 
hemorrhage simulating hemoptoe. Differentiation between bronchial 
and pulmonary bleeding is decided by the history, later physical exami- 
nation and clinical evolution. 



452 DISEASES OF THE LUNG 

Hematemesis vs. Hemoptysis. 

(a) The blood is acid (unless a very large Is alkaline. 

amount is voided) . 
(6) The patient always recognizes whether it is vomited or coughed up. 

(Blood from the lung is very rarely (Hemoptysis, very rarely, causes consensual 

swallowed and then vomited.) vomiting.) 

(c) Is often dark (though large amounts Nearly always bright (though when stag- 

of bright red blood may be vomited, nating in a cavity it may become dark 

as in ulcer). or buff). 

(d) Is mixed with food, HC1, ferments, etc. Mixed with air, which is also found in the 

clots. (Not infrequently tubercle bacilli 
or heart disease cells are found.) 

(e) In 16 per cent, of cases blood is in the Is very rare in stools. 

stools. 

Prognosis and Course. — Spontaneous cessation is the rule. The imme- 
diate prognosis is good, as early death occurrs in 3 per cent, only, except 
in profuse pneumorrhagia, resulting from aneurysmal rupture (even 
then the patient may live years). Drowning of the patient in his own 
blood is rare. The final outcome depends on the etiology. In Ware's 
386 cases 62 per cent, recovered. 

Treatment. — Prevention. — In tuberculosis (q. v.) the patient should 
be kept quiet, the cough suppressed and exertion and vocal efforts 
avoided; in heart disease and marantic thrombosis, rest is indicated 
to obviate detachment of the thrombi. 

Therapy. — Absolute physical and mental quiet should be enforced. 
Movement and talking are prohibited; coughing is suppressed by hypo- 
dermics of morphine, which allay the mental excitement (opiates are 
employed guardedly in very large hemorrhages, for bronchial occlusion 
may result). The patient is assured of a favorable outcome; no physical 
examination should be made except auscultation of the chest in front, 
for treatment takes precedence of diagnosis; if rales indicate the side 
of the hemorrhage, the patient should lie on that side to prevent aspira- 
tion into the contralateral bronchus. 

Arterial pressure should be reduced by inhalation of 10 to 15 drops 
of amyl nitrite, which lessens tension in the pulmonary and arterial 
circulation. A liquid diet is ordered. Alcohol, coffee and tea should be 
interdicted. Even if the patient collapses cardiants should be avoided, 
for syncope is nature's hemostatic; the old practice of venesection in 
this way promoted thrombosis. Cardiac excitement is lessened by plac- 
ing a large ice-bag over the precordium. Active purgation by croton 
oil is very beneficial. 

Hemostatics do not control the lesser circuit, which is independent of 
drugs which operate on the arterial circuit. Ergot raises the blood-press- 
ure in the lungs. Calcium lactate, gr. xxx, and common salt on the 
tongue are of some value (salt acts reflexly, by way of the vagus, on the 
pulmonary vessels). Horse serum may be used in urgent cases and the 
beneficial effects of turpentine have long been known. Nature, as a rule, 
effects the cure. Hippocrates employed ligature of the extremities, i. e., 
binding tightly for a few minutes the vessels of the groin and axilla, to 
lessen the return flow of blood. Artificial pneumothorax, to compress 
the bleeding lung, is advocated in desperate and persistent hemoptysis. 



PLEURISY 453 



DISEASES OF THE PLEURA. 

PLEURISY. 

Definition. — An inflammation of the pleura, secondary to tuberculosis 
or other lung disease, general and septicemic infections and disease in 
contiguous tissues. Hippocrates recognized the dry and humid types and 
tapped for empyema and pneumothorax. The first full description dates 
from Laennec. 

Pleurisy constitutes 3 per cent, of internal maladies and is the most 
common of all postmortem findings (in over 50 per cent.). It is suscep- 
tible of division into infinite varieties, acute, subacute or chronic accord- 
ing to its course, dry or effusive according to its consistence, primary or 
secondary as to its cause, diffuse or circumscribed as to its distribution, 
and serofibrinous, hemorrhagic or suppurative as to its nature. It seems 
preferable to describe all its symptoms first and group special types later. 

Etiology. — 1. Tuberculosis. — So-called primary, spontaneous or 
cryptogenetic pleurisy is usually tuberculous. Landouzy considers that 
98 per cent, of all pleurisies are tuberculous and Le Damany proved by 
inoculation that 92 per cent, of "primary" pleurisies were tuberculous. 
Lord states that two-thirds of pleuritics have no obvious disease in other 
organs and three-quarters respond to tuberculin. The causal lesion may 
be recognized at autopsy in calcified bronchial glands or as small lung 
foci (v. page 459). 

2. Diseases of the Lung Substance. — Pneumonia, abscess, gan- 
grene, infarcts, tuberculosis, tumors, pneumothorax, etc., are etiological 
factors; according to Koplik, 95 per cent, of pleurisies in children follow 
pneumonia. It is less frequent in diseases involving the bronchi, as in 
grippe or measles. 

3. Acute Infections. — Rheumatism, sepsis, endo- and pericarditis, 
scarlatina, and other acute infections may result in pleurisy. It develops 
in about 2 per cent, of typhoid cases. 

4. Diseases of Adjacent Organs. — (a) Intrathoracic affections, 
involving the ribs, spine, esophagus, mediastinum, lymph glands, dia- 
phragm and pericardium; and (b) abdominal affections, as of the stomach, 
spleen or liver (abscess, tumor or cirrhosis), subphrenic abscess, sup- 
purative, carcinomatous or tuberculous peritonitis (in 25 per cent.), 
perinephritic abscess, etc., may excite pleural infection by direct local 
invasion or by the lymph and blood streams; in neglected appendicitis, 
hepatic and diaphragmatic invasion are the steps to pleural infection. 

5. Tumors. — Echinococcus and endothelioma are the most important 
types; carcinoma, sarcoma, ecchondroma and rarely lipoma are also fac- 
tors; pleural neoplasms are far more frequently secondary than primary. 

6. Altered Conditions of the Blood. — Gout, nephritis and scurvy 
are often causative of pleurisy, as reduced physiological resistance pre- 
disposes to infection. 

7. Terminal Pleurisy. — Various forms of sepsis are often fatal to 
subjects of chronic disease of the heart, liver and kidneys. 



454 DISEASES OF THE PLEURA 

8. Ag?e, Sex, Localization. — Age: most cases occur between the 
twentieth and fiftieth years, but no age is exempt. Sex: Eichhorst 
observed pleurisy in 3 per cent, of all his male and 2 per cent, of all his 
female cases, and found the following localizations: right-sided in 54 
per cent., left-sided in 42 per cent, and bilateral in 4 per cent. Cases 
following nervous disease, cold or exposure, venous thrombosis or 
trauma can usually be brought within the above given classification. 

Bacteriology. — The above etiological classification does not correspond 
to the bacteriological division. Suppurative pleurisy may result from 
the streptococcus, pneumococcus, tubercle bacillus or less often from 
the staphylococcus or typhoid or colon bacillus; serous pleurisy may 
be due to the tubercle or pyogenic organisms. The frequently negative 
cultural results favor the hypotheses that chemical products may induce 
pleurisy or that bacteria produce pleurisy and then die. It must be 
remembered that cultures are made, not from the pleura directly, but 
from the fluid effused from it. The organisms found are most frequently 
the pneumococcus, tubercle bacillus and streptococcus; less often the 
staphylococcus, pneumobacillus of Friedlander, typhoid, paratyphoid, 
colon, influenza and diphtheria bacilli, gonococcus, meningococcus, ray 
fungus, etc. (a) Purulent pleurisy (empyema) is due most often to the 
streptococcus in adults and the pneumococcus in children. About 10 
per cent, of empyema is tuberculous; empyema giving no results cul- 
turally or by inoculation is usually tuberculous— a cold abscess of the 
pleura. Other bacteria (v. s.) are infrequent factors, (b) Serous pleurisy 
is usually tuberculous, as shown by the increasing percentage of successful 
inoculations. Tubercle bacilli when found, suggest a direct communica- 
tion with a tuberculous focus in the lung or lymph glands; Eichhorst 
found them by direct examination in 15 per cent, of serous pleurisies, 
though inoculations were positive in 62 per cent, (c) So-called primary 
pleurisy which is non-tuberculous is usually pneumococcic. (d) Meta- 
and parapneumonic pleurisy is most frequently pneumococcic, but some- 
times streptococcic and staphylococcic. 

Symptoms. — Physical findings are absolutely essential for diagnosis 
and all subjective symptoms are ambiguous or may be wholly absent. 
In the main, all types have much the same signs which differ more 
quantitatively than qualitatively; serous pleurisy nearly always shows 
friction, and fibrinous pleurisy is always accompanied by some exudation. 

Inspection. — (a) Inspiratory retraction of the intercostal spaces 
may result from imperfect ingress of air, pain or adhesions. Epigastric 
retraction during inspiration is due to contraction of the diaphragm. 
(b) The patient often lies during the dry stage on the sound side to avoid 
pain from pressure on the inflamed surfaces ; later, he lies on the diseased 
side to allow freer expansion of the sound lung, especially when the exu- 
date is large; the patient may sit up for breath, or assume the diagonal 
decubitus, (c) Ectasia (distention) of the affected side occurs especially 
in children, and is determined by mensuration and inspection. The 
interspaces are obliterated, the costal arch is immobile during respira- 
tion, the skin glistening, the spine curved toward the diseased side, the 
shoulder higher and the nipple and scapula are farther from the median 



PLEURISY 455 

line. (The right chest is normally one or two centimeters larger.) The 
sound side exceeds, by three centimeters, its normal dimensions on 
account of compensatory emphysema. In some very large effusions 
the writer has observed an apparent retraction of the diseased side. 
(d) Respiratory movement of the affected side is decreased or absent 
both in dry and exudative pleurisy. Pain alone may reflexly decrease 
the respiratory expansion and variation on the same side may occur, 
there being more movement above and less below. The frequency of 
respiration is increased from lung compression, heart luxation, the low 
diaphragm, fever, pain or paresis of the intercostal muscles, (e) The 
arrays show a dark shadow. (/) Inspection reveals cyanosis, dislocation 
of the apex and occasionally edema (v. i.). (g) Absence of Litten's pheno- 
menon and (h) rarely pulsation of the effusion, (i) C. L. Greene describes a 
rhythmic lateral displacement of the heart most marked in medium-sized 
effusions. The heart approaches the affected side in inspiration and moves 
outward in expiration, movement often amounting to two inches, measured 
by fluoroscopic examination, percussion of the free cardiac border, or by 
inspection of the apex. 

Palpation confirms inspection, (a) An up-and-down friction-rub 
is felt; it increases on pressure, which also increases the pain and ten- 
derness, and it is the more readily distinguished the coarser the rub. 
The friction develops before the effusion, is often present with it and 
after it is absorbed. The rub is due to roughening of the pleura, which 
•loses its glistening appearance and looks like glass upon which one has 
breathed; the two raw pleural surfaces scrape on each other. It may 
last a few hours or days, even disappearing when the patient takes a 
deep breath; or it may last for months or even years, (b) Pressure on 
a tender interspace may cause a sudden contraction of the rectus muscle 
on the side of lesion, (c) Vocal fremitus, normally greater on the right 
side, varies according to the level at which it is tested, (i) Above the 
effusion it is normal, (ii) Near the spine over the compressed, relaxed 
lung it is increased, (hi) Below it is weak or absent, from exudation of 
thick fibrin or fluid, though less change is observed in dry than effusive 
pleurisy. The condition of the lung and the bronchial secretion are 
important, whence before testing, the patient should cough and take a 
few deep breaths. The results are irregular in cases of loculated effusion 
and of adhesions bringing the lung closer to the chest wall in given places. 
(d) By tapping with the finger tips the increased resistance is clearly pal- 
pated, (e) Edema of the chest wall on the diseased side may be inflam- 
matory in serous and purulent pleurisy, or mechanical (and more intense) 
from pressure on the azygos or hemiazygos veins. (/) Fluctuation is 
extremely rare. (17) Palpation determines the dislocated apex beat, the 
dislocated liver or spleen, the bulging of the diaphragm and sometimes a 
furrow between the diaphragm and liver (Stokes). 

Percussion is negative in dry pleurisy, except when a very thick 
fibrin causes some dulness and weak breathing; after an effusion has 
resorbed, the residual plastic lymph maintains the dulness. In effusion 
(a) dulness is found typically between the fifth and eighth ribs in the 
left axilla or over the liver and posteriorly on the right side. Dulness 



456 DISEASES OF THE PLEURA 

also results from old adhesions, or atelectasis of the lung. As in pneumo- 
thorax, emphysema of the lungs and calcification of the ribs may some- 
what obscure the dulness of an effusion. In doubtful cases the apparently 
sound side should be percussed first. Thirteen ounces of fluid are neces- 
sary in the adult for recognition and four ounces in children, and 
sometimes six ounces, which produce a dulness two fingers in height, 
may be recognized, especially in children and women having thin tho- 
racic walls. The effusion must be one inch thick to produce dulness. 
Before percussion the patient should breathe deeply several times to 
eliminate partial collapse of the lung and accumulated bronchial secre- 
tion. Percussion is absolutely essential to diagnosis. Not merely the 
audible dulness should be regarded, but also the palpable sense of resis- 
tance, on light percussion. In larger effusions, the distinct flatness, at 
first located posteriorly, increases along the spine and laterally in the 
axilla, and in massive exudates, may reach above the clavicles. 

The dulness is highest posteriorly as the patient lies on the back. 
When he sits the line of dulness describes a parabolic curve (courbe de 
Damoiseau or the Garland-Ellis line) which is lowest behind and due 
to the uneven thickness of the chest wall or to adhesions. If the fluid 
should effuse with the patient out of bed, the upper level would be 
horizontal. Dulness is found one or two centimeters higher than the 
fluid, due to plastic exudate, (b) Right-sided effusions merge with the 
liver dulness, but the lower limit of left-sided effusions can usually be 
determined because they invade Traube's semilunar space, which lies 
between the heart's apex above and tenth rib below, representing the 
supplementary pleural space and is designated as the " half -moon" 
space because of the curve at its upper portion, produced by the apex; 
its tympanitic note is decreased or replaced by flatness in left-sided 
effusions (without adhesions). Dulness here may not be confused with 
the spleen, for there is no respiratory excursion in pleurisy, and the 
dulness lies more toward the heart than toward the spleen, (c) Res- 
piratory excursion and Litten's sign are absent, (d) Change of the upper 
line of dulness with change of position, emphasized by most writers, 
cannot be established, because of adhesions at the upper level; the 
patient must lie hours in another posture before any alteration 
occurs. 

The following findings are less important : (e) A vertical strip of tym- 
pany along the spine, often measuring 3 cm. wide, may be detected in a 
large exudate, due to compression of the lung. Tympany in the lower 
left chest results from the gaseous stomach and intestines. (/) Tympany 
over an upper lobe from compression or relaxation of the lung, was 
observed by Avenbriigger and Skoda — the Skodaic note, (g) "Cracked- 
pot" resonance occasionally appears on short, forcible percussion over 
the upper lobe, and results from sudden expulsion of air through the 
rima glottidis. (h) William's tracheal note is observed on the left more 
than on the right side and most clearly in the first and second interspaces. 
It is obtained chiefly when the entire side is dull and is due to transmission 
of percussion vibration from the fluid to the trachea, giving a tympanitic 
note, (i) Grocco's sign is a small triangular dulness on the sound side 



PLEURISY 457 

along the vertebrae, due to displacement of the mediastinum and, with 
it, the sound lung, which is pushed away from the vertebral column 
by fluid in the lower chest; it also occurs in subphrenic abscess, cysts 
or ascites; Koranyi first described this sign in 1897 and Grocco in 1902. 
(j) Dislocation of other organs. There is no parallelism between the 
amount of exudate and the amount of luxation, which, of course, is 
absent if the organs are adherent. The average increase of intrathoracic 
pressure is 10 mm. mercury (0 to 26). The heart is usually dislocated 
in toto and seldom suffers change of the direction of its axis. The right 
ventricle pulsates to the right of the sternum, even at the right nipple 
line, in left-sided effusion. In right-sided effusions the apex is pushed 
to the left and downward, for the diaphragm is lower. The liver is less 
easily displaced than the heart, but in right-sided effusions is pushed 
down (especially in empyema) and the left lobe tipped somewhat upward ; 
both lobes are dislocated downward in massive pleurisies. In left-sided 
effusions the spleen is dislocated downward and forward, undergoes some 
torsion and may stand perpendicular to the costal arch. 

Auscultation. — This is most important in dry and effusive pleurisy. 
(a) The friction-rub may be hard or soft, is superficial, i. e., close to the 
ear and resembles the sound made by scratching the finger upon the 
ear or the crunching of snow under the shoe; it often develops in the 
first twelve hours. It is most frequent during inspiration, but is very 
often detected in expiration, but seldom during expiration alone. It 
may disappear after several long breaths which smooth the pleural 
roughening. It may be increased by pressure and its duration is subject 
to no law; Gerhardt heard a pleural rub which lasted six years. It is 
heard most frequently over the anterolateral portion of the chest, and is 
detected more clearly with the stethoscope than with the naked ear, 
but may be heard at a distance of several feet, as in a case seen with 
Dr. H. M. Richter. It may rarely be present in miliary tuberculosis 
and in tumors of the lung or pleura without actual pleurisy. It usually 
becomes less clear when exudation develops, and its reappearance indi- 
cates absorption or extension, (b) The breath sounds are modified not 
only by the effusion, but also by the condition of the lung, and the 
conditions of conduction in the pleura and thoracic walls. In general, 
and especially in men and children, the respiratory sounds are tveakened 
even in fibrinous pleurisy, from repressed breathing and perhaps from 
pain alone; cog-wheel breathing is common. In moderate effusions 
three zones are observed: (i) Absence of breathing in the lower parts 
from compression of the lung by the exudate, which lessens the conduc- 
tion of the vesicular sounds; (ii) bronchial breathing in the middle 
zone from moderate collapse of %he alveoli of the lung, with fair con- 
duction through the bronchi; (iii) an upper zone of sharp vesicular 
breathing. In larger effusions the lower zone extends higher and 
bronchial breathing may be heard near the clavicle or between the 
scapula and spine. In the largest effusions the breathing is indistinct 
everywhere (with metallic bronchial breathing when the lung is wholly 
collapsed) . (c) The voice sounds are not heard over the fluid or over very 
thick, plastic exudate. They may persist where islets of lung adhere to 



458 DISEASES OF THE PLEURA 

the chest wall, (d) Bronchial breathing and increased fremitus may 
be present, especially in children with empyema, under the following 
conditions: if the bronchi are patent, if there is no great fibrin deposit 
on the pleura and if the lungs are retracted but not absolutely com- 
pressed. The bronchial breathing may sometimes be as intense as in 
pneumonia. In adults increased fremitus may be observed between 
the spine and scapula where the lung is compressed, (e) Bronchophony 
depends upon the same conditions as bronchial breathing. (/)" Egophony, 
which is an exaggerated bronchophony, was described by Laennec; it 
is found chiefly in middle-sized effusions, usually at the level of the 
fluid; in large effusions it is rare, the compression being too great. It 
is caused by the voice sounds passing through the compressed smaller 
bronchi to the chest wall ; it may be present when the exudate is increas- 
ing or decreasing at a given point, (g) Baccelli's symptom of the ''whis- 
pering voice," which he thought was more frequent in serous effusions, 
also occurs in other forms of pleurisy, in induration of the lungs, pneu- 
monia, hydrothorax and cavities, (h) A ivide propagation of the heart 
tones — if consolidation is excluded — suggests dislocation of the heart 
by an effusion. Murmurs may result from bending of the large vessels 
by dislocation of the heart, as well as accidental murmurs resulting 
from a heart weakened by toxemia. 

Diagnostic puncture determines: (a) the existence of pleurisy, 
excluding pneumonia, hypostasis, tumor, etc.; (b) the character of the 
fluid; and (c) the prognosis. It is indicated in all doubtful cases. Punc- 
ture with aspiration is also an important therapeutic measure. Negative 
results may result from a thick, fibrinous exudate, from failure to reach 
an encapsulated effusion, as in interlobar pleurisy, and from the mem- 
brane being pushed in before the needle. In dry taps, after withdrawal 
of the needle, examination should be made to see that no fibrin or cells 
plug the needle. If a plug is obtained it should be examined under 
the microscope. No carbolic acid or alcohol should remain in the syringe 
or needle, which, by coagulating the serum, may explain some dry 
punctures. The puncture should be made with a large needle. Positive 
results: when the needle is introduced, resistance due to a callous pleurisy 
or indurated lung may be felt. After introducing the needle, the point 
may be freely movable, as in a cavity. In rare cases serum may be 
obtained from a high puncture and from a lower one a cellular deposit, 
the cells settling to the bottom; oftener puncture in different localities 
shows serum in one and pus in another sac— Galliard's polymorphous 
pleurisy. A pocket of sterile effusion often indicates a contiguous encap- 
sulated empyema or a lung abscess. Bacteriological examinations made 
with 20 to 30 c.c. of the serum give frequent positive results. The 
special chemical, bacteriological, cellular and other characteristics will 
be discussed under individual forms. 

X-ray Findings. — It is usually stated that fluid first accumulates 
under the lung, between it and the diaphragm. Englebach and Carmen 
found this was the case in but 25 per cent, of cases; in another 25 per 
cent, the fluid stood like a vertical column and in 34 per cent, laterally 
— nearer the chest wall than the mediastinum; the column was oblique 



PLEURISY 459 

in 16 per cent. The arrays confirm the lack of mobility on change of 
position and show how adhesions may prevent luxation of organs, inva- 
sion of Traube's space, respiratory excursion, etc. Small or deep pockets 
of fluid near the diaphragm or in the interlobar fissures are thus detected 
which may escape physical examination. 

Symptoms. — Symptoms may be absent (latent pleurisy); if present 
they are not distinctive and there is no relation between them and the 
physical findings, (a) The temperature rise is usually gradual and 
without a rigor. Temperature is no positive index as to the character 
of the fluid. For weeks there may be no temperature, even in purulent 
exudates, especially in marantic and diabetic subjects and in terminal 
infections. When present it is more frequently subcontinuous or remit- 
tent than continuous. The average elevation is 101° to 102°. Exacer- 
bations of fever are ominous, expecially when no change occurs in the 
physical findings. Recovery is not expected until the temperature has 
been normal for some time, (b) The pulse is increased; it is sometimes 
of the paradoxical type or unequal in the two radials. (c) Dyspnea 
seldom attends pleurisy, for effusions may attain enormous proportions 
without respiratory difficulty, particularly when they are gradual in de- 
velopment. Urgent dyspnea is usually referable to coincident pneu- 
monia, pericarditis, arteriosclerosis, nephritis or bilateral pleuritis. (d) 
Pain is usually an initial symptom. It is in no way proportional to the 
physical findings; it may be absent when auscultation shows a marked 
rub. Its character is usually dull, tearing, stabbing and sometimes very 
severe, crampy or colicky. The pain is pleural (Cruveilhier) and is present 
in the diseased side, well down over the ribs, liver, epigastrium or low 
in the back, and sometimes may radiate to the sound side, into the 
arm, spine or abdomen, especially in children, in which case it may 
simulate appendicitis, (e) Coughing, an early and frequent symptom, 
results most often from pleural irritation. It may occur after tapping 
or change of posture. It is usually unproductive. (/) Other symptoms 
are anorexia, vomiting, headache, and difficult swallowing due to involve- 
ment of the foramen esophageum; the sweats of pleurisy rank third in 
importance after those of sepsis and rheumatism. The urine is scanty 
but increases during resorption, when peptonuria and transient albumin- 
uria are often found. The skin may be pale and cachectic from purulent 
accumulations, red from high temperature, cyanotic from poor oxygena- 
tion or suddenly pallid from hemorrhage into the pleura, when also there 
is a sudden increase of fluid. Emaciation is common in chronic tuber- 
culous or purulent pleurisy. 

Special Forms.— 1. Character of the Inflammation. — In 790 cases 
Eichhorst found serous pleurisy in 81, fibrinous in 12, purulent in 5, 
ichorous and hemorrhagic each in 1 per cent. 

(a) Serous pleurisy is the prototype of pleuritis. The fluid is lemon- 
colored. Its specific gravity ranges between 1.015 and 1.023, which 
characterizes inflammation. Albumin amounts to 3 to 7 per cent.; 
sugar is frequently present. The fluid clots after puncture. All pleuritic 
exudates, serous and otherwise, contain white and red blood cells and 
endothelial cells, which may show fatty degeneration. 



460 DISEASES OF THE PLEURA 

Cytodiagnosis. — Widal, Sicard and Revault (1900) insisted that lym- 
phocytes are characteristic of primary pleural tuberculosis and afford 
diagnostic data long before the results of inoculation are available; the 
fluid must be examined before it coagulates; in other pleurisies the poly- 
morphonuclears prevail and that over 50 per cent, lymphocytes indi- 
cates tuberculosis; the " lymphocytic formula" proves tuberculosis, the 
" polymorphonuclear formula" indicates pyogenic infection or pleurisy 
secondary to well-developed phthisis and the "endothelial formula" 
denotes irritation, transudation or malignancy. The tuberculous nature 
of pleurisy is established by inoculation tests (positive in 66 to 94 per 
cent.), by apical or other involvement, by the finding of tuberculosis 
in cases of sudden death in the course of pleurisy, by the usually intensely 
positive ophthalmoreaction (see page 164) and by the fact that 25 to 33 
per cent, of cases become obviously tuberculous. It is well to suspect 
the tuberculous nature of all so-called rheumatic pleurisies and carefully 
watch the sputum and lungs. The leukocytes are not much increased 
in the blood. 

(6) Fibrinous pleurisy usually shows some fluid, serous or purulent, 
if systematic punctures are made. 

(c) Purulent pleurisy (empyema) usually begins as a serous exudate 
which soon becomes purulent. In contrast to serous pleuritis two-thirds 
of this group are secondary : (i) the streptococcic form, which is observed 
chiefly in adults, in which the thin fluid separates on standing into an 
upper serous and a lower denser layer, with slight fibrin formation; and 
(ii) the pneumococcic form, which is more common in children; the 
fluid is more homogeneous and viscid, like " laudable" pus, fibrin forma- 
tion is abundant and the odor peculiar; it is more often accompanied 
by endocarditis, pericarditis and meningitis, and is more often febrile 
and more susceptible of spontaneous recovery. In Netter's series of 
empyema the streptococcus was causal in 47 per cent., the pneumococcus 
in 39, the tubercle bacillus in 11 and the staphylococcus in 3 per cent. 
Over 80 per cent, of juvenile empyemas are pneumococcic. It is remark- 
able that the pneumococcus has far less pyogenic propensities in the 
lung than in the pleura. Microscopically, various bacteria are present, 
polymorphonuclear and often fatty white cells, and sometimes choles- 
terin and Charcot-Leyden crystals. Greater visceral luxation and dis- 
tention of the chest than in any other type may occur ; Krause reported 
22 pounds of pus. Leukocytosis and hectic fever are mentioned under 
symptoms. 

Empyema pulsans (Walshe); Sailer collated 95 cases in 1904; 95 per 
cent, of all pulsating effusions are purulent; 93 per cent, are left-sided. 
A pulsating tumor as large as the fist may be noticed, which usually 
decreases during inspiration, or the effusion may simply pulsate behind 
the ribs; in either case the pulsation may be expansile, and usually 
lies between the second and fourth ribs, anteriorly, but may be seen 
lower or even in the back. Pulsation is probably propagated from the 
aorta. The apparent conditions for pulsation in an empyema are cardiac 
energy, massive exudation and paresis of the intercostal muscles. Empy- 
ema pulsans may be confused with aneurysm, which latter is much 



PLEURISY 461 

slower in its evolution, is much oftener located above and to the right, 
and has its own signs, murmur and thrill; it may be confused with 
pulsating abscess, pneumonia, gangrene or tumor of the lung. The 
pulsation ceases after aspiration. Expansile pulsation of the chest wall 
has been observed without any organic change (Lafleur and Edwards). 

Empyema may rupture externally, empyema necessitatis, usually 
along the sternum or lower ribs. Gravitating abscesses may result, 
as pulsating tumors in the groin and loin, confusable with aneurysm 
or spinal caries. Rupture into the air passages may cause suffocation 
during sleep; 25 per cent, of postpneumonic empyemas rupture into 
the bronchi. Fistulse, hectic fever and amyloidosis are frequent sequelae. 
Hippocrates knew of the "mouthful" expectoration and also the fact 
that pus may penetrate the lung like a sponge without perforation 
or pneumothorax (perforation into the lung without pneumothorax is 
caused by a small opening which allows the escape of fluid into the lung 
but not of air into the pleura, because of higher tension in the exudate). 
Empyema may rupture into the pericardium, peritoneum, esophagus, 
stomach, etc. Hellin (1905) found 114 cases of bilateral empyema 
recorded in the literature; 67 per cent, occurred in males and 90 per 
cent, in young persons under fifteen years old; the mortality was 30 
per cent. 

(d) Putrid pleurisy is usually associated with gangrene of the lung, 
pneumothorax, esophageal carcinoma, appendicular abscess and kindred 
lesions. The fluid is extremely fetid; fat, leucin, tyrosin, cholesterin 
and sometimes hematoidin crystals are found; the colon bacillus and 
other gasogenic bacteria are frequently present. 

(e) Hemorrhagic pleurisy is usually serofibrinous and the exudate is 
tinged with blood. Five to six thousand red cells per c.mm. are necessary 
to produce a reddish tinge. Its character is seldom suspected before 
puncture, (i) Most cases are tuberculous and Dieulafoy speaks of them 
as having "hemoptysis into their pleurae." After puncture more fluid 
is frequently formed but recovery is possible, (ii) Some cases are can- 
cerous; hemorrhagic pleurisy is found in but 12 per cent, of pulmono- 
pleural cancer; pain, dyspnea, luxation and rapid pulse are frequent 
symptoms; the fluid is dark red and contains little fibrin; a case of Desnos 
was punctured thirty times in six months, (iii) Some cases occur in 
liver cirrhosis, in nephritis and in hemorrhagic fevers or exanthemata; 
profuse hemorrhage into the pleura was called pleural hematoma by 
Wintrich and pachypleuritis hemorrhagica by Chouppe. 

(/) Chyliform pleurisy (v. i. Chylothorax) . 

2. Location of the Exudate. — (a) Pleuritis diaphragmatica produces 
notable subjective disturbance, as pain which may resemble angina 
pectoris, pain with tenderness in the epigastrium, between the tenth rib 
and the xiphoid ; tenderness in the lower interspaces near the spine ; ten- 
derness over the cervical portion of the phrenic nerve, with pain reflected 
along the acromial branches of the cervical nerves to the shoulder. An 
inspiratory spasm of the upper part of the rectus muscle; dysphagia 
from inflammation of the foramen esophageum; if left-sided, vomiting 
and singultus may be noted, and if right-sided, icterus is not uncommon. 



402 DISEASES OF THE PLEURA 

Cough may occur spontaneously or on pressure. Dyspnea is usually 
great, the temperature is generally normal, the lower chest moves but 
little, the respiratory murmur is very weak and friction may be heard 
over the liver or in Traube's space. If there is no exudate the diaphragm 
may remain high. Fluid, accumulating between the diaphragm and 
lung without reaching the chest wall, causes no dulness. Fibrinous is 
more common than serous effusion. 

(b) Interlobar pleurisy occurs most frequently in pneumonia or tuber- 
culosis. Previous pleurisy may favor this localization by obliterating 
the general pleural space. As Laennec noted, it is almost always sup- 
purative. Its early diagnosis is uncertain, for the fever, rales, hemoptysis, 
cough and dyspnea suggest a lesion of the lung, e. g., lung abscess from 
which differentiation is sometimes impossible; tenderness is frequently 
elicited along the interlobar fissure; later a zonular surface dulness is 
found conforming to the fissure, bounded above and below by a normal 
or somewhat over-resonant note. The heart may be pushed to the right 
in left-sided localization, but the liver is not luxated in right -sided locali- 
zation. Interlobar pleuritis may be shown clearly by the £-rays. Large 
effusions may break internally, pus suddenly appearing in the sputum, 
but spontaneous recovery is infrequent. Puncture may infect the lung 
during the withdrawal of the needle. The outlines of the lobes are shown 
in Figs. 33-35. 

(c) Mediastinal pleurisy is most often tuberculous or pneumococcic, 
and more frequently purulent than serous. The symptoms of lung 
compression are less distinctive than those of the compression of medias- 
tinal tissues. There may be dyspnea, dysphagia, intrathoracic oppres- 
sion, a pertussis-like cough, enlarged thoracic veins, deviation of the 
trachea, and dulness between the scapula and spine; the a:-ray picture 
may be suggestive. The sudden onset and febrile course differentiate 
it from aneurysm, tumor and adenopathies. Without operation the 
outlook is unfavorable. 

(d) Peri- (para-) pleuritis is inflammation outside of the parietal 
pleura, and is usually purulent. Most cases are actinomycotic. Fistula? 
and the evacuation of the characteristic sulphur granules are common. 
The symptoms are more local and irregular than those of pleurisy; 
fluctuation is more frequent; heart dislocation and lung compression 
are rare; the respiratory excursion is free, and heavy percussion elicits 
lung resonance beneath the dulness. Metastatic inflammation, perfora- 
tion and burrowing are common. 

3. Pleurisy in Children. — In children pleurisy is attended by more 
toxemia, higher temperature, pulse and respiration. Bronchial breath- 
ing is more frequent; there is less dulness, less luxation and less friction. 
It often follows pneumonia, where, in the majority of cases, the empyema 
is more benign; tuberculosis is less frequently causative in children. 

Issue. — 1. Resorption. — Even purulent pneumococcic pleurisy may 
exceptionally resorb in part without operation or rupture, leaving 
inspissated caseous accumulations. Serous pleurisies may be absorbed 
after three to six months, during which time persistent friction is common 
over the lower chest. A proteolytic ferment in the white cells dissolves 



PLEURISY 



463 



the fibrin and the serum is taken up by the lymph- and bloodvessels. 
Dieulafoy reports a case of serous pleurisy, in good health after ten years, 
which was tapped over 100 times and 230 liters removed. 

2. Adhesions. — The thickness of pleural adhesions is more important 
than their extent. Universal obliteration of the pleural sac by thin 



Fig. 33 




Fig. 34 



Fig. 35 





Figs. 33, 34, and 35. — Cuts from Dieulafoy, showing: Fig. 33, the posterior surface of 
the lungs and their interlobar fissures; Fig. 34, the lateral aspect of the left lung; and Fig. 
35, that of the right lung. 



adhesions is of no consequence. Compensatory emphysema, pain, 
thoracic oppression, obliteration of the complementary pleural space, 
dulness, decreased vocal fremitus and breathing, failure of Litten's 
phenomenon and stagnation of bronchial secretion may occur when the 
adhesions are thick, and stasis may ensue. Peritonitis, mediastinitis 



464 DISEASES OF THE PLEURA 

and obliterative pericarditis may complicate the case. In some instances 
the pleura calcifies or ossifies, leaving a deposit measuring 3 cm. or more 
in thickness. 

3. Sudden death may result after exertion, coughing, urination or defe- 
cation; it results chiefly from such extreme venous compression that the 
venous trunks can return little blood to the heart. Less frequent causes 
are cardiac paralysis or thrombosis, pulmonary edema, and rarely bend- 
ing of the aorta, pulmonary embolism, rupture of fluid into the bronchi, 
which may drown the patient during sleep, and death from hemo- or 
pneumothorax or brain embolism. 

4. Retractio thoracis is characterized by increased resistance, 
decreased fremitus, decreased circumference of the affected side and 
often by bronchiectasis. The percussion-note is dull and the breathing 
is usually decreased, but sometimes bronchial. The causative factors 
are atmospheric pressure, retraction of the pleural scars, or pleurogenous 
interstitial pneumonia, also known as pleuritis deformans, which some- 
times lobulates the lung. Retraction is generally a slow process but the 
writer has seen marked deformity develop in three weeks. 

5. Changes in Other Organs. — Retraction may raise the liver 
and the lung may shrink away from the heart, the spleen and the heart 
may lie higher and Traube's space may be increased. Organs displaced 
by exudate may in rare cases remain luxated after the exudate is absorbed. 
Pleural callosities may produce recurrent laryngeal paralysis which may 
also follow pressure by an exudate or adenopathy. Other complications 
are acute and chronic infiltration in the lung; extension to other serous 
surfaces; septicopyemia; stasis in the liver, stomach, extremities, etc.; 
chronic nephritis; amyloid degeneration and various visceral or miliary 
tuberculosis. Scagliari reports 47 cases of brachial paralysis. 

Diagnosis. — The physical findings only are final; symptoms are most 
unreliable. Diagnosis of the malady is the first step, and the second is 
the determination of its cause. 

Differentiation. — 1. Pleuritis sicca is recognized only by feeling or 
hearing the friction, (a) The crepitant rale is largely inspiratory, and 
is heard as a number of small crackles at the end of inspiration; it is 
altered or removed by coughing and deep inspiration, but the pleural 
rub is increased by pressure and deep breathing. It may disappear 
after a number of deep inspirations, which make the two surfaces tem- 
porarily smooth, (b) It must be differentiated from sacculated breathing 
and the physiological, bilateral crackling in the chest muscles on deep 
breathing, (c) Intercostal neuralgia is intermittent, occurs in typical 
attacks and is limited to the interspaces; Valleix's points are present at 
the angle of the ribs, in mid-axilla and anteriorly, and correspond to the 
exit of the three perforating branches of the nerve. Intercostal neuralgia 
is increased less on deep breathing, (d) In caries of the ribs pain is local- 
ized directly over one rib and not between the ribs, (e) Differentiation 
from rheumatism of the thoracic muscles may be difficult, for both affec- 
tions induce pain on breathing, tenderness and disturbed breathing; 
there may be a history of exposure or repeated attacks; there is no 
fever or cough; movement increases the pain more than in pleurisy. 



PLEURISY 465 

(/) The rub in pericarditis (q. v.) more distinctly depends upon the cardiac 
movements. In pleurisy along the left border of the heart, over the 
lingual lobe, on holding the breath the pleuritic rub is heard near the 
heart, but decreases after a few heart beats. On deep inspiration the 
pleural rub ceases and the pericardial rub is increased; pericarditis most 
commonly produces a rub over the conus pulmonalis arteriosus. 

2. Pleuritis humida (pleuritis effusiva) must be distinguished (a) from 
pneumonia (page 74). (b) Tumors of the lung produce a characteristic 
exudate; this is often brown, sometimes chyliform, and contains fat 
globules and large, degenerated cells which may show mitoses; the 
glands above the clavicle may be enlarged, as well as those in the medias- 
tinum, which produce recurrent laryngeal paralysis. Tumor particles 
are rarely obtained by puncture or in the sputum, and are only found 
in carcinoma, for sarcoma rarely ulcerates. A trocar rather than a 
needle should be used. Unverricht observed the development of car- 
cinoma at the seat of puncture. In tumors there is less displacement, 
less invasion of Traube's space and less widening of the chest than in 
pleurisy, arid the breathing is often bronchial, the flatness intense and 
the fremitus increased, (c) Hydrothorax (q. v.), usually described as 
bilateral, may be unilateral (right-sided), especially in disease of the 
liver, kidneys and heart. The fluid readily shifts its level on change of 
posture, which does not occur in pleurisy. The claim that salicylic 
acid, iodine and potassium iodide pass readily into transudates and 
but slowly into exudates, is disproved. In hydrothorax the specific 
gravity is below 1.014, the albumin is 1 to 3 per cent, and the sediment 
shows few white cells and some endothelial cells. Cytology, etc., may 
point to hydrothorax, while inoculation reveals tuberculosis, (d) The 
presence of hemothorax is determined only by puncture. 

3. Circumscribed pleurisy requires differentiation (a) from pericarditis; 
pleurisy shows a more irregular outline, the apex beat is not altered and 
there is no pericarditic friction, (b) Lung cavities show dulness when 
full of secretion and resonance when it is voided; the fluid obtained by 
puncture (under a wrong diagnosis) has a higher specific gravity and a 
larger percentage of fat. (c) Differentiation from splenic tumors is 
determined by respiratory excursion and palpation of the lower edge of 
the spleen, (d) Liver enlargements rarely occur solely upward, save in 
in echinococcus and in abscess of the convexity; these are prone to occur 
anteriorly, and pleurisy more frequently posteriorly. In tumors of the 
liver there is usually respiratory excursion, (e) Subphrenic abscess 
(v. Localized Peritonitis) may be intraperitoneal (as from liver abscess) 
or extraperitoneal (e. g., perinephritic) . The liver stands higher in the 
chest because of the paretic diaphragm. There may be a history or 
physical signs of an abdominal disease. The needle reaches the pus only 
when thrust deep in the lower interspaces. The pus frequently has a 
fecal odor. The manometer shows increased pressure during inspiration 
and decreased pressure during expiration, the converse of the findings 
in pleural effusion. (/) Abscess of the liver: Pleurisy, serous or suppura- 
tive, may complicate abscess of the liver. Differentiation is easy when 
abscess of the convexity is located forward; when it is situated poste- 

30 



466 DISEASES OF THE PLEURA 

riorly, aspiration alone will distinguish it; the pus shows liver cells, 
amebee, cholesterin or bile, (g) 43 case's of pleural echinococcus are 
reported; 11 per cent, of hepatic cysts reach the lung and pleura. 

Course and Prognosis. — 1. The course: Acute cases last two, subacute 
three to eight and chronic eight or more weeks. The onset is no index 
of the issue. No cycle is seen in any form of pleurisy. Friction along 
the lowest limits of the pleura and in front rarely attends great effusions 
and therefore, after the exclusion of tuberculosis, carcinoma or pyemia, 
the prognosis is relatively good. In the average case dry pleurisy precedes 
and succeeds exudation. Persistence, recurrence and exacerbations 
render the prognosis unfavorable. The author has seen recovery of 
secondary carcinomatous pleurisy. 

2. The immediate mortality is under 5 per cent., and depends upon 
the etiology and the nature of the fluid. Fibrinous pleurisy is the most 
favorable type, except when it occurs at the apex of the lung. The 
outlook in effusive forms is most favorable in metapneumonic serous or 
purulent pleurisy; next most favorable in serous pleurisy due to the 
staphylococcus, less favorable in staphylococcus empyema, and least 
favorable in tuberculous, fetid or putrid forms. It is usually poor in 
hemorrhagic, chyliform, peracute and bilateral (generally hemorrhagic 
or purulent) effusions. It is more favorable in effusions relatively rich 
in solid constituents; effusions containing little solids are apt to recur. 
Since Hippocrates, the belief has prevailed that right-sided are less 
favorable than left-sided efTusions. Sudden death is not infrequent. 
The author saw 3 cases in one year. 

3. Opinions vary as to the ultimate prognosis; 87 per cent, of cases 
become tuberculous in one or two years (Fiedler); 33 per cent, die in 
five years (Bars); 15 per cent, die of tuberculosis; 90 per cent, are in 
good health after two to five years; and 80 per cent, are healthy after 
five years (Cabot). 

Treatment. — In fibrinous pleurisy, or in the fibrinous or first stage of 
exudative pleurisy, pain is the main indication; morphine may be given 
in severe cases, especially with hard coughing; the ice-bag, poultices, cups 
and hot fomentations give little relief; blisters cause as much discomfort 
as the disease itself; the pleura should be splinted by four strips of zinc 
oxide adhesive plaster two inches wide, overlapping the median line before 
and behind by about three inches, and running around the chest horizon- 
tally and obliquely; these should be applied firmly during expiration, 
that the lung in its lower part and the pleural surfaces may be well 
immobilized. Personal experience with the salicylates has not been 
satisfactory. The patient shoidd be kept in bed. 

In serous pleurisy the patient should be kept in bed and the cough 
and fever treated expectantly. Laxatives are given solely to obviate 
straining at stool which may induce cardiac weakness; they do not 
reduce the effusion. If at the end of the second week the effusion remains 
stationary, various measures are indicated; Schroth's treatment limits 
the fluid ingested to one quart daily, but the method gives no results, 
as exudation is an active, not a passive, process; tincture of iodine is 
seldom beneficial, and when old is distinctly a local irritant; potassium 



* PLEURISY 467 

iodide, digitalis, drastics to produce copious evacuations, cotton jackets 
and sweats are useless, and pilocarpine is dangerous. Transudates may 
be removed in this way but not exudates. 

Aspiration. — Trousseau's indications were (a) the vital indication, 
when life is threatened by a large exudate; (b) moderate effusions with 
slow resorption, and (c) persistent or residual exudates. The author 
believes that early puncture and aspiration are indicated in every case, 
where two quarts or more (2000 or 2500 c.c.) of fluid are effused, 
whether the temperature is still high or not, and whether dyspnea is 
present or not; this amount of effusion causes dislocation of the heart, 
liver or spleen, compression of the lung, torsion of the large vessels, or 
ectasia of the chest; high intrathoracic pressure may cause sudden 
death, sometimes without warning symptoms. Early puncture does 
not irritate the pleura or favor recurrence or suppuration. Puncture 
was first performed by Hippocrates and exploited by Schub and Skoda 
(1841), but aspiration dates from Bowditch of Boston (1848). 

Method of Aspiration. — After the usual surgical antisepsis, a small 
trocar or large aspirating needle is introduced, which has an elbow con- 
necting with a rubber tube, to siphon the fluid to a vessel below or 
connecting with a bottle which can be exhausted by a pump. There is 
no rule as to the site of puncture, which must be governed by the physical 
signs; adhesions which hold the lung to the surface vitiate any set law; 
fluid is usually obtained low down in the chest between the scapular 
and postaxillary lines. The trocar is introduced perpendicularly to 
the chest wall and not obliquely, in order to avoid injuring the intercostal 
artery lying above the rib, as a result of which the author twice saw 
fatal hematoma and hemothorax. Hypodermics should be at hand, 
against a possible syncope. The pump is necessary in but 10 per cent, 
of cases, for the fluid can usually be siphoned readily ; a tube is attached 
to the needle or trocar, filled with boric acid solution, clamped with an 
artery forceps and undamped, after its lower end is placed in a basin con- 
taining the same solution and held at a lower level. The fluid, if pumped, 
should be withdrawn gradually; caution is necessary lest air be pumped 
the wrong way, i. e., into the pleura. The blood-pressure during aspira- 
tion should be controlled by the sphygmomanometer. The amount 
removed need not be great, as moderate relief of intrapleural tension 
often promotes absorption; it is estimated arbitrarily at one quart 
(1000 c.c.) to three pints (1500 c.c). Complete or nearly complete evacua- 
tion may cause the accidents enumerated below and is thought by Litten 
to induce miliary tuberculosis. Aspiration should be discontinued when 
the exudate becomes bloody from lung injury, when friction develops, 
when pain is felt or when from congestion of the relaxed lung coughing 
begins. Repetition of puncture; a second puncture is necessary in 25 
per cent, and a third in 5 per cent, of effusions. Favorable results are 
relief of pressure on the lung and absorption of the exudate, strengthen- 
ing of the pulse, and return of luxated organs to their place. Unfavorable 
results are (a) syncope due to cerebral anemia from reflux of blood 
to the expanding lung which contained little blood before it was relieved 
by the puncture, a relatively uncommon occurrence; (6) pulmonary 



468 DISEASES OF THE PLEURA 

edema — albuminous expectoration — which is due to the sudden with- 
drawal of too much fluid (2 to 5 liters) at one tapping; it should take 
a half-hour to evacuate one and a half quarts or 1500 c.c. (Frantzel); 
edema pulmonum is treated (and prevented) most successfully by hypo- 
dermics of morphine gr. J; Sears records 10 deaths from simple punc- 
ture; Capps and Lewis ascribe sudden death or syncope to the irritation 
of a pleural reflex; (c) sudden death from pulmonary embolism or 
cerebral embolism; the latter results from discharge of clots from vessels 
in the relaxing lung, and causes the so-called pleuritic hemiplegia; (d) 
injury to the heart, liver or spleen; (e) pneumothorax and subcutaneous 
emphysema may occur. Doubtless some, if not most, instances of 
pneumothorax after tapping are primary pneumothorax with secondary 
pleurisy; the tapping opens up the closed point of rupture and pneumo- 
thorax again dominates the clinical picture. (/) The author twice 
witnessed an extensive hemothorax and subcutaneous hematoma after 
pleural puncture, in which the trocar was impatiently thrust in and 
out during an unsuccessful thoracocentesis. Naunyn writes of death 
following puncture of an atheromatous intercostal artery, (g) Fibrinous 
bronchitis has followed paracentesis, (h) The needle has been broken 
by moving the patient during tapping, (i) Anaphylaxis has followed 
tapping. When repeated punctures fail the advisability of operation 
should be considered, as in empyema. Various modifications are sug- 
gested : Holmgren advises two openings, one to admit air and the lower 
to withdraw fluid; others inject nitrogen to replace the fluid withdrawn, 
adrenalin to constrict the vessels, etc. 

Gilbert's autoserotherapy consists of aspirating 1 c.c. (10 to 20 c.c), 
but before the needle is withdrawn entirely, reinjecting the fluid into 
the subcutaneous tissues; the results are uncertain. 

Empyema in all cases necessitates operation (practised by Euryphon 
and after him by Hippocrates). Rarely, patients may recover spon- 
taneously. A day or two before operation aspiration is indicated when 
the fluid is under high tension. Some surgeons advocate treating tuber- 
culous empyema without operation, as Volkmann treated other cold 
abscesses. The mortality in Velpeau's cases was 100 per cent, and 
Dupuytren himself " chose to die of empyema at the hands of God rather 
than to die at the hands of man under operation.'' In Schede's series 
the mortality of tuberculous empyema was 77 per cent., of metastatic 
32 per cent., of metapneumonic 13 per cent, and of primary 8 per cent. 

After-treatment is directed toward prevention of thoracic retraction, 
to which end gymnastics and deep breathing are essential. A patient 
having suffered from a "primary" effusive pleurisy should be treated 
as one with latent tuberculosis. 

PNEUMOTHORAX. 

Definition. — Pneumothorax is an accumulation of gas or air in the 
pleural sac. It was named by Itard of Paris (1803) and was described 
fully by Laennec (who in 1819 made the first diagnosis) and Skoda. 
Hippocrates described succussion. As it excites pleurisy in 90 per cent. 



PNEUMOTHORAX 469 

of the cases, the following varieties are distinguished: pyo-, sew- and 
hemopneumothorax. 

Etiology. — 1. Diseases of the lung and pleura cause about 95 per cent, 
of all cases. In Biach's collection of 918 cases in Vienna, pulmonary 
tuberculosis caused 77 per cent., gangrene 7 per cent., empyema 5, trauma 
3, bronchiectasis and abscess each 1 per cent., the etiology was unknown 
in 2 per cent, and the remaining 4 per cent, were due to emphysema, 
infarct, thoracocentesis, echinococcus and contiguous disease perforating 
into the pleura, as gastric or esophageal ulceration or caries of the ster- 
num, (a) Acute is more important than chronic tuberculosis in which 
there are protecting pleural adhesions; pneumothorax develops in 5 
per cent, of tuberculous cases, (b) Ulcerative lesions of the lung may 
erode the pleura and admit air (v. s.). (c) Trauma or stab wounds 
occur far less frequently than one would expect, and here hemopneumo- 
thorax is the type. (For "pneumothorax following paracentesis," see 
page 468.) (d) Empyema may rupture into the lung without allowing 
ingress of air from the opposite direction, (e) Rupture of a healthy 
lung by tearing away of the lung, as pleural adhesions give way in 
coughing, muscular straining or violent coughing is very exceptional. 

2. Perforative lesions in the mediastinum, esophagus, peritoneum, 
stomach or colon and subphrenic abscess are uncommon causes (v. s.). 

3. The view held by Oppolzer and Biermer that pneumothorax may 
occur spontaneously (without rupture) has received confirmation by 
discovery of the Bacillus aerogenes capsulatus and other gasogenic 
organisms (Welch, Lewy). It is always possible, however, that the 
point of rupture in the lung has healed; the fact remains that air enters 
the pleura chiefly from the lung or from a gas-containing organ. 

Pneumothorax occurs largely in adults and four to seven times as 
frequently in males as in females. Cozzolino (1906) found only 41 cases 
in children; of these but 40 per cent, were tuberculous. 

Pathology. — When the chest is opened, air or gas escapes with a force 
sufficient to blow out a candle. The volume of air may exceed 2000 
c.c, and its tension, studied first by Wintrich and Weil, collapses the 
lung — overcoming the normal negative pressure of 3 to 6 mm. Hg., 
due to its elasticity — dislocates the heart and mediastinum and depresses 
the diaphragm and subphrenic organs. The gas may be odorless or 
fetid. The pathological and clinical findings vary (a) as the gas is encap- 
sulated or occupies the entire pleural cavity; (6) as the air is aseptic 
(producing a pure pneumothorax, or one with slight exudation) or is 
infected by the organisms of the primal disease which excite serous, 
purulent or putrid pleurisy; (c) as the air-containing cavity is " closed," 
"open" (into a bronchus, or sometimes also externally) or possesses a 
valve, allowing passage of air in one but not in the opposite direction 
(v. I). 

Symptoms. — The onset is usually sudden, occurring spontaneously or 
following coughing or exertion; it is characterized by sudden pain in 
the side, cyanosis, dyspnea and collapse, due to reflex action on the 
vagus; the onset may resemble angina pectoris, pulmonary embolism or 
abdominal perforation; there may be sudden evacuation of pus from the 



470 



DISEASES OF THE PLEURA 



breaking into the lung of an empyema; urticaria occasionally develops; 
decreased diuresis, albuminuria, stasis and subcutaneous emphysema are 
sometimes observed. The onset may be insidious — with no symptoms 
and with only physical signs; indeed pneumothorax sometimes con- 
stitutes an unexpected postmortem finding. In other instances the 
history or course may justify a presumptive diagnosis, as in a case 
clearly tuberculous; and in still other cases, a small, latent caseous 
focus may burst and thus produce its first symptom. 

Physical Findings. — 1. Inspection.— (a) The affected side is distended 
2 to 4 inches and immobile, and contrasts sharply with the widely moving 
sound lung, (b) The interspaces are obliterated, (c) The heart and liver 
or spleen are dislocated, (d) There is dyspnea and cyanosis, (e) The 





I II 

Fig. 36. — I. Left-sided effusive pleurisy, showing relative heart dulness (A), effusion 
(B), liver flatness (C), and fluid impinging on Traube's half-moon space, of which but a 
small part remains resonant (D). In larger effusions reaching, e. g., up to the dotted black 
line, the relative heart dulness may be pushed over to the dotted line (over C). II. Left- 
sided pneumothorax marked by tympany (T, T), pushing over the mediastinum and also 
the heart to the right, and pushing down the left lobe of the liver and the spleen. 



attitude is characteristic; the patient most often lies on the affected side 
to afford ample play to the sound lung; sometimes there is orthopnea 
and if the point of rupture opens into the lung or bronchus a peculiar 
decubitus may be assumed in order to drain the pleura. (/) The .T-rays 
show the lung flattened near the spine, the diaphragm depressed and 
motionless, and the shadow of the effusion. 

2. Palpation. — (a) Vocal fremitus is absent, unless adhesions hold the 
lung to the chest wall, (b) The chest wall feels resistant and (c) some- 
times splashing, fluctuation or a " pillow sensation" is noted, (r/) The 
dislocated apex beat and the edge of the liver or spleen are felt. 

3. Percussion. — Results vary according to the tension of the gas and 
chest wall : (a) In open pneumothorax the note is tympanitic or even 
metallic when percussion is made on a solid object, as a coin; this 



PNEUMOTHORAX 471 

bruit d'arain is found in 75 per cent, of cases; cracked-pot resonance and 
Wintrich's change of note may be elicited when the mouth is opened. 
(b) In closed pneumothorax the note is full and loud; it is tympanitic 
when there is moderate pressure and the intercostal muscles are relaxed; 
again the note may be dull if the tension is great or if the chest muscles 
are spasmodically contracted, as in sudden pneumothorax (vagus reflex 
action), (c) Flatness over the lower thorax usually results from pleural 
effusion. The author has seen tympany over the entire side, in great 
pleural effusion. Skoda said that the fluid is .twice as much as we antici- 
pate, (d) On change of posture a changing level of the fluid is readily 
elicited, the gas being found above, like a spirit-level, and the fluid below. 
(e) The pitch over the gas-distended part changes with change of posture 
(Biermer's change of note). It becomes deeper as the patient sits, 
because the vertical dimension of the chest is increased by the pushing 
down of the diaphragm, (f) The heart dulness is replaced by resonance 
in left-sided pneumothorax, and is found to the right of the sternum; in 
right-sided pneumothorax the luxation is less and toward the left axilla. 
(g) The liver or spleen dulness is pushed well dotvnward. 

4. Auscultation. — (a) The breath sounds are usually absent in the 
closed variety of pneumothorax, and this, with ectasia and hyperreson- 
ance, is most characteristic. In the open and sometimes in the closed 
form, the breath sounds are bronchial, amphoric or metallic, the voice 
sounds, especially under the clavicle, are metallic, and coincident rales 
in the bronchi are also metallic. Amphoric sounds were referred by 
Laennec to a fistula but probably are due to the air acting as a sounding 
board, (b) Air passing through the point of rupture may produce 
curious snapping or ivhistling sounds; the point of rupture is oftenest 
between the second and fourth interspaces and the mammary and axil- 
lary lines, (c) The gutta cadens (the metallic "falling drop") may be due 
to rales or dripping of fluid from fibrin shreds as the posture is changed. 
(d) The Hippocratic splashing (succussio Hippocratis) was carefully 
described by Laennec and is elicited by placing the ear to the chest and 
sharply shaking the patient; in one of James's cases it was heard over 
a large clinical amphitheatre; three patients called the author's attention 
to a "splashing in the chest"; it is heard in three-quarters of the cases, 
usually before dulness develops, (e) The heart tones may be metallic, 
and the heart's action may even cause splashing sounds. Hellin collected 
54 cases of double pneumothorax; it is not incompatible with life. 

Diagnosis. — The ectasia, resonant note, suppressed or amphoric breath- 
ing, luxations and succussion are characteristic. 

Type. — Dislocation occurs in all types, though it varies in degree, (a) 
In the open form Wintrich's change of note, metallic sounds, fistula 
murmur, periodic expectoration of large amounts of pus, or of methyl 
blue injected into the pleura, moderate cardiac and other dislocations 
and no manometric increase of the tension in the pleura are distinctive. 
(b) The closed type is distinguished by increased manometric tension, 
absence of breath sounds, marked ectasia, change of note on sitting but 
not on opening the mouth and marked luxations, (c) In the valvular 
form air may enter the pleural cavity but cannot escape back and there- 



472 DISEASES OF THE PLEURA 

fore pus cannot be voided. Some of the auscultatory findings of the 
open type are noted. The manometer shows increased pressure. 

Differentiation. — (a) Cavities may be simulated by circumscribed 
pneumothorax, but the interspaces are sunken, the fremitus is increased 
when the cavities are empty, luxation is absent and the Hippocratic 
succussion and coin sound are extremely rare. (6) Pleurisy can be dis- 
tinguished on careful examination, (c) Meteorism is at once excluded 
by filling the stomach or colon with water, (d) Diaphragmatic hernia 
is very frequently confused with pneumothorax; out of 481 cases only 
12 were recognized. The a>rays determine the condition. Respiratory 
excursion is present and the tympany and metallic sounds are accom- 
panied by symptoms of incarceration, as vomiting, colic, obstipation and 
indicanuria. The intestines push the heart to the right. Ninety per 
cent, of cases are left-sided, (e) Pyopneumothorax subphrenicus (q. v. 
under Peritonitis, Localized Forms), results from abdominal lesions, 
such as cancer, ulcer, appendicitis, disease of the gall tracts, etc., whose 
histories are suggestive. Thoracic symptoms, as cough, sputum and 
dyspnea, are not conspicuous early in the process and the lungs may 
show perfect excursion. The manometric pressure is increased during 
inspiration and decreased during expiration; the converse is true in 
pneumothorax. By the arrays the diaphragm is above the fluid, while 
in the pneumothorax it is below the fluid. 

Prognosis. — The prognosis varies with the cause, the condition of the 
lungs and the character of the fluid. Cases in a healthy lung following 
exertion, trauma or infarct are relatively favorable. The closed and 
open are more auspicious than the valvular type. In tuberculosis, 
pneumothorax seems to arrest the tuberculous focus if it is small and if 
no mixed infection occurs; even in these cases complete recovery is 
infrequent. Eichhorst observed one case which lasted for five years. 
Gabb's case recovered and relapsed four times, the attacks being two to 
four years apart. West observed a mortality of 70 per cent., of which 
three-quarters died within two weeks, nine-tenths in less than a month 
and one case in twenty minutes. 

Treatment — The results are disappointing. (a) Narcotics and stimu- 
lants are imperative at the time of the rupture, for collapse, dyspnea 
and cyanosis, (b) Aspiration is of most value in the serous forms; early 
aspiration may open a healing fistula by relieving the pressure which 
closed it. As a rule aspiration is resorted to only when pressure menaces 
the heart and lungs, and when pyothorax threatens sepsis, (c) The 
radical operation is indicated in putrid or purulent pneumothorax. 
Leyden reported 66 per cent, and Richardiere 50 per cent, of recoveries. 

HYDROTHORAX. 

Definition. — Hydrothorax is a serous transudation into the pleura. 

Etiology. — (a) Stasis, from cardiac, pulmonary or vascular factors, 
is a frequent cause. In failure of the right heart the superior cava is 
imperfectly drained, which congests the azygos and hemiazygos, leading 
in turn to pleural transudation. It may occur alone but is oftener 



CHYLOTHORAX 473 

part of a general dropsy. Local venous obstruction from mediastinal 
tumor or aneurysm may induce hydrothorax. (b) Blood and vascular 
changes resulting from multitudinous anemic, marantic or cachectic 
states, as nephritis, cancer and blood diseases. The chief factors are 
cardiac and renal. 

Symptoms and Diagnosis. — 1. The symptoms of hydrothorax do not 
include pain or fever. The condition accentuates the dyspnea attending 
the causal stasis or cachexia. The amount of fluid varies from ounces 
to quarts (or even to two gallons). 

2. The physical signs are those of moderate effusive pleurisy, except 
that the rub is absent, the fluid shifts with change of posture and pro- 
duces a moderate compression of the lungs and luxation of the heart, 
liver and spleen. The transudate is usually described as bilateral, but 
in over half the cases it is unilateral (adhesions obliterating the opposite 
pleura) and often right-sided, in cardiac, renal and hepatic disease, by 
pressure on the azygos or pulmonary veins by the dilated heart or cava 
or the luxated root of the lung. 

3. The fluid is clear, slightly green, possibly moderately blood-tinged 
if it develops during the death agony, and shows a specific gravity of 
1.010 to 1.015; at the most it develops only light delicate flocculi of 
fibrin; the albumin ranges between 1 and 3 per cent. Centrifuging 
brings down only a few leukocytes, endothelial cells and red disks, but 
no bacteria. Right hydrothorax may prove very obstinate, because a 
low grade of inflammation eventually supervenes. 

The treatment is causal; aspiration often prolongs life. 

HEMOTHORAX. 

Blood effusion into the pleura is a rare malady. It may be caused by 
trauma, scurvy or allied blood diseases, aneurysmal rupture, ulceration 
of the pulmonary or pleural veins and by various necrosing lung diseases. 
It may occur with pleurisy, pneumothorax or thoracocentesis. Its 
symptoms are essentially those of hydrothorax; it is suspected only by 
a sudden onset with signs of acute anemia, and is proved only by the 
exploring needle. Its treatment is symptomatic, stimulants, ice applied 
to the chest, horse serum for hemostasis or operation for trauma. 

CHYLOTHORAX. 

A very rare affection, in which true chyle or chyliform fluid is found 
in the pleura. Its etiology is disputed; (a) in genuine cases chyle con- 
taining sugar is found (though sugar has been found in many forms of 
serositis and in most transudates); only 60 cases are recorded. In 11 
cases (of which 4 died and 9 were right-sided), traumatic rupture of the 
thoracic duct has been found. In others the duct was obstructed by 
thrombosis of the subclavian vein or by glands and tumors, (b) In a 
second group, the pseudochylous (chyliform or adipose), there is no 
chyle and the milky appearance is due to fatty or minute albuminous 
granules held in suspension. This variety is chiefly tuberculous or 



474 DISEASES OF THE MEDIASTINUM 

carcinomatous. It has been thought that old empyemas may become 
chyliform. The characters of both forms of fluid will be considered 
under chylous and adipose ascites, with which they are frequently 
associated. 

PLEURAL TUMORS. 

Pleural tumors are nearly always secondary by contiguity or metas- 
tasis to pulmonary, mediastinal or extrathoracic growths. Carcinoma 
and sarcoma are the most frequent forms; enchondroma, lipoma, hyper- 
nephroma and dermoids are very uncommon. Of primary endothelioma 
of the pleura, 50 cases are reported, but it is considered by some as 
solely inflammatory; clinically it presents the picture of chronic pleurisy 
plus occasional metastatic deposits in the liver, lungs, kidneys, muscles 
and lymph glands. The signs are those of lung tumor plus those of 
pleurisy; the diagnosis of primary tumor is impossible. 



DISEASES OF THE MEDIASTINUM. 

MEDIASTINAL TUMORS. 

Mediastinal tumors are very rare. They are usually primary. Sar- 
coma is the most common form and then carcinoma; lipoma (7 reported 
cases), substernal struma, thymic growths, fibroma, myoma, osteoma, 
enchondroma, echinococcus, dermoid (64 cases collected by Christian, 
1908), teratoma, gumma, tubercle, leukemic, pseudoleukemic and 
chloromatous adenopathies are rarer forms. Sixty per cent, occur in 
males between twenty and thirty years of age. 

Symptoms. — Symptoms develop gradually. 1. Local signs: (a) 
Bulging may be present in the jugulum or under the sternum, especially 
in lymphosarcoma, (b) There may be pulsation, imparted by the 
heart, aorta or its branches; it is rarely expansile, (c) The tumor or 
secondarily involved glands may be palpable deep in the jugular notch. 
The vocal fremitus varies, (d) The sternum may be exquisitely tender 
from erosion, (e) Dulness may be elicited under or near the sternum, 
or, if the posterior mediastinum is involved, in the back; the dulness 
may blend with the heart, suggesting aneurysm or effusive pericarditis, 
though far more irregular. (/) Sometimes there is bronchial breathing, 
or if the bronchi are closed the breath sounds may be absent. 

2. Compression symptoms, as in aneurysm, may predominate in tumors 
of the posterior and middle mediastinum, though local physical findings 
may be slight or absent, (a) Paroxysmal asthma and orthopnea are 
common; dyspnea is the earliest and most frequent symptom, due partly 
to compression of the vagus and partly to tracheal, cardiac and pleuritic 
involvement. Other vagus symptoms are brazen cough from paralysis 
of the vocal cords, tachy- or bradycardia, hiccough, vomiting or esopha- 
geal spasm, (b) The trachea or bronchi may be compressed from without 



MEDIASTINITIS 475 

or occluded by growth into their lumina, in which case the symptoms of 
tracheal or bronchial stenosis may be pronounced. Tracheal tugging 
and shrinking of one side of the chest (instead of bulging) may be noted, 
perhaps with dulness of the right apex. The sputum may contain blood, 
tumor tissue or hair. The larynx may show lateral deviation, (c) The 
arteries of the neck may show a systolic stenotic murmur, but the veins 
are more often compressed, especially the innominates or the superior 
cava, which cause bilateral or unilateral edema and, less often, cyanosis 
of the face, neck and arms; enlargement of the veins on the thorax 
indicate the collateral circulation, (d) The heart may be compressed 
and dislocated, downward and outward if the growth emanates from the 
anterior mediastinum, forward if from the posterior mediastinum. Dis- 
location of the liver and spleen are less common, (e) Compressive 
dysphagia may cause death from inanition. (/) Inequality in the pupils 
is uncommon. Neuralgia, muscular paralysis or even spinal paraplegia 
may result. Boring pain is rare. 

Diagnosis. — A diagnosis is positive from the signs or presumptive 
from the symptoms. Dyspnea, ectasia, irregular substernal dulness, 
venous stasis, bronchial stenosis, heart luxation and the skiagram make 
the diagnosis probable; puncture may withdraw tissue or dermoid 
material; the sputum sometimes voids tumor particles, hooklets or 
hair. Deep aneurysm (q. v.) is difficult to eliminate. The irregular 
dulness excludes pericarditis. Tumors of the lung and pleura produce 
less pressure symptoms, though such differentiation is rather academic. 

Prognosis and Treatment. — The prognosis is unfavorable, as death from 
inanition, compression, exhaustion or pneumonia results within a few 
months. Benign tumors run a longer course, sometimes five to seven 
years, or even forty in Lebert's dermoid. Treatment is palliative. A 
few successful operations are reported; in 20 operated cases of dermoid, 
70 per cent, recovered (R. S. Morris). 

MEDIASTINITIS. 

Acute inflammation is uncommon, but may follow various local 
lesions, as pleurisy, pericarditis, pneumonia, acute lymphadenitis and 
kindred processes, by contiguity or by metastasis, (a) Acute non- 
suppurative cases begin with chill, fever, pain in the mediastinum and 
tenderness anteriorly over the sternum or high in the back; there may 
be edema over the sternum; dysphagia, dyspnea and vague cardiac 
symptoms may develop. A presumptive diagnosis is made from acute 
inflammatory symptoms with mediastinal localization. The prognosis 
is grave and the treatment is symptomatic; an ice-bag should be applied 
over the sternum and opiates should be given for pain, (b) Of medias- 
tinal abscess, Hare (1899) collected 115 cases in most of which the 
anterior mediastinum was affected . Acute cases, most often traumatic 
or sequential to eruptive diseases, were more frequent than chronic 
cases, which were usually tuberculous (v. Mediastinal Pleurisy). 

Symptoms. — The symptoms are mediastinal, as in simple acute medias- 
tinitis, and general or septic. A throbbing retrosternal pain is common 



476 DISEASES OF THE MEDIASTINUM 

and dyspnea may result from pressure by large pus pockets. Edema, 
fluctuation, pointing or rupture in the upper interspaces or in the jugular 
notch may be noted. Fatal hemorrhage may follow simultaneous erosion 
of the aorta and bronchus. Internal rupture also occurs into the air 
passages, esophagus or pleura, or deep burrowing to the abdomen. The 
exploring needle is of great diagnostic aid in doubtful cases. Auvray 
(1904) found in the literature 36 operations with 33 recoveries. 

(c) Chronic mediastinitis is discussed under Adhesive Pericarditis. 

MEDIASTINAL HEMORRHAGE. 

Small hemorrhages of no clinical importance may occur in icterus, 
hemorrhagic blood diseases or acute infections. Larger hemorrhages 
may follow trauma or erosion of the large vessels, both of which over- 
shadow the mediastinal incident. 

INTERSTITIAL EMPHYSEMA. 

(See Differentiation of Emphysema.) 



SECTION IV. 

DISEASES OF THE DIGESTIVE TRACT. 



DISEASES OF THE MOUTH. 

CATARRHAL STOMATITIS. 

Etiology. — Simple, acute stomatitis is the most frequent form. In 
children it may develop with dentition, rude cleansing of the mouth 
and digestive disorders, especially in the poorly nourished; it is part of 
the exanthemata and syphilis. In adults it results from hot food, alcohol, 
tobacco, iodine, mercury, arsenic, etc., acidulous vomiting, carious 
teeth, throat disease, uncleanliness, etc. 

Symptoms. — Symptoms are chiefly redness, swelling and increased 
secretion, and in the acute forms pain which makes eating difficult. The 
increased and usually acid saliva irritates the lips or chin if it flows 
over them. The gums are turgid (gingivitis) and the tongue broadened, 
lax and indented by the teeth, as is also the buccal mucosa. The tongue 
is coated. Vesicles sometimes form and break down into small erosions. 
The whitish areas sometimes seen are epithelial thickening. Fever, 
thirst and general symptoms are absent, except in some infantile cases. 
Acute stomatitis lasts but a week or two. Transient stomatitis is physio- 
logical in the newborn. 

Treatment. — In children the mouth should be gently washed after 
each nursing. Boracic acid is excellent and safe. In adults the teeth 
should be cared for. Cold water or ice mitigates pain. Tincture of 
myrrh and of rhatany (equal parts) are excellent. Stronger antiseptics 
may be used in adults but children may swallow them; for instance, 
2 per cent, chlorate of potash, or 1 per cent, phenol; erosions may be 
touched with 1 per cent, silver nitrate. 

STOMATITIS ULCEROSA. 

Etiology. — Its bacteriology is unknown. In some cases the micro- 
organisms of Vincent's angina are found. Epidemics may occur in 
asylums or prisons. It may be induced by malnutrition, uncleanliness, 
oral or dental disease, phthisis, leukemia, diabetes, toxic factors (mer- 
cury) and dentition. (See Acute Pharyngitis and Diagnosis of 
Diphtheria.) 



478 DISEASES OF THE MOUTH 

Symptoms. — The symptoms are those of catarrhal stomatitis plus 
necrosis and ulceration. The gums, especially about the incisors and 
canines, are red, swollen and spongy; they bleed, secrete pus and ulcerate; 
over the ulcers a membrane develops. The teeth are exposed and 
loosened. The tongue and cheek ulcerate less often and the pharynx is 
nearly exempt. The breath is fetid, the saliva is increased, the sub- 
maxillary lymph glands and salivary glands are swollen and mastication 
is almost impossible. Fever, prostration and signs of sepsis may mark 
the severest cases. Acute cases last one or two weeks and chronic cases 
weeks or months. 

Varieties. — (a) Mercurial stomatitis may be industrial or therapeutic. 
The author saw a case in which five grains of calomel caused necrosis of 
the tongue, which rotted off at its root. (See Intoxications.) Mer- 
curial and other stomatitis may cause "erosions" of the enamel in the 
developing teeth of children; they become pitted, discolored and trans- 
versely furrowed. (6) In Riga's disease, described by Riga (1881) in 
South Italy, there is a pearly induration between the tip of the tongue 
and frenum; it appears with the first dentition, sometimes ulcerates, 
is occasionally epidemic, is often observed with the status lymphaticus 
and is invariably fatal, (c) In nursing women ulcers may develop from 
the lymph follicles of the lip and cheek; they usually indicate mal- 
nutrition, sometimes are painful and respond to tonics and hygiene, (d) 
Herpetic or pemphigoid stomatitis is seen in neurotics and is frequently 
recurrent (Jacobi's stomatitis chronica neurotica), (e) Bednar described 
(aphthous) white plaques on the posterior part of the hard palate near 
the alveolar border of the jaw, which may ulcerate; they occur in the 
first three months of life, and are apparently due to sucking. Fatal 
cases are due to hemolytic streptococci. (/) Parrot's ulcers occur in 
marantic newborn children on the hard palate near the median line; they 
seldom heal. 

Treatment. — Potassium permanganate 1 to 1000 relieves the fcetor 
ex ore. Necrotic areas may be touched with silver nitrate solution or 
equal parts of tincture of the chloride of iron and glycerin. Potassium 
chlorate gargles may be combined in children with gr. x-xx every day 
internally and twice the amount for adults. Opium and belladonna are 
indicated by pain and salivation. 

APHTHOUS STOMATITIS. 

Etiology. — It may occur sporadically or epidemically. It is probably 
contagious; when due to milk it ceases on its withdrawal. Besides 
the causes of stomatitis (u. s.), it occurs chiefly in children between ten 
and thirty months old. 

Symptoms. — Fever, thirst, salivation and pain in the mouth precede 
the round, yellowish-white and slightly elevated areas as large as a pea 
on the tongue and less often on the lip and buccal mucosa. The mucosa 
is slightly reddened about them. Attempts to scrape them off produce 
bleeding. They are areas of superficial necrosis into which exudation of 
fibrin and round cells occurs (stomatitis fibrinosa disseminata). Vesicles 



GANGRENOUS STOMATITIS 479 

are no part of the process, though they may occur on the skin near 
the mouth. Occasionally there is tumefaction of the lymphatic and 
salivary glands. They last one or two weeks, and recurrence is frequent. 
The treatment is that of stomatitis. 



PARASITIC STOMATITIS. 

Etiology. — -Thrush, muguet, soor or stomatomycosis o'idica is due to the 
Oi'dium albicans, closely allied to the saccharomyces, which consists of 
branching mycelia and ovoid granular and refracting spores. It occurs 
chiefly in young or marantic children whose mouths have been improperly 
cared for, especially among the poor and in institutions. Thrush may 
develop in tuberculous and diabetic adults. 

Symptoms. — A few punctate, whitish spots develop on the tongue, 
cheek and soft palate; they become yellowish as the areas grow or fuse. 
The fungus is at first deposited on the epithelium, between the layers of 
which it proliferates and penetrates. The mouth is dry or moist from 
increased salivary flow. In severe cases the fungus may reach the 
pharynx, larynx, esophagus and even the stomach and intestine. It 
is generally limited to areas with flat epithelium, and epithelia of the 
cylindrical and ciliated order usually escape. It may, in exceptional 
cases, cause esophageal occlusion, bronchopneumonia, cerebral, renal, 
and other embolism. The outlook is good except in marantic subjects. 

Treatment. — Prophylaxis is most essential in regard to sterilization of 
bottles and nipples and maintenance of the general health by fresh air 
and early treatment of dyspeptic disorders. Stomatitis may persist 
until a wet-nurse is secured. Cleansing the mouth with borax, sodium 
bicarbonate and lime-water is most effective. If unusual extension occurs 
a teaspoonful of a resorcin solution (1 to 200) may be given every two 
hours. 

Stomatitis may in rare cases result from the sarcina, leptothrix, pneu- 
mococcus, gonococcus, etc. 

GANGRENOUS STOMATITIS. 

Etiology. — Gangrene of the cheek, noma or cancrum oris, is a rare 
affection. Of Brun's 415 cases, only 11 were over fifteen years of age 
and only 6 infants; the author saw noma in a man forty years old. 
More cases occur in girls. Malnutrition causes* some cases; 50 per cent, 
follow measles; typhoid, scarlatina, etc., are less frequent factors. An 
organism resembling that of diphtheria (Bac. necroseos) and those of 
Vincent's angina may be seen. 

Symptoms. — Ulceration of the gums or buccal mucosa near the angle 
of the mouth is followed by rapid necrosis, gangrene and extensive 
brawny edema of the face. The fetor is intense and much tissue is fre- 
quently sloughed off. Perforation of the cheek, necrosis of the jaw and 
extension to the throat, orbit or ears are not uncommon; 70 per cent, 
die within a week with septic symptoms as fever, weak heart, diarrhea, 



480 DISEASES OF THE TONGUE 

colitis and meningitis or lobular pneumonia. The mortality was 92 per 
cent, in Springer's collation. 

Treatment. — Treatment is ineffectual. A full diet, alcohol (salvarsan) 
and disinfectants applied to the necrotic focus are indicated; excision, 
the live cautery and caustics are employed without success and sometimes 
aggravate the necrosis. 



DISEASES OF THE TONGUE. 

ECZEMA. 

In eczema the epithelium thickens and desquamates, leaving red, 
smooth and circular, serpiginous or geographical areas, which heal 
centrally and extend peripherally. It may cause local irritation or worry 
the patient, who may think he has syphilis or cancer. Again, it is an 
accidental finding. Its cause is unknown, its course is chronic and its 
treatment by silver nitrate is quite inadequate. 

LEUKOPLAKIA. 

Leukoplakia (psoriasis, ichthyosis, keratosis) closely resembles the 
"geographical tongue/' in connection with which it is often described. 
Irregular, smooth, pale plaques of thickened epithelium measuring 1 or 
2 centimeters, develop on the tongue and less often on the lips, cheeks 
or tonsils. Eighty to ninety-eight per cent, occur in men; tobacco, 
alcohol, gout and gastric disease are probable factors; Fournier's experi- 
ence with 324 cases convinced him that 80 per cent, came from syphilis 
and 20 per cent, from tobacco. Its symptoms are slight, its course very 
chronic and its treatment uncertain; salvarsan is suggested. Sodium 
salicylate, 10 per cent.; chromic acid, 5 per cent.; strong silver nitrate; 
corrosive sublimate (1 to 500 parts) and the galvanocautery are recom- 
mended. Excision is necessary for papillomatous or epitheliomatous 
outgrowths which are said to develop in one-third to one-half the cases. 

ACUTE GLOSSITIS. 

Acute glossitis may be localized or diffuse, and ends in suppuration 
in 33 per cent. It follows burns, erosions, trauma or the entrance of 
pyogenic cocci through the lymph follicles. The painful, swollen tongue 
may protrude beyond the lips. In 145 cases the mortality was 3 per 
cent. (Bennett, 1906). Eating, speaking and oral breathing are impos- 
sible. Incision is indicated. 

GLOSSITIS DESICCANS. 

Glossitis desiccans is a rare, chronic, intractable affection in which 
deep indentations of the margins of the tongue and consequent lobulation 



PAROTITIS 481 

occur. Melanoglossia (nigrities lingua?) results from proliferation of the 
filiform papillae at the base of the tongue (melanotrichia linguce, black- 
haired tongue); 50 cases are on record; the hair is removed by a 10 per 
cent, salicylic acid solution or by curetting. The mucor niger may cause 
a black coating on the tongue. 



DISEASES OF THE SALIVAEY GLANDS. 

PTYALISM, SALIVATION, HYPERSECRETION, SIALORRHEA. 

Etiology. — The chief causes are (a) disease of the mouth, stomatitis, 
dentition; (b) toxic substances, as jaborandi, tobacco, mercury and 
iodides; (c) nervous affections, as trigeminal neuralgia, paretic dementia 
or hydrophobia; a distinction is drawn between oversecretion and lesions 
like bulbar paralysis, in which the saliva cannot be swallowed; (d) 
reflex salivation, which may occur from diseases of the tympanum through 
the chorda tympani, from gastro-intestinal disease (ulcer, pancreatic 
lesions, etc.) by way of the vagus and sympathetic nerves and from 
genital conditions, as pregnancy. 

Symptoms. — A pathological salivary flow of over twelve quarts has 
been recorded. The salivary glands are tense, swollen and hard. The 
reaction of the saliva may become neutral or acid; it may contain ropy 
mucous or scattered pus cells; the ptyalin and potassium sulphocyanide 
disappear. The saliva may trickle into the larynx during sleep, and cause 
coughing; it may flow into the stomach and produce vomiting of an 
alkaline or neutral vomitus, especially in the morning; it may stream 
from the lips and redden the skin. 

Prognosis and Treatment. — Both depend on the causal affection. In 
nervous and reflex types potassium bromide and iodide are often valuable. 
Severe cases necessitate opium and belladonna. 

XEROSTOMIA. 

Hyposecretion or arrested secretion occurs in diabetes insipidus and 
rnellitus, in some cases of contracted kidney and as a neurosis or a neurotic 
symptom (Hutchinson, 1888). Women are more often affected (80 per 
cent.). The mouth is dry, red and glistening, interfering with speaking, 
chewing, swallowing and digestion of carbohydrates. The tongue may 
cleave to the roof of the mouth. Treatment consists in painting the 
mouth with iodine, potassium iodide and glycerin (1, 10, 100 parts), 
pilocarpine hydrochloride, grain y 1 ^- to -§-, and galvanism to the parotid. 

PAROTITIS. 

Besides specific parotitis (mumps), infection may reach the salivary 
glands by way of their ducts or the blood stream. Acute parotitis may be 
31 



482 DISEASES OF THE SALIVARY GLANDS 

simple or oftener suppurative (staphylococcic). (a) Any acute infec- 
tion may be complicated by parotitis, particularly typhoid, (b) Paget 
drew attention to diseases of, or operations on, the alimentary and genito- 
urinary tracts, peritoneal disease, pancreatitis, abdominal trauma, etc.; 
many of these cases are clearly attenuated sepsis. Zezas, in 1910, 
collected 162 cases of postoperative parotitis; the mortality is 33 per 
cent, (c) Facial neuritis and the starvation therapy of gastric ulcer 
may cause parotitis. 

Chronic parotitis sometimes follows epidemic or symptomatic parotitis, 
poisoning by mercury or lead, syphilis or chronic nephritis. Mikulicz 
described a ''chronic symmetrical hypertrophy of the salivary and lachry- 
mal glands," which may be independent or symptomatic of pseudo- 
leukemia, leukemia, etc. There is a round-cell infiltration, epithelial 
degeneration, and structures like giant cells. 

Treatment. — In acute parotitis, leeches, cold and later, hot fomentations 
and surgical incision, if there is pus formation, are indicated. Chronic 
forms respond slowly to iodine or mercurial ointment, and Mikulicz's 
disease to arsenic and x-rays. 

ANGINA LUDOVICI. 

Ludwig's angina is a streptococcic infection beginning in the sub- 
maxillary gland, and extending to the floor of the mouth and the cervical 
cellular tissue (Ludwig, 1836). Trauma may be its immediate antece- 
dent, but most cases are secondary to typhoid, diphtheria and kindred 
infections. The inflammation spreads rapidly, causing fever, redness, 
pain and swelling under the tongue, cellulitis and sometimes gangrene 
in the neck (cynanche gangmneuse) . Mastication and deglutition may be 
impossible. The parotids are sometimes invaded. Resolution is very 
exceptional and external pointing of pus is not likely to occur, whence, 
without early surgical intervention, septic and pyemic complications or 
laryngeal and pharyngeal edema or phlegmon (of which it is the analogue) 
very frequently develop. The mortality is 40 per cent. 

SIALODOCHITIS FIBRINOSA. 

Inflammation of the salivary ducts with formation of membrane 
(Kussmaul) results from infection ascending from the oral cavity and is 
characterized by fever, tenderness, pain and tumefaction of the gland. 
The duct is kept patent by pressure or sounding. 

SIALOLITHIASIS. 

Stones of calcium phosphate or carbonate occur usually from stagna- 
tion of the salivary secretion by foreign bodies, bacterial invasion or 
stricture following ulceration. Roberg found stones in Wharton's duct 
fifty times, in the submaxillary gland twenty-eight times, in Stenson's 
duct six times and in the, parotid gland twice. Bendixen collected 216 
cases (1908). 



CHRONIC PHARYNGITIS 483 



DISEASES OF THE PHARYNX. 



ACUTE PHARYNGITIS. 

Etiology. — Acute, simple angina may be caused by (a) rheumatism, 
cold or exposure; (b) infections, either acute (measles, scarlatina) or 
chronic (syphilis); (c) gout, dyspepsia or smoking; (d) in many cases 
the cause is obscure, probably always mycotic; no single virus is found. 
It is most common in youth. 

Symptoms; (a) Local: The throat is red, glazed and streaked with 
mucopus which is easily wiped away. Swelling or vesicles on the soft 
palate and uvula, superficial erosions, and swollen mucous follicles are 
occasionally seen. In some cases the local findings, hidden in the naso- 
pharynx, are very slight in proportion to the local pain and general 
symptoms. A scratching sensation in the throat may radiate into the 
posterior nares or ear. The patient hawks, but raises little, unless there 
is coincident rhinitis or laryngitis. Swallowing is rather painful, slight 
deafness is common, the speech is slightly nasal and the angular lymph 
nodes are painful, (b) Constitutional symptoms are usually slight. At the 
onset there are chilliness, moderate fever, aching in the muscles and in 
some individuals extreme cutaneous hyperesthesia, which may be falsely 
attributed to changes in the deeper parts of the body. With or without 
coincident tonsillitis, there may be high fever, and in labile individuals, 
marked nervous intoxication. Herpes facialis occasionally develops. 
Complications, as acute endocarditis or nephritis, are very uncommon. 
In a few days convalescence is complete. 

Treatment. — (a) Local: Painting the pharynx with a 20 per cent, 
silver nitrate solution affords local and general relief, (b) General- 
Dover's powder and acetylsalicylic acid, each ten grains, may be ex- 
hibited for unusual pain, calomel, followed by salines, for elimination 
and a 1 per cent, phenol gargle for the throat. 

The imeumococcic sore throat may be suppurative, pseudodiphtheritic, 
follicular, like tonsillitis, erythematous or herpetiform; its onset is 
severe, it produces a thicker and more adherent membrane than does 
the streptococcus and the prognosis is generally poor. 

CHRONIC PHARYNGITIS. 

Etiology. — (a) Recurrent pharyngitis; (b) tobacco or alcohol ; (c) abuse 
of the voice, as in clergymen, venders, etc.; (d) extension from chronic 
nasopharyngitis; (e) chronic nephritis, syphilis, etc. These factors are 
most common in adolescence and middle life. 

Symptoms. — The nasopharynx is red and lined with turgid venules; 
the pillars are relaxed and the drooping uvula may tickle the tongue or 
epiglottis, causing chronic coughing. The sides of the pharynx may show 
isolated whitish epithelial thickenings or more often, reddish, hyper- 
trophied lymph follicles {pharyngitis granulosa). The pharynx is dry and 
burning, exciting hawking efforts which are unproductive and may 



484 DISEASES OF THE PHARYNX 

cause morning vomiting. Slight bleeding occasionally causes unneces- 
sary worry. Middle-ear involvement is common, through the Eustachian 
tube. Pharyngitis sicca is an atrophic type and marked by a pallid glazing 
of the pharynx wall and crust formation. 

Treatment. — (a) The causal factors, as straining of the voice, alcoholism 
or smoking, etc., are corrected. Alkaline laxatives are frequently bene- 
ficial, (b) Galvanopuncture of the turgid veins or hyperplastic follicles 
is indicated; improvement is probably more frequent than aggravation 
by overzealous treatment, (c) Local medical treatment is less efficacious. 

1$ — Phenolis gr. xx 

Acidi tannici 3ss 

Glycerini gij 

Aquae rosa q. s. ad. gv 

M. et ft. gargarismus. 

S. — As gargle, properly diluted. 

1$ — Tincturae guaiaci 5iv 

Liq. potassae 5ss 

Alcoholis gj 

Aquae cinnamomi q. s. ad. giv 

M. et S. — One teaspoonful in one-half glass of water as gargle. 

(d) For atrophic pharyngitis the best formula is: 

1$ — Iodi gr. iij 

Potassii iodidi 3ss 

Glycerini gj 

M. et S. — Massage thoroughly into the pharynx. 

PHLEGMONOUS PHARYNGITIS. 

Angina phlegmonosa invades the submucosa (Senator). It is usually 
primary but may be metastatic. The throat is painful, swollen and 
edematous, the neck enlarges and suppuration occurs with high fever, 
sepsis, dysphagia and dyspnea, especially when the subject lies down. 
The inflammation may be hemorrhagic or necrotic. Phlegmonous 
angina is the analogue of suppurative submucous laryngitis and angina 
Ludovici. Without surgical intervention or early spontaneous rupture 
into the throat, death occurs from septicopyemia, mediastinitis or glottis 
edema. 

RETROPHARYNGEAL ABSCESS. 

(a) The primary form occurs in children under two years of age, with 
dysphagia, a nasal voice and retropharyngeal suppuration, as a visible 
protrusion or a palpable fluctuation on the posterior pharyngeal wall; 
dyspnea, cyanosis and inspiratory retraction of the chest develop. It 
is primarily a lymphadenitis. (6) Secondary types are less common in 
caries of the cervical spine, diphtheria, erysipelas, scarlatina and suppu- 
rative inflammation in the retropharyngeal lymph glands, or rarely by 
metastasis. Unless surgical measures are instituted or spontaneous 
rupture occurs early, death results from asphyxia, mediastinitis, glottis 
stenosis, inhalation pneumonia or sepsis. After incision the head should 
be promptly thrown forward to obviate occlusion of the air passages. 



ACUTE FOLLICULAR OR LACUNAR TONSILLITIS 485 

PHARYNGEAL ULCERATION. 

Syphilitic and tuberculous ulceration have been considered. Follicular 
ulcers are superficial and, like all ulcers in the mucous membrane only, 
heal without a cicatrix. Ulceration also occurs in diphtheria and the 
diphtheroid group, due chiefly to the streptococcus. Malignancy too, 
causes ulceration. 

Vincent's angina (see page 85) constitutes 2 per cent, of all anginas 
including diphtheria. It occurs especially in children between six and 
ten years, medical students and servants in anatomical laboratories. 
Tobacco, tuberculosis, syphilis, scarlatina, measles and the eruption 
of wisdom teeth are predisposing factors. The two causative organisms 
were first described by Rauchfus (1893): (a) The fusiform bacillus has 
pointed, sometimes rounded ends, is sometimes bent, measures 6 to 
12/x in length and may be flagellated; (b) the spirillum or Spirochete 
darticola is long, delicate and twisted. They stain with carbol-fuchsin 
but not by Gram's method. 

Symptoms. — In the first period, there is congestion and edema. Then 
a grayish-yellow membrane forms which is friable, cheesy and usually 
removable. Under the membrane, an ulcer develops; it is usually 
single, oval and has an irregular edge and an uneven granulating floor. 

The general symptoms are lassitude, indigestion, vomiting or epistaxis; 
fever over 100° is uncommon and complications rare (albuminuria, enter- 
itis or noma). The breath is fetid and the cervical nodes enlarge. Lesions 
are recorded in the larynx and bronchi alone. Syphilis and diphtheria 
require differentiation. It is communicable within narrow limits. The 
affection heals under applications of iodine, pencilling with silver nitrate 
and gargles of hydrogen peroxide or chlorate of potash. Salvarsan locally 
has given rapid results. Mercury is contra-indicated (v. page 226). 



DISEASES OF TONSILS. 

ACUTE FOLLICULAR OR LACUNAR TONSILLITIS. 

Definition. — An acute mycotic parenchymatous inflammation of the 
tonsils, usually attended by decided constitutional reaction. 

Etiology. — (a) Bacteriologically, the streptococcus is the most frequent 
cause, then the staphylococcus, pneumococcus and diphtheria bacillus 
(at the time of diphtheria epidemics, but such cases are a subtype of 
diphtheria). (6) The virus of rheumatism probably gains access to the 
blood by way of the tonsils; affections associated with rheumatism, as 
erythema nodosum, chorea and endocarditis may follow acute tonsillitis. 
Tonsillitis may begin the rheumatic cycle, as described under Rheuma- 
tism in Children, or it may appear later with endocarditis, pericarditis, 
arthritis and chorea. Tonsillitis is contagious, (c) Cold and dampness are 
directly predisposing causes, largely in the spring, (d) Tonsillitis occurs 



486 DISEASES OF THE TONSILS 

chiefly in youth and adolescence, (e) Individual predisposition depends 
on some unknown factor and one attack favors recurrence. (/) Poor 
hygiene and possibly sexual activity, especially in young married people, 
may be conducive to tonsillitis (Shepard) . 

Symptoms. — (a) The onset occurs with chilliness or rigor, severe pains 
in the back and limbs, fever, rising within a day to 103° or even 106° 
in children or susceptible adults, pain in the throat, particularly on swal- 
lowing, and tenderness of the glands at the angle of the jaw. (b) The 
tonsils are swollen and show on the deeply injected surface three to ten 
yellowish- white points, corresponding to the lacunar; these crypts con- 
tain bacteria, epithelium and leukocytes and are small abscesses; the 
tonsil is the seat of serocellular infiltration. Occasionally there are small 
superficial areas of necrosis, slight erosions or even membrane. The 
voice may acquire a nasal twang, the pain increases for a few days and 
the angular glands remain painful and tender, whence the head is often 
held rigidly forward and the jaws are opened with difficulty. Pain in 
the ear is common, (c) The constitutional symptoms (v. s.) also include 
anorexia, coated tongue, hyperesthetic skin, depression, accelerated 
pulse and respiration; in two adult cases seen by the writer, retraction 
of the neck with headache, delirium and vomiting was mistaken for 
meningitis. Herpes facialis is frequent. 

"Septic Sore Throat." — English writers have long believed that milk 
conveys streptococcic tonsillitis; such epidemics were observed in Chris- 
tiana in 1908 and, in 1911-12, 1043 cases developed in Boston with 5 per 
cent, mortality and 10,000 cases in Chicago. In 75-87 per cent, of cases, 
infection was traced to certain dairies, where bovine mastitis and human 
sore throat prevailed. The disease is due to streptococci (of a type half- 
way between the S. pyogenes and S. mucosus) or to pneumococci. The 
local findings are tonsillitis with a milky gray membrane ; the onset is severe, 
or first mild with later severe symptoms — -fever 102-106°, bradycardia 
(40-90), prostration, chill, moderate leukocytosis; later marked lymphad- 
enitis, which suppurates in about 10 per cent., and suppurative tonsillitis 
in 5 per cent. ; and finally septic generalization in the severerst types, 
with peritonitis particularly, empyema, meningitis, arthritis and endo- 
carditis. 

Complications. — Complications are uncommon. Acute pericarditis, 
endocarditis, functional heart murmurs, febrile albuminuria, otitis and 
erythema (from the toxins or medication) are not very infrequent. Con- 
valescence is complete within a week, though marked prostration and 
considerable residual swelling remain for some time. Repeated attacks 
may cause chronic nephritis or endocarditis. 

Diagnosis. — The typical case cannot be confused, (a) Diphtheria 
produces a white membrane, with a pathognomonic tendency to spread 
to the uvula, soft palate or pharynx; it leaves bleeding raw points when 
it is stripped off; it recurs after removal; it sometimes extends to the 
larynx; it is followed not infrequently by paralysis, responds to sero- 
therapy and shows the Klebs-Loefner bacillus. (6) Tonsillitis necrotica 
leaves an ulcer; some cases showing the fusiform bacillus and spirillum 
of Vincent and others are alleged to be diphtheritic; in some cases there 



SUPPURATIVE TONSILLITIS 487 

is much fever, in others none; the general reaction is severe, (c) The 
possibility of incipient scarlatina should be kept in mind. 

Treatment. — 1. Prevention. — The subject should be hardened by cool 
baths or sponges, and tonsillectomy should be performed. 

2. Local Measures. — After cocainizing the throat, a small probe, 
bent at right angles near its end, is introduced into each swollen crypt 
to secure free drainage; then undiluted Dobell's solution is applied on 
bits of cotton to each crypt, followed by 20 per cent, silver nitrate solu- 
tion; the results are often immediate, sometimes abortive. Squeezing 
out the crypts with a spatula is painful. Hot fomentations may be 
applied to the neck. 

3. Constitutional Treatment. — In a small number of cases sodium 
salicylate, given as in rheumatism, affords relief. Hydrarg. biniodide, 
gr. 5^0", every fifteen minutes for ten doses may abort the process; tr. 
guaiaci ammoniat., lUx-xl, every two hours is unsatisfactory. Ac. 
acetylsalicylicum and Dover's powder, aa gr. x, relieve pain in the throat, 
body and limbs. Aconite and belladonna are beneficial in children with 
high fever, but less so in adults; they are given as in coryza or influenza. 

SUPPURATIVE TONSILLITIS. 

Etiology. — The etiology is almost identical with that of the follicular 
type. Suppurative tonsillitis is most common in adolescence, and for 
unknown reasons individual disposition is an important factor. 

Symptoms. — The symptoms resemble those of the follicular type but 
are more severe from the onset; one, or less often both, tonsils are greatly 
swollen, tense, edematous, and deep red. The pain often radiates to 
the ears. The swollen tonsils may come in contact; one swollen tonsil 
may reach over to the sound side. There is often coincident stomatitis, 
a free salivary flow, and edematous palate and uvula. Swallowing causes 
great pain, the jaw cannot be depressed because of the swollen, painful 
angular glands, and the speech is nasal. The toxemic prostration is often 
profound, the fever ranges between 103 and 105 degrees and the pulse 
between 100 and 140. 

Incision in the first two or three days evacuates only blood and serum. 
In a few days fluctuation is felt anterior to and above the tonsil (peri- 
tonsillar abscess). Introduction of a probe into the early incision is 
followed by escape of pus and immediate relief. The abscess may break 
spontaneously, usually forward and rarely toward the throat, when, in 
rare cases, suffocation or aspiration pneumonia may follow. Very rarely 
ulceration may reach the carotid with fatal hemorrhage. Minute sup- 
purative foci may cause septicemia. 

Treatment. — (a) Tonsillectomy is indicated after an individual tendency 
is manifested. (6.) An ice-bag over the neck is beneficial. Local applica- 
tions are uncertain. It is good practise, early in the course, to introduce 
a knife, with extreme care, covered with adhesive plaster to within half an 
inch of its point, above and inside the tonsil; blood and serum escape, 
tension, edema and pain are relieved and the later abscess more readily 
points toward the cut; the wound is opened with a blunt probe every 



488 DISEASES OF THE TONSILS 

day. (c) Salicylates help, and possibly hasten maturation. Opium and 
coal-tar products relieve the pain to some extent, (d) In exceptional 
cases intubation or tracheotomy is indicated, because of great swelling. 
(e) The diet is necessarily liquid. (/) In convalescence, iron and strychnine 
overcome the resulting prostration and anemia. 

CHRONIC TONSILLITIS. 

Synonyms. — Chronic inflammation; tonsillar hypertrophy; hyperplasia 
of the pharyngeal or lingual tonsils; adenoids; aprosexia. 

Etiology. — (a) Repeated acute attacks of tonsillitis cause chronic hyper- 
trophy in some cases, and in others the tonsils gradually indurate and 
shrink. (6) Waldeyer's " Schlundring" of lymphadenoid tissue consists 
of the two tonsils, the adenoid tissue in the nasopharyngeal vault ("ade- 
noids" in the common acceptation) and the lingual tonsil. Variously 
combined hypertrophies of these structures may be noted, occasionally 
as congenital growths, but most frequently from the third year until 
puberty. Adenoids are found in 1 per cent, of children. Rickets, the 
lymphatic constitution and acute infections involving the throat pre- 
dispose. 

Symptoms. — 1. Local Changes. — (a) From the enlarged tonsil may 
be expressed cheesy plugs, which occasion an extreme fcetor ex ore; calculi 
may result from a deposit of lime salts. The pharyngeal mucus is 
increased, sometimes tinged with blood and expectorated with difficulty. 
(b) Adenoids occur alone or with tonsillar hyperplasia. They are papillo- 
matous, vascular and range up to the size of a bean, (c) Hypertrophy 
of the "lingual tonsil" often disturbs deglutition. Enlarged tonsils and 
adenoids produce the following changes by stenosing the posterior 
nares: 

2. Sequences. — (a) Oral breathing is the earliest symptom and is 
first noticed at night, when sleep is disturbed by night terrors (pavor 
nocturnus), by disordered and irregular breathing, for a time stertorous 
and then interrupted, asthmatic seizures or Balne's paroxysmal cough. 
(b) The palatal vault is high from atmospheric pressure in the mouth, 
and the transverse measurement between the upper teeth is diminished; 
there is less room for the teeth to erupt, (c) The anterior nares are small 
and retracted and the voice is nasal (rhinolalia claustra) ; the consonants n 
and m are pronounced with difficulty. Bloch associated oral breathing 
with stuttering. The sense of smell or taste is obtunded. Hearing is 
impaired by pressure of adenoids on the Eustachian tubes, or retraction 
of the tympana from low atmospheric pressure in the nasopharynx, (d) 
The fades is characteristic; it is vacuous and apathetic, the nose is pinched, 
the mouth open and the lips swollen. The "adenoid habitus" may be 
observed as a stigma of degeneracy, (e) In chronic cases the cerebral 
reaction is slow, the memory tardy, the disposition sullen and the power 
of concentration diminished (aprosexia), due perhaps to some cyto toxin 
elaborated in the lymphoid tissue. (/) Nervous symptoms embrace 
headache, habit-spasm, night terrors and enuresis nocturna. (g) Devel- 
opment is sometimes retarded, (h) Deformity of the thorax was noted 



PLATE XIII 



FIG. 1 




FIG. 2 




Types of the "Adenoid" Faeies. (Posey and Wright.) 



IN FLA MM A TION— NECROSIS— ULCER A TION 489 

by Dupuytren (1828). The pigeon- or chicken-breast is the most common. 
The sternum juts forward, from which the ribs slant sharply backward; 
at the level of the diaphragm there is a circular depression, and inspira- 
tory retraction is caused by the contraction of the diaphragm. The 
funnel-breast, marked by a deep depression of the lower part of the 
sternum, is less commonly due to adenoids, and like the chicken-breast 
also results from other causes. The emphysema chest may result from 
adenoids, (i) Mouth-breathers may develop collapse-induration resem- 
bling apical tuberculosis (see page 158). (j) The cervical lymph glands are 
enlarged and the blood evidences decreased hemoglobin, increased white 
cells and distinct lymphocytosis. (Plate XIII.) 

Diagnosis. — The oral breathing, adenoid facies, mental disturbance, 
palpation of the adenoids in young children and their rhinoscopic detec- 
tion in older ones, and the inspection of hyperplastic tonsils determine 
the diagnosis. In the prognosis of untreated cases, the possibility of 
deafness, mental deficiency, retarded growth, arthritis, endocarditis, 
nephritis, asthma and emphysema should be borne in mind. Acute 
recurrent tonsillitis, diphtheria and other infections are more likely to 
develop and produce disproportionate symptoms. Rarely the hyper- 
plastic tissues may atrophy spontaneously. 

Treatment. — The general health should be maintained by out-door 
life, an ample diet, hydrotherapy and iron. Hypertrophied tonsils should 
be removed when they harbor chronic infection, or when growth is 
retarded, etc. Adenoids causing symptoms should be removed early 
under ether anesthesia; chloroform frequently causes death in the status 
thymicus or lymphoid constitution. Oral breathing, persisting after 
operation, is a habit hard to break; at night a bandage should be used 
to close the mouth. 



DISEASES OF THE ESOPHAGUS. 

INFLAMMATION, NECROSIS, ULCERATION. 

I. Esophagitis. — This is an uncommon finding at autopsy. Its causes 
are (a) mechanical, as from foreign bodies, strictures or dilatation of 
the esophagus; (b) chemical, as corrosive poisons or acid vomitus; (c) 
hypostatic, in cardiac or pulmonary affections; (d) rarely extension 
from pharyngeal or laryngeal inflammation; (e) acute infections, as 
smallpox and diphtheria. Esophagitis is physiological in the newborn 
after the ingestion of the first meals of life. Its pathology is local or 
diffuse, acute or chronic redness, swelling and hypersecretion. Special 
forms are follicular catarrh, sometimes resulting in ulcers or retention 
cysts; exfoliative esophagitis; the fibrinous form, observed in acute 
infections and uremia; genuine diphtheria; the' pustules of smallpox; 
the toxic form from caustics or acids; only 12 cases are on record of the 
single bulging submucous abscess or diffuse submucous suppuration which 
perforates into the esophagus which then presents a sieve-like aspect; 



490 DISEASES OF THE ESOPHAGUS 

forms due to the Oidium albicans or ray fungus. In chronic cases the 
epithelium may thicken (leukoplakia) or hypertrophy (papilloma). 

Symptoms. — Only in marked cases is there pain, continuous, substernal 
or elicited by speaking, or movement of the spine. Dysphagia is constant 
in marked inflammations. Mucus, blood, pus or eschars, depending on 
the nature of the inflammation, are brought up by gagging efforts. Fever 
is common in the more severe types, in which the local symptoms are 
wholly obscured by the causal diphtheria, smallpox, etc. In inflammation 
due to acids or alkalies, the history, local symptoms and eschars in the 
mouth and pharynx are distinctive. 

Treatment. — Treatment is palliative. Narcotics are given for pain, 
demulcents as acacia and ice-cream and a liquid diet for local irritation, 
or nutrient enemata are given. 

II. Necrosis. — This may be due to corrosive poisoning; pressure 
from struma, aneurysm, sounds left in the esophagus to dilate strictures; 
or "bed-sores of the gullet," described by Dittrich (1850) in laryngeal 
perichondritis, due to pressure of the larynx upon the gullet. Esophago- 
malacia is softening due to regurgitation of the gastric acid, chiefly after 
death, or during the death agony. 

III. Ulceration. — Aside from cancer, follicular ulceration, caustic 
ulcers, syphilis and tuberculosis, there is the peptic ulcer first described 
by Cruveilhier, who identified it with ulcer of the stomach. Forty cases 
were collected by Tileston (1908). It appears in four conditions (a) 
by extension from the round ulcer of the cardiac orifice, (6) in ulcers 
at the pylorus or duodenum, which produce gastric dilatation, (c) in 
multiple hemorrhagic infiltrations of the esophagus, stomach and duo- 
denum and (d) in alcoholism and arteriosclerosis. Its chief symptom is 
dysphagia (50 per cent.) ; its pathology, complications and treatment are 
those of gastric ulcer. 



STENOSIS OR STRICTURE OF THE ESOPHAGUS. 

Stenosis is the most frequent esophageal disease. The esophagus is a 
closed tube only in its cervical segment, and its cardiac orifice is not 
physiologically closed. 

Etiology. — (a) Interstitial factors, i. e., in the wall of the esophagus, are 
the most important; cancer causes 90 per cent, of all stenoses; ulceration, 
by caustics and acids comes next; then stenosis by diverticula or pouches 
which, bulging out of and beside the esophagus, exert upon it a lateral 
compression; rarer ulcerative stenoses result from healing gummata, 
tuberculous lesions, smallpox and peptic and diphtheritic ulcers; mus- 
cular spasm causes many cases; congenital stenosis or atresia, of which 
Dickie (1906) collected 76 cases, occurs chiefly as a cul de sac, incom- 
plete development or fistulous communications with the trachea or 
bronchi. (6) Extra-esophageal factors, compressing the tube from with- 
out, include aortic aneurysm or abnormal branches of the aorta; vertebral 
tumor, cold abscess, exostosis or deformation; anthracotic lymphadenitis 
and malignant lymphoma; thyroid or thymic enlargements; medias- 



STENOSIS OR STRICTURE OF THE ESOPHAGUS 491 

tinitis, pericarditis and pulmonary neoplasms. (c) Intra-esophageal 
factors are the rarest, as foreign bodies, pedunculated polyps, 
etc. 

Stenosis occurs chiefly (a) at the lower third of the esophagus, (b) 
near the level of the bifurcation of the trachea or (c) high in the esopha- 
gus. The stenosis is more often single than multiple and more often 
annular than longitudinal; it varies from slight stenosis to complete 
atresia. Above the stenosis the tube is dilated and its musculature is 
hypertrophied to force food through. 

Symptoms. — Dysphagia may be secondary to aortic aneurysm and 
vary from time to time with the pressure exerted upon it; in cicatriz- 
ing ulcers dysphagia is the only symptom. In advanced stenosis the 
food and later the fluids regurgitate after a short time if the stenosis is 
low, or at once if the stenosis lies just below the pharynx. The regur- 
gitated food is neutral, often fermented and contains round cells, mucus 
or blood, but never HC1 nor pepsin. Esophageal pain is common. 
Singultus is frequent when the lesion lies near the diaphragm. Dyspnea 
may result from pressure upon the air passages by the dilated portion 
of the esophagus above the stricture. 

Signs and Diagnosis. — The chest should be examined for aneurysm, 
retrosternal struma and lung tumor and the finger should be introduced 
down the throat to exclude lesions situated high in the esophagus or 
larynx. Esophagoscopy may give excellent results if done by an expert. 
Local signs are elicited in three ways: 

1. Sounding. — A soft sound is far less dangerous at least for the 
first examination in cases of acute esophagitis, aneurysmal compression 
and ulcerating cancer; as there may be other strictures lower down, the 
sound should be passed into the stomach. The length of the esophagus 
is 10 inches or 25 cm. ; from the upper incisor teeth to the esophagus, 6 
inches or 15 cm.; from the teeth to the cardia, 16 inches or 40 cm. (19.7 
inches or 50 cm.). The length of the cervical portion is 2 inches or 5 cm., 
of the thoracic, 6f inches or 17 cm., and of the abdominal part, 1\ inches 
or 3 cm. From the teeth to the level of the tracheal bifurcation is 9 
inches or 23 cm. 

2. Auscultation. — Physiologically, two murmurs are heard with the 
stethoscope six to eight seconds after the beginning of deglutition, first 
a short and then a longer murmur. In marked stenosis the swallowing 
sound is heard at a point just above the lesion, of value when aneurysm 
is suspected and sounding is feared. In the cervical part the noise 
results from the movements of the pharynx; in the thoracic segment, 
to the left of the spine from the first to ninth dorsal vertebra, there is 
a delayed first murmur, and a gurgling, spurting character in both mur- 
murs; in the lowest segment the murmurs are heard above the cardia, 
at the tenth dorsal vertebra. 

3. X-rays. — The ^-rays outline the dilatation (v. i.). 

Prognosis. — Cancerous stricture may ulcerate, relieving the local symp- 
toms, though cachexia increases. Strictures from caustics often improve. 
Where the cause cannot be relieved, the same symptoms result as in 
esophageal cancer (q. v.). Perforation into the lungs, pleura 3 , air passages, 



492 DISEASES OF THE ESOPHAGUS 

mediastinum or vessels may follow. Aspiration pneumonia, which often 
becomes gangrenous, is not infrequent. 

Treatment. — The remediable etiological factors are few. Foreign 
bodies can sometimes be removed by long forceps, with the direction of 
the esophagoscope. In cancerous and aneurysmal strictures, dilatation 
by sounds is attended by the risk of perforating the esophagus. Sounds 
should be introduced beside the index finger, with the patient's head 
thrown slightly backward; severe gagging may be overcome by painting 
the pharynx with cocaine, though it is often as much psychical as esopha- 
geal. The subject should first swallow some olive oil to facilitate passage 
of the sound, which is held like a pen and pushed with exceeding gentle- 
ness. Trousseau's ivory olive points are excellent, but care is necessary, 
and successively larger sizes should be used. Sounds may be left in 
the esophagus for some minutes or an hour, or even permanently, but 
pressure necrosis may then result. It is at times necessary to introduce 
filiform bougies. Silver balls (2 to 7 mm. in diameter) with threads 
attached, may be swallowed and carefully pulled out after remaining 
in over night. When the obstruction is high, external esophagotomy is 
advisable. After opening the stomach, dilatation may be employed 
from below. Impermeable strictures call for gastrostomy. 

DILATATION. DIVERTICULUM. 

Etiology. — Dilatation involves the entire circumference; diverticulum 
involves but part of it. Secondary dilatation may occur above stenosis 
of the esophagus or above the cardiac end of the stomach. It seldom 
extends more than an inch and a half (4 cm.) above the stricture; it 
may follow enteroptosis, ulcer or pyloric stenosis. Marked dilatation 
above the cardia, Luschka's so-called "f ore-stomach" is a local form, 
usually congenital. The diffuse idiopathic dilatation results from cardio- 
spasm (Purton, 1821). It is seen chiefly between the years of twenty and 
forty. Most clinicians incline to Meltzer's view, that cardiospasm is 
due to abolition of cerebral inhibition on the cardia; Kraus reports a 
case with great atrophy of both vagi; others accuse a primary esophagitis 
or the angular insertion of the esophagus in the stomach. Cardiospasm 
produces a great hypertrophy of the cardia muscle, even six times its 
normal thickness, and diffuse total dilatation so that the esophagus may 
measure 46 cm. instead of 25 cm. in length, or 30 cm. in circumference. 
Though Zenker collected but 18 cases in 1878, in 1912 Plummer published 
91 personal cases. The mucosa is catarrhal, thickened or eroded, and the 
muscularis is hypertrophied. 

Symptoms. — There is gradual or sudden dysphagia, which may be over- 
come by effort; the patient feels that the food does not reach the stomach. 
Regurgitation of the food, especially the portion last swallowed, occurs 
soon after eating or lying down; it may measure two quarts, is neutral, 
decomposed if retained for some time, and contains no hydrochloric 
acid, pepsin or rennet. The regurgitated food may again be swallowed. 
Vomiting is impossible. The pressure of the stagnant food or fluid in 
the gullet may produce dyspnea or palpitation. The sound moves freely 



DILA TA TION—DI VER TIC UL UM 493 

from side to side, but meets temporary resistance at the cardia, though 
pressure usually overcomes an obstructing cardiospasm. One sound, 
introduced into the stomach, may recover HC1, pepsin, etc., but another, 
introduced to but not beyond the cardia, recovers fluid or food with a 
neutral reaction; methylene blue solution poured through the first 
tube returns blue; that recovered by the second tube is colorless. Dis- 
tention of the esophagus with water gives dulness, to the left of the sixth 
to the ninth dorsal vertebra, sometimes above the left costal arch, or 
even in the epigastrium. The esophagoscope reveals the dilatation; a 
distinct shadow is seen by using the arrays after the patient has eaten 
potatoes mixed with bismuth. The second swallowing bruit may be 
absent or sounds like fluid running into fluid. Marasmus, constipation 
and often death result, but the clinical course may cover decades. 

Treatment. — Treatment is unsatisfactory. Olive oil §ss before meals 
may help the fluid (or the sound) to pass the cardia. Continued use of 
the stomach-tube may cause esophagitis; its life-long use is often re- 
quired. Lockwood's pneumatic bag may be introduced empty on a sound 
into the stomach, then inflated and withdrawn gently through the 
cardia. Gastrostomy and rectal feeding may be indicated. Operation 
should not be delayed too long — entering the stomach and divulsing the 
cardia. 

Diverticulum involves only an arc of the esophageal circumference. 
Two types are distinguished: 1. Zenker's pressure diverticulum (pulsion- 
diverticulum) of which Rosenthal (1902) collected 180 cases. It is 
found chiefly in men (77 per cent.), and is a pouch which forms on the 
posterior esophageal wall, near its junction with the pharynx, and con- 
sists only of the mucosa and submucosa — a bottle-shaped esophageal 
hernia. Its onset is very gradual, for the muscle, probably congenitally 
weak, yields before intra-esophageal pressure, trauma, foreign bodies 
and the stagnating food. The early symptoms are signs of pharyngo- 
esophagitis, hawking and dysphagia, and food entering the sac rather 
than the esophagus; the axis of the sac, which dips between the gullet 
and the spine, is roughly parallel with that of the esophagus; many of 
its symptoms are those of a high esophageal stenosis. The food stag- 
nates and regurgitates with a fetid odor. Cooper describes a succussion 
splash. In 33 per cent, of cases a tumor appears in the supraclavicular 
region, which is dull when filled with food or tympanitic when dis- 
tended with carbon dioxide; it sometimes can be smoothed out, whereon 
the food regurgitates. The murmurs on swallowing are protracted in 
50 per cent. A sound usually enters the sac, and another, if slightly 
bent, enters the gullet, which differentiates a diverticulum lower in the 
gullet, which is even less common. Examination by the esophagoscope 
is generally negative, but the .r-rays show a characteristic shadow. There 
may be pressure on the heart, trachea, vagus, recurrent laryngeal nerve 
and brachial plexus. The clinical course is protracted, even to forty- 
nine years, and the evolution is inanition in over 50 per cent., gangrene 
(15 per cent.) or perforation with cervical phlegmon. Treatment includes 
feeding by means of the tube, rectal nutrition, gastrostomy and surgical 
resection, first performed by von Bergmann, with 20 per cent, mortality. 



494 DISEASES OF THE ESOPHAGUS 

2. Rokitansky's traction-diver liculum, found in 3.5 per cent, of autopsies, 
is due to extra-esophageal traction, which draws part of the gullet out into 
a funnel-like form. Over 80 per cent, are due to indurative periadenitis 
around caseous or anthracotic lymph glands. Cicatricial mediastinitis 
from pleuritis, pericarditis or vertebral disease produces the same effect. 
It usually, therefore, occurs at the level of the tracheal bifurcation; 
it begins early in life, is usually single, less marked on the anterior or 
lateral wall, rarely exceeds 5 to 10 mm. in depth and is rarely discovered 
except with the esophagoscope. Its chief danger is ulceration at its apex 
and perforation, with resulting gangrene of the lungs, fatal hemorrhage, 
pneumothorax or phlegmonous mediastinitis. 

CANCER OF THE ESOPHAGUS. 

Etiology. — Its frequency is rated at 0.25 to 1 per cent, of autopsies, 
ranking third among cancers (stomach 33, uterus 15, and esophagus 6 
per cent.). Scars, ulceration and traction are promoting causes; 75 per 
cent, occur in males and 80 per cent, between the fortieth and sixtieth 
year and 8 per cent, occur before the fortieth year. 

Pathology. — Cancer of the esophagus is single and primary; cancer 
of the stomach, pharynx or mediastinum rarely involves the esophagus 
secondarily. Most cases are squamous epithelioma, arising from its 
pavement-epithelium; scirrhous, colloid and medullary forms are rare. 
Most cases (57 per cent.) develop in the lowest third of the esophagus, 
33 per cent, in the middle, and 10 per cent, in the upper third; its favorite 
sites are near the cardia, tracheal bifurcation level and back of the cricoid 
cartilage. The muscularis sometimes hypertrophies above the cancer, 
where some dilatation may occur. 

Symptoms. — Signs of esophagus stenosis (v. s.) develop in varying 
grades; stenosis generally advances slowly but occasionally is sudden. 
It may lessen as the cancer ulcerates. Its symptoms are those of stenosis, 
as dysphagia, rather indefinitely located pain, regurgitation of food and 
perhaps also of bloody mucus or necrotic cancer tissue. Its signs are also 
identical, as obstruction on sounding, fluoroscopic findings, detection 
by the esophagoscope of a papillomatous or ulcerated neoplasm, and 
rarely tumor particles found in the fenestras of the tube. Salivation 
(Roger's syndrome) was noted in 22 cases. Cachexia develops; con- 
stipation, indicanuria and acetonuria are frequent. Extension, by 
contiguity, occurs to the spine, mediastinum and cardia, or in 60 per 
cent, by metastasis; the mediastinal lymph nodes are usually invaded, 
the supraclavicular often, and upper cervical seldom. 

Complications. — There may be pressure on the recurrent laryngeal, 
vagus, mediastinal vessels, sympathetic ganglia or brachial plexus. 
Perforation occurs in over 50 per cent., most often into the air passages, 
when aspiration pneumonia or gangrene may follow; into the lung, 
pleura (ichorous pleurisy or pneumothorax resulting), aorta (fatal hem- 
orrhage), heart, pericardium and mediastinum. Pyemia, tuberculosis 
and thrombosis occur in some cases. Death is usual within thirteen 
months, with emaciation, subnormal temperature, small, slow pulse, 



MOTOR AND SENSORY DISTURBANCES OF THE ESOPHAGUS 495 

slow, shallow breathing, flattened abdomen and perhaps acidosis, 
coma and fever. 

Diagnosis. — The diagnosis is based (a) on a stricture of the esophagus, 
which in 90 per cent, of all cases is carcinomatous; (6) on cachexia, 
nodes, metastases and perhaps tumor particles on the sound. Other 
tumors, as lipoma, myxoma, myoma or fibroma are of little clinical 
importance, except accessible fibropapillomata of the upper gullet. 
Von Hacker (1908) collected 21 cases of sarcoma; 81 per cent, were in 
the lower thoracic segment. 

Treatment. — The treatment is that of stricture, nutritive enemata, 
feeding by the stomach-tube, gastrostomy and narcotics. Less than 
10 per cent, are accessible to surgical interference. As to gastrostomy, 
45 per cent, do not live longer than a week and 90 per cent, not more 
than one hundred days. 

PERFORATION, RUPTURE; HEMORRHAGE OF THE ESOPHAGUS. 

1. Perforation may result from causes within or without the esophagus. 
Internal causes include ulcers, foreign bodies, diverticula, cancer and use 
of the sound; external causes are aneurysm, gravitating abscess, lung 
cavities or gangrene, suppurating lymph glands or trauma. It is marked 
clinically by mediastinitis and cervical cellulitis, which are usually 
phlegmonous. Esophageal fistula? may communicate with the air 
passages, from which by the laryngeal mirror fluid or food is seen to be 
expectorated; a communicating tuberculous cavity may become flat 
when the patient drinks or eats, and the flatness changes to tympany 
when the food or drink is expectorated; this is tested by giving the 
patient milk, which will be brought up from the larynx. Aspiration 
gangrene, pneumopericardium, pneumothorax and fatal hemorrhage are 
common causes of death. 

2. Spontaneous rupture (so-called) is a very rare affection, there being 
only 39 cases on record (Cohn, 1908). It is often confused with esophago- 
malacia, in which the rupture is not longitudinal or clean-cut as in 
genuine rupture. The first case, and one of the clearest, was reported 
by Boerhaave (1714); in all cases, except Boerhaave's, the rupture 
was longitudinal. It follows overeating or severe vomiting, and most 
victims have been alcoholics. There is great and sudden pain over the 
lower esophagus (where most ruptures occur) and over the xiphoid, 
hematemesis, collapse and subcutaneous emphysema. Death results 
from collapse, phlegmonous mediastinitis, pleuritis or pneumothorax. 

3. Hemorrhage may follow esophageal ulceration, external or internal 
trauma, toxic esophagitis, softening and aneurysmal or other perforations. 
Varicose veins in the lower esophagus, first described by Le Derberden 
(1837), most often complicate liver cirrhosis, less often syphilis and 
pylethrombosis. The diagnosis and localization of the bleeding-point is 
only suggested by the history and previous physical findings. Treatment 
consists chiefly of absolute quiet, morphine and rectal feeding. 

MOTOR AND SENSORY DISTURBANCES OF THE ESOPHAGUS. 

(See Affections of the Vagus under Nervous Diseases.) 



496 DISEASES OF THE STOMACH 



DISEASES OF THE STOMACH. 



ACUTE GASTRITIS (ACUTE CATARRH, ACUTE DYSPEPSIA). 

1. Simple Gastritis. — Etiology. — It is a common primary and secondary 
affection, (a) Its most important mechanical cause is improper food 
or improper eating; rich food, an excessive amount, partial mastication, 
washing down food with water, hurried eating when very hungry, articles 
containing bacteria or ptomaines and excessive ingestion of cold water 
and fruit are accessory factors, (b) Thermal factors include too hot 
or too cold foods, especially when taken on an empty stomach, (c) 
Chemical causes; aside from toxic gastritis (v. i.), alcohol ranks foremost; 
autotoxins may excite acute gastritis, as in nephritis, cholemia or gout. 
(d) Some cases are clearly infectious; the condition may occur in variola, 
typhoid, grippe and pneumonia, as a secondary manifestation ; occasion- 
ally it is an independent febrile affection, as in the Christiana epidemic 
reported by Hausemann (1880), in which 6000 persons were affected 
within three weeks (Gartner's Bacillus enteritidis, paratyphoid bacillus 
or Bacillus botulinus). (e) Stasis from diseases of the heart, lung or liver, 
tuberculosis, cancer, chlorosis and affections of the higher alimentary 
mucosa are predisposing factors. In some cases a nervous, familial or 
even hereditary tendency is noted, "the delicate stomach." 

Symptoms. — 1. Digestive Symptoms. — These are sometimes absent, 
as demonstrated by Beaumont in the celebrated St. Martin case of 
gastric fistula. The appetite is usually lost or perverted. The tongue 
is thickly coated with white fur and dry mucus. The mouth is dry and 
there is a disagreeable taste and thirst, even though the salivary flow 
be increased. Hiccough, eructations, a sense of gastric distention, pressure 
or pain and tenderness over the stomach are common. Nausea and 
vomiting characterize the more marked cases ; the vomitus is pale yellow, 
bitter and contains little or no hydrochloric acid, though lactic, butyric 
and fatty acids are common; there is much mucus, frequently flecked 
with blood. Gastric intolerance, pain, nausea and vomiting summarize 
the situation. Few uncomplicated cases come to autopsy; the mucosa 
is red, swollen, smeared with adherent mucus, sometimes slightly eroded 
or dotted with ecchymoses; the dilated vessels, seen by the gastroscope 
or through a gastric fistula, are less conspicuous at autopsy for the 
blood leaves the organ after death; microscopically the main findings 
are leukocyte emigration, granular degeneration and swelling of the 
mucous and other glandular cells. 

2. General Symptoms. — Herpes is an occasional finding. Constipation 
is the rule. The urine is scanty because of the vomiting; it deposits a 
lateritious sediment and sometimes contains indican or acetone. Frontal 
headache, vertigo, intercostal neuralgia and depression are common; 
convulsions (acetonemia) and other marked nervous manifestations occur 
infrequently in sensitive individuals. Fever is uncommon; when present, 
it is irregular and ephemeral. 



ACUTE GASTRITIS 497 

Diagnosis. — With fever or constitutional symptoms it is excellent 
practise to regard acute gastritis as a symptom, until typhoid, exanthe- 
matous disease or nephritis is excluded. Confusion is possible with a 
tabetic crisis, the vomiting of pregnancy, hysteria, appendicitis or gall- 
bladder disease. 

Treatment. — (a) Prophylaxis embraces the etiological factors, (b) 
Complete rest of the stomach is the first indication; no rectal feeding is 
required for twenty-four to forty-eight hours, by which time the gastric 
equilibrium is restored; warm water by rectum unloads the bowels and 
allays thirst, (c) If gastric irritation persists, the stomach is washed out 
by the stomach-tube (using warm water with sodium bicarbonate) ; lavage 
is better than calomel, salines and apomorphine or ipecac which irritate 
the inflamed mucosa. Epigastric fomentations alleviate pain. 

]$ — Phenolis gr. iv 

Ac. hydrocyanici dil 5ss 

Bismuthi subnitratis, 

Cerii oxalatis aa 5iss 

Mucilaginis acacias q. s. 

Aqua? menthse piperita? q. s. ad. gij 

M. et fac emulsum. S. — One teaspoonful without dilution every half to one hour for six 
to ten doses, or till vomiting ceases. 

Opiates give relief, but secondary nausea is an insuperable obstacle 
to their use. (<i) In convalescence, dilute hydrochloric acid TTlv-xv and 
bitters are given after meals, to stimulate the gastric secretion. The 
food should be simple and thoroughly chewed. 

II. Gastritis Toxica (Venenata). — Etiology and Pathology. — Acute 
toxic gastritis is caused by various alkalies, acids and metallic poisons. 
Sulphuric acid produces a gray eschar, nitric acid a yellow one, alkalies 
a brown, copper a greenish-blue, silver a deep black eschar and phos- 
phorus produces an opaque, milky stain. The pathological changes are 
severest in places with which the corrosives remain longest in contact, 
as the pylorus and posterior wall; they range from epithelial desqua- 
mation and catarrh, to hemorrhagic infiltration, diphtheroid patches, 
suppuration and ulceration. 

Symptoms. — They are those of simple gastritis, but more severe; 
pain is intense in the mouth, throat, esophagus and stomach, and the 
vomitus is often bloody and the epigastrium tender. 

Prognosis. — The outcome varies; (a) collapse after a few hours or 
days is frequent, with small pulse, shallow breathing, subnormal tempera- 
ture, bloody, albuminous urine, etc. (b) The gastric symptoms subside 
and death occurs later from blood or visceral changes, (c) Stricture 
may develop, or (d) there may be atrophy of the secretory glands. 

III. Phlegmonous Gastritis. — Etiology. — Only 131 cases are reported 
since Borel's in 1656. It is an acute suppurative gastritis, usually caused 
by the streptococcus, which usually enters some small erosion at the cardia 
and infiltrates the submucosa and other coats diffusely or circumscribes 
as a mural abscess. It occurs secondarily #(75 per cent.) in sepsis, acute 
infections, or in local diseases as gastric cancer; 85 per cent, occur in 
adult males. Alcoholism and traumatism are predisposing factors. 

32 



498 DISEASES OF THE STOMACH 

Symptoms. — Besides an acute gastritis, the vomitus sometimes contains 
pus, the epigastric pain is intense, with meteorism and many symptoms 
of peritonitis, which is a most common complication. In a few cases an 
epigastric tumor marks the circumscribed variety. Sepsis causes the high 
fever, the pronounced status typhosus, the small pulse, occasional icterus 
and petechia?. 

Diagnosis and Treatment. — A diagnosis is almost impossible, the out- 
come is fatal in 96 per cent, during the second week and the treatment is 
symptomatic, viz., rectal nutrition, stimulation, narcotics, and if the 
affection is suspected, operation. Some cases heal by rupture into the 
stomach with cicatrization. 

IV. Diphtheritic Gastritis. — Genuine diphtheria is very rare. Diph- 
theroid gastritis, caused by streptococcic and other infections, may 
develop after gastritis toxica, pneumonia and kindred maladies. 

V. Parasitic Gastritis. — This rare form is due to Oidium albicans, 
favus, anthrax, larvae of insects and tinea?. 

CHRONIC GASTRITIS. 

Chronic catarrh is characterized pathologically by degeneration of the 
parenchymatous and infiltration of the interstitial tissue, and clinically 
by mucus formation and decreased secretion. 

Etiology. — (a) The factors are those of acute gastritis, from repeated 
attacks of which chronic inflammation may result. Abuse of drugs, 
especially cathartics, alcoholism and improper eating, eating hurriedly 
or at irregular hours, inadequate mastication, washing down the food 
with fluids, excessive use of coffee, tea, ice-water, pastries or fried foods 
are salient factors. Chewing and smoking tobacco, stomatitis, carious 
teeth and pyorrhea are important causes. Most cases occur in adult 
males. (6) It often accompanies other gastric diseases, as cancer or 
ectasia, or (c) tuberculosis, anemia, stasis, nephritis, gout, diabetes, 
syphilis, amyloidosis, etc. 

The acid form is usually caused by excesses in eating, drinking and 
smoking; the subacid form by the abuse of spirits. 

Pathology. — The pathological changes are observed chiefly in the 
pyloric region. The vessels are dilated, imparting a reddish-brown 
color, which later changes to gray. The mucosa is swollen, lax and 
covered with tenacious mucus or sometimes punctate hemorrhages 
or erosions. In a few cases the mucosa is rough, even papillomatous 
{gastritis polyposa, etat mamellone). The muscularis is occasionally 
hypertrophied near the pylorus. Histologically, the glandular cells 
show granular, fatty or mucoid degeneration; the parietal cannot be 
distinguished from the principal cells, the glands are often large or 
cystic and the tubules show ramifications; the glandular structures 
may completely atrophy (see Achylia). The interstitial tissues show 
leukocytic infiltration. 

Symptoms. — The symptoms begin insidiously. 

1. Oral Symptoms. — \The tongue is generally coated with moist white 
fur, reddish at its tip and indented on its edges, which (like salivation) 



CHRONIC GASTRITIS 499 

may also result from alcoholic or nicotine stomatitis. There is frequently 
a bitter, sour, salty taste in the mouth and sometimes a marked factor ex 
ore. The throat frequently aches. 

2. Gastric Symptoms. — (a) Gastric pain is less frequent than a sense 
of distention or pressure after eating, or sometimes when the stomach 
is empty; actual pain is characteristic of the alcoholic type. Soup and 
fluids, unless they are cold, generally cause no distress; coarse or hard 
foods, as beefsteak, bread, smoked meat, cabbage, hard-boiled eggs or 
cheese, cause distress. (In nervous dyspepsia, any kind of food may 
cause discomfort.) Tenderness is much less than in cancer or ulcer. 
(b) Belching indicates atony. Eructations of hydrochloric acid are 
rare, (c) Nausea and vomiting are infrequent, except in alcoholics, 
in whom the morning vomiting (vomitus matutinus potatorum) consists 
chiefly of saliva and mucus swallowed during the night. 

3. Gastric Chemism. — Our knowledge dates from the introduction 
of the stomach-tube by Kussmaul and Leube and especially the work of 
Riegel, Ewald and Boas. After washing out the stomach the Ewald 
test breakfast is given, consisting of a piece of dry bread and a cup of 
weak tea without sugar or cream. In an hour the gastric contents is 
withdrawn (the patient compressing the abdomen and straining) by 
Ewald's aspiration bag. Innumerable errors result from confidence in a 
single examination and assigning undue importance to the gastric chemism 
alone. It is best to examine the contents without filtration. 

(a) The gross examination shows coarse particles of food when the 
hydrochloric acid is absent or greatly reduced, or fine subdivision when 
it is present in fair amounts. A rancid odor denotes fatty acids, and a 
foaming appearance, fermentation. Mucus is seen in practically all 
cases; most clinicians do not recognize a simple gastritis without mucus 
formation, though Ewald distinguishes (i) simple gastritis in which the 
acid and ferments are decreased; (ii) a mucous gastritis, in which the 
acid is greatly decreased, the ferments are present and there is much 
mucus; and (hi) an atrophic gastritis (v. Achylia). Mucus usually 
indicates a reduction in the hydrochloric acid. Normally there is little 
gastric mucus, though rather more with an amylaceous than with a 
proteid diet. Mucus of gastric origin is intimately mixed with the food 
and is not yellow, nummular, pigmented or mixed with air or cells, as 
is swallowed mucus. 

(b) The HCl is reduced. Of Gunzburg's solution (2 gm. phloroglucin 
and 1 gm. vanillin dissolved in 30 c.c. of absolute alcohol), a few drops 
are added to an equal amount of gastric contents and heated, without 
boiling, in a porcelain dish, when a carmine-red color develops, indi- 
cating free hydrochloric acid; the solution should be kept in a dark 
bottle and not over two months, for it deteriorates. Boas's test gives 
the same reaction and is less expensive: resorcin 0.5, sugar 0.3, dilute 
alcohol q. s. ad. 10 gm. 

Total free HCl. 10 c.c. of gastric contents plus a few drops of the indi- 
cator (0.5 per cent, solution of dimethylamidoazobenzol in strong alcohol) 
are placed in a beaker and, if free HCl is present, the yellow color imparted 
by the indicator will change to bright red; a decinormal solution of 



500 DISEASES OF THE STOMACH 

caustic soda is then added drop by drop until the color of the indicator 
has been changed from red to bright yellow; the number of c.c. of deci- 
normal solution used is multiplied by 0.00365 and again by 10 to give 
the amount of free HC1. Often the result is expressed in terms of the 
number of c.c. of decinormal solution used; i. e., if 4 c.c. were employed, 
4X10 = 40, the free HC1. The usual amount is 30 to 40. 

The total acidity (HO, lactic and other organic acids, acid phosphates, 
albumins, albumoses and peptones) is estimated by adding two drops 
of a 1 per cent, alcoholic solution of phenolphthalein (as an indicator) 
to 10 c.c. of the gastric contents; to this is added, drop by drop, a deci- 
normal solution of caustic soda until the red color, due to the alkali 
acting upon the phenolphthalein, is no longer even deepened in hue by 
it. As 4 to 8 c.c. of the decinormal solution are usually required, 
4 to 8 X 10 = normal total acidity; i. e., 40 to 80 expressed in terms 
of the decinormal solution (corresponding to 0.15 to 0.25 per cent. HC1). 
In most cases determination of the total acidity is sufficient. The bread 
of the test breakfast (phosphates chiefly) accounts for a total acidity of 
from 5 to 8; this figure indicates that the gastric glands are atro- 
phied. 

In chronic gastritis the hydrochloric acid is found decreased or absent. 
A few cases, usually light or incipient, show a total acidity of 40 to 50; 
this form is called gastritis acida, though its separation as a type is 
scarcely justifiable. 

(c) Rennet and pepsin are rarely absent, though usually decreased; 
25 c.c. of gastric juice will dissolve 0.05 gm. of serum albumin in one 
hour, of fibrin in one and one-half hours and of egg albumen in three 
hours. A few drops of hydrochloric acid liberate the enzyme (pepsin) 
from the pro-enzyme (pepsinogen). If no rennet is present the filtrate 
will not coagulate milk. 

Lactic acid is seldom found. Leukocytes and epithelial cells are found 
at times, and in rare cases shreds of gastric mucosa (gastritis exfoliativa, 
Parisier) . 

4. Other Symptoms.— (a) Vertigo e -stomacho lasso, gastric vertigo, is 
probably neurasthenic rather than gastric. Dyspeptic dyspnea probably 
results from pressure of the distended stomach on the heart. Headache, 
physical and mental depression, intercostal neuralgia, tender points 
between the shoulders or over the lower cervical spines and palpitation 
are common toxemic symptoms. (6) The bowels are constipated; diarrhea 
and tympany at times result from marked gastric fermentation or 
extension of the catarrh to the gut, when catarrhal icterus may result. 
Boas and Schmidt find undigested connective tissue in the movements. 
(c) The urine is reduced and shows a lateritious deposit, phosphates and 
oxalates, (d) The general nutrition is maintained if the intestines 
functionate well, (e) The motive and absorptive power of the stomach 
may be impaired, normal or even exaggerated, the food being hurried 
into the intestine. 

Diagnosis. — Its cardinal points are its steady, chronic course, the 
presence of mucus and decreased secretion. (For its differentiation, v. i. 
Ulcer.) 



CHRONIC GASTRITIS . 501 

Treatment. — 1. Prophylaxis. — Recurrence is prevented by treatment 
of the causal conditions. 

2. Hygiene. — Hygiene concerns regularity in living, moderation, 
recreation, rational exercise and careful mastication. 

3. Diet.— Everyone "has the stomach he deserves." Slowness of 
eating, drinking only after meals and thorough mastication are frequently 
curative without medicinal treatment; insalivation of the food is vital, 
since the ptyalin operates for nearly an hour in the unchurned contents 
of the cardiac end of the stomach. As Ewald states, "die Diat der 
Magen-Kranken fangt im Munde an." The teeth require care, as pyorrhea, 
carious teeth and fitting of proper plates Food should be taken in moder- 
ate amounts, and the stomach given sufficient rest. The relish of food 
excites the flow of the gastric juice, the "appetite juice" (Pawlow). 

Kind of Food. — "Easily digestible food" is less important than 
careful mastication and insalivation. In severe or alcoholic cases equal 
parts of milk and Apollinaris water, may be tried, to which grains x 
each of sodium bicarbonate, sodium chloride and magnesium oxide are 
added. Predigested milk is indicated in severe catarrh with much mucus 
formation or atrophy. The diet should be mixed, but proteids are superior 
to carbohydrates, which are prone to ferment. The proteids given are 
chopped lean meats, scraped beef, boiled mutton, veal, roasted steak, 
broiled tenderloin, pigeon, chicken and eggs boiled one minute. Beef- 
tea, fresh beef, hard-boiled eggs, pork, game, fish, warmed-over (therefore 
hardened) meat, turkey, goose, duck, smoked or cured meat (except 
bacon) and cheese must be interdicted. Carbohydrates are withheld when 
there is obstinate fermentation. Those allowed are arrow-root, well- 
cooked sago, tapioca or rice, white bread, zwieback and toast; those 
occasionally allowed or tried later are mealy potatoes, spinach, pea or 
bean soups; those forbidden are substances containing much cellulose, 
as hard or brown bread, oatmeal, coarse vegetables, uncooked green 
vegetables, most fruits, pies and pastries. Soups (containing meat extract), 
dextrin, maltose, dextrose, and proteoses, reaching the pyloric region and 
duodenum, liberate a hormone (gastrin), which, absorbed and carried 
by the blood to the gastric glands, excite secretion from them. Carbo- 
hydrates should be eaten before the proteids, as they leave the stomach 
earlier. Fats are a necessary part of the diet, especially moderate amounts 
of butter and cream; greasy soups are injurious. Liberal quantities of 
salt may be used; condiments in moderate amounts are helpful. Tea, 
coffee, alcoholic beverages and smoking should be interdicted or re- 
stricted. 

4. Gastric Lavage. — Lavage is considered when there is formation 
of mucus, fermentation, deficient secretion and delayed digestion, but 
in the writer's experience is seldom indicated as there is no stagnation of 
food. Morning lavage is best for removal of mucus, and lavage before 
the evening meal for delayed digestion or fermentation. Warm water 
is used, to which sodium bicarbonate (1 to 100) is added to dissolve the 
mucus, or salicylic acid (1 to 1000) to modify fermentation. The stomach 
is washed until the water returns clear. When the stomach-tube is contra- 
indicated, the patient may drink before breakfast two glasses of warm 



502 DISEASES OF THE STOMACH 

water to which a teaspoonful each of sodium chloride and sodium bicarbon- 
ate has been added — essentially the same as drinking the Kissingen, 
Wiesbaden and other waters. Sodium bicarbonate acts locally and 
sodium chloride locally and systematically, for small doses increase the 
hydrochloric acid and large doses reduce it. Carbonated waters stimulate 
secretion and neutralize abnormal acids. 

5. Medical Treatment. — (a) The first indication for hydrochloric acid 
is to convert pepsinogen into pepsin, whence it is useless in atrophic 
gastritis save as it stimulates pancreatic and possibly biliary secretion. 
Its second indication is as a digestant; we employ 20 drops of the dilute 
acid every thirty minutes until 3j~ij have been given; it dissolves 
the glutin covering on vegetables and some connective tissue in meats. 
Its third indication is as an antizymotic, which Boas holds is its sole 
indication; it should not be given until about half an hour after meals, 
during which period the saliva is acting upon the carbohydrates; its 
fourth indication is its appetizing action, (b) Pepsin should be given 
as a powder, for solutions rapidly deteriorate and are strongly alcoholic; 
many forms on the market are inert. Pancreatin is usually ineffective. 
Taka-diastase is beneficial in some cases, (c) Bitters, best exhibited 
before meals, increase the appetite and flow of saliva, gastric and 
probably also the pancreatic juice. Strychnine and nux vomica are 
the best drugs and are expecially valuable in alcoholic cases; bitters are 
given in solution, as their taste is their chief mode of action. 

1$ — Strychninse sulphatis gr. j 

Acidi nitrohydrochlorici 5j 

Tr. gentianse comp §iv 

M. et S. — One teaspoonful half an hour after meals in half a glass of water.' 

Condurango bark (fluidextract 5 ss) is prepared by macerating the bark 
in cold water. Some bitters, as gentian, may irritate the stomach and 
induce diarrhea, (d) Antijermentatives often cause irritation. Phenol 
gr. j, creosote TflJ, thymol gr. ss— j, resorcinol gr. ij-v, after meals, 
act on the stomach and salol gr. x and betanaphthol gr. x (in capsule 
because of its bitterness) are intestinal antiseptics, (e) Gastric sedatives 
are seldom indicated except in the hyperacid type (see page 55) . Silver 
nitrate is sedative, astringent and alterative, but may cause nephritis 
or argyria; it is given in pill form, half an hour before meals, gr. J (per- 
haps with small doses of opium or belladonua). Zinc oxide, gr. iij-v, 
before meals, is valuable in alcoholic gastritis. Extract of belladonna, 
gr. |, relieves pain, especially in hyperacid gastritis. In pyrosis of fatty 
and other organic acids, alkalies may be employed, sparingly, sodium 
bicarbonate, creta preparata and magnesium carbonate, each grains x, 
after meals. Spasm from gas, erosions near the pylorus, or overloading 
of the stomach is modified by tincture of asafetida 5j\ extract of bella- 
donna gr. J and subnitrate of bismuth gr. x. (/) Faradization, massage 
and hydrotherapy, are less valuable than in gastric atony and sensory 
neuroses of the stomach. Cathartics cause irritation and constipation 
recurs; hot water, colonic flushings and perhaps the mildest saline 
aperients are indicated. 



ACHY LI A 503 

Achylia Gastrica. — Etiology. — The term was introduced by Einhorn 
to designate total suppression of gastric digestion. Achylia occurs 
secondarily in cancer of the stomach, various gastritides, cancer of distant 
organs, diabetes, pernicious anemia, tabes and as a functional disorder. 
In rare cases it develops as a seemingly primary affection, possibly as a 
congenital condition. It occurs oftenest in middle or advanced life. 
Atrophy of the stomach was described by H. Jones, Flint and Fen- 
wick. 

Pathology. — Pathologically two main forms exist, (a) cirrhosis ventriculi, 
in which the stomach is very small and its walls measure several centi- 
meters in thickness, and (b) phthisis ventriculi, in which the walls are thin 
or " wasted" and the stomach is lax or dilated. The glandular structures 
are wasted (anadenia). In neurotic achylia there is no anatomical 
change. 

Symptoms. — Symptoms may be absent if gastric motility is good and 
the intestinal glands are normal. If the same process exists in the gut 
diarrhea, marasmus and death result. 

1. Gastric Symptoms. — None are pathognomonic. Pain may be 
absent, moderate or in some cases lancinating, like that of hyperchlor- 
hydria. The appetite is variable. When vomiting is present the vomitus 
contains coarse, poorly digested particles. 

2. Test Meal. — The recovered food is coarse; the total acidity 
corresponds to the amount in the food ingested. No HC1 is found 
(achlorhydria), no pepsin (therefore no peptones), no rennet (therefore 
no coagulation of milk), no blood and according to most writers no mucus; 
mucus may be due to metaplasia of the gastric mucosa to one resembling 
that of the intestine, the cells of which secrete mucus; as they in turn 
atrophy the mucus disappears. Lactic acid is found but rarely. The 
gastric motor power is usually increased and the stomach is emptied in 
less than an hour. In the contracted cirrhotic form, a sound is introduced 
into the stomach with difficulty, hydrochloric acid is present, the stomach 
cannot be distended with gas and its capacity is enormously decreased; 
in the phthisic form ectasia may occur. 

3. Other Symptoms. — Headache, vertigo and constipation are the 
rule; in some cases diarrhea may be the sole salient symptom, simulating 
an intestinal lesion; these morning movements are inoffensive and usually 
painless. Symptoms like those of pernicious anemia or like gastric cancer 
mark some cases. 

Prolonged observation may be necessary to exclude the atrophic gas- 
tritis of cancer and amyloid gastric disease. In one instance the autopsy 
showed only atrophic gastritis, whereas clinically hematemesis, achylia, 
lactic acid, edema, ascites and extreme emaciation had led to a suspicion 
of cancer. 

Prognosis. — Life may be prolonged for years by compensating intestinal 
digestion, but recovery is impossible after atrophy develops. 

Treatment. — Treatment is necessarily palliative. Thorough masti- 
cation of food is imperative. Cellulose is to be avoided and thick, plain, 
leguminous purees should be given. Butter is well tolerated. The 
meals should be small and given every three or four hours. HC1 should 



504 DISEASES OF THE STOMACH 

be given in full doses (lUxx-xxx), stimulating the pancreatic flow and 
controlling the pylorus (thus averting diarrhea) . Water relieves the pain, 
which resembles hyperchlorhydria. 

DILATATION OF THE STOMACH; MOTOR INSUFFICIENCY. 

Gastrectasia is only a symptom, and is understood as a more or less 
lasting dilatation with motor insufficiency. 

I. Acute Dilatation. — Acute dilatation was first fully described by 
Fagge (1883); 217 cases are recorded ' (Laffer, 1908). 

Etiology. — (1) Most cases follow abdominal trauma or anesthesia, 
affecting the vagus (45 per cent.) ; gall-bladder operations are the most 
frequent type. The two cases seen by the writer were in women operated 
on for fibroids of the uterus. (2) It may follow acute infections as pneu- 
monia or typhoid; or (3) mechanical causes; in one of Kolisko's autopsies 
the author saw an enormously dilated stomach in a man who on a wager 
had taken a large number of charged siphons. Unconscious aerophagia 
is Mathieu's explanation. (4) Traction or obstruction of the superior 
mesenteric artery in the duodenal mesentery is the most favored etiological 
factor, though no proof exists that it is not a result rather than cause. 
(5) Most cases occur between twenty and thirty years of age. 

Symptoms. — The stomach is enormously distended; there is vomiting 
of brown or black material which often runs out of the mouth, may be 
very copious, sometimes offensive and rarely fecal. Succussion sounds are 
frequent. The abdomen is greatly distended and often painful. There 
is much collapse. 

Prognosis and Treatment. — Sixty-four per cent, die, usually within five 
days. The indications are: the knee-chest position or lying on the face 
or the right side; interdiction of all food and fluid; early and frequent 
use of the stomach-tube, which may be left permanently in the stomach; 
rectal feeding; atropine (under which the writer observed one recovery), 
or eserine gr. ^-; salt solution under the skin, and other measures 
for shock; gastrostomy or gastroenterostomy is contra-indicated. 

II. Chronic Dilatation and Motor Insufficiency. — Various grades of 
distention and atony may occur; dilatation may be associated with 
increased power of the gastric musculature or with atony; and motor 
insufficiency (inability of the stomach to propel food into the intestine) 
is not necessarily, though very often, associated with dilatation of the 
stomach. Dilatation and motor insufficiency are most prevalent in 
middle or advanced life. 

Etiology. — 1. Pyloric Stenosis. — Its causes are twofold, malignant 
and benign. It is most often cancerous, but may follow round or corrosive 
ulcers, gastritis leading to hypertrophy of the pyloric musculature 
(stenosing gastritis), benign tumors, as pedunculated polyps, and con- 
genital stenosis. (In pyloric obstruction in nurslings, the cause is either 
pylorospasm or hypertrophy of the pyloric musculature, from its repeated 
irritation.) It may also result from congenital duplicature, volvulus 
of the stomach, angular bending of the fixed pylorus or from chole- 
cystitis. Garre collected 25 cases of tuberculous pyloric obstruction. 



DILATATION OF THE STOMACH 505 

Stenosis of the duodenum produces essentially the same results as pyloric 
stenosis and may follow duodenal ulcer, diverticulum or twisting. The 
pylorus may suffer compression stenosis from tumors of the liver, colon, 
kidney or pancreas. Pyloric stenosis may be associated with intestinal 
stenosis (chiefly from round ulcer). Temporary or permanent pyloric 
spasm from fissure, erosion, ulcer, hyperchlorhydria or from appendicitis 
may cause obstruction. The pathological sequence of pyloric stenosis is 
retention of food within the stomach and hypertrophy of its musculature 
in attempts, sometimes partially successful and at other times vain, 
to force the food through the narrow or closed pylorus. Dilatation of the 
stomach may be considered as a disturbed compensation, analogous 
to hypertrophied and dilated bladder from prostatic enlargement or 
hypertrophy with dilatation in obstructive valvular disease. In all 
three instances the hypertrophied muscle eventually degenerates. 

2. Muscular Weakness. — Motor insufficiency, atony or myasthenia 
gastrica constitutes, in contrast with the first group of causes, a functional 
and, generally speaking, a more reparable type, (a) Atony dependent on 
general causes may occur in acute infections, anemia, rickets and neuroses. 
The tendency may be acquired or congenital, (b) Atony may result 
from gastric conditions, as cancer, gastritis, hypersecretion, peritoneal 
adhesions, cholecystitis with pyloric adhesions, diaphragmatic pleurisy 
and diastasis of the recti muscles. Overloading the stomach with heavy 
meals, indigestible foods, vegetables, carbohydrates, beer, milk in large 
quantities, much water ingested with heavy meals, as in diabetics, 
swallowing of foreign bodies by insane subjects, etc., may develop 
muscular insufficiency. The stomach is usually enlarged and shows a 
lax, often wasted and thinned, musculature but seldom contains residual 
food. ■ 

Symptoms.— The symptoms differ greatly, ranging from absolute pyloric 
stenosis to the least motor weakness, and are partly mechanical, partly 
chemical. 

1. Gastric. — (a) The appetite is variable; the tongue is sometimes 
coated, sometimes clean, (b) There is usually thirst and dryness of the 
throat, most frequently in hypersecretion, (c) Singultus, pyrosis of 
fatty acids, oppression over the stomach and eructation of gas are 
frequent. Gases are never formed without motor insufficiency; they 
include hydrogen sulphide, hydrogen, oxygen, nitrogen, carbon dioxide 
and even inflammable gases, (d) Vomiting is always present in pyloric 
obstruction and marked motor insufficiency. It occurs easily and is 
often rather belched up than vomited. It frequently occurs during the 
night or at intervals of days; five quarts may be evacuated. Large 
amounts argue directly for stagnation and dilatation. The vomitus is acid, 
sour and often greatly decomposed. Three layers are noted: a brownish 
foam, a grayish-brown fluid and a sediment of food, stones and seeds, which 
may have lain for days in the stomach. Gas often bubbles up as the 
vomitus stands. If gastric juice only is found, it indicates hypersecretion 
with motor insufficiency. Chemically, butyric acid, peptones and, in 
cancer, lactic acid, are found; when the obstruction lies in the duodenum 
below the papilla of the common duct, bile is also present. Micro- 



506 DISEASES OF THE STOMACH 

scopically undigested meat or starch, in benign stenosis sarcinse and in 
cancer the Oppler-Boas bacilli and yeast are found. HC1 is absent in 
cancer, (e) Pain is cramp-like, boring or burning. 

2. Motility and Resorption. — (a) The chemism depends on the 
causal affection (see Ulcer, Cancer, Hyperchlorhydria, Hyper- 
secretion). Hyperchlorhydria and hypersecretion are usually present 
except in malignancy and are sequential rather than causative, (b) 
Motility is best tested by Leube's test dinner, consisting of 13 ounces beef 
soup, 7 ounces beefsteak, one or two ounces bread and 7 ounces water, 
which should leave the stomach physiologically in not more than seven 
hours; jam is added, for seeds are a ready index of stagnation. If food 
is found later, stagnation is present; if found in the morning when 
Leube's meal has been given at night, there is great stagnation and 
fermentation. Fluid is not absorbed by the stomach, whence the measure 
of its residual amount is important. There is more fluid in the stomach 
than was ingested, which is accounted for by hypersecretion, transu- 
dation, mucus and perhaps regurgitation from the intestine or hemor- 
rhage. (Other tests are less reliable — the oil test, administering 100 c.c. 
of olive oil, 70 to 80 per cent, of which should leave the stomach in two 
hours; and the salol and potassium iodide tests.) In general a homo- 
geneous chyme means that the motor function is normal ; coarse particles 
occur when there is motor insufficiency. 

3. Physical Signs. — (a) Inspection in a good light is very important. 
A visible prominence of the dilated organ may be seen below the navel, 
sometimes showing clearly the abnormally low upper and lower curva- 
tures, the upper curvature never being seen normally. In obstruction a 
peristaltic wave passing from left to right or an antiperistaltic wave in 
the opposite direction often tells the whole story. Peristalsis disappears 
when the gastric musculature is exhausted or infiltrated, e. g., by carci- 
noma. " Stiffening" of the stomach is an infallible sign of pyloric stenosis. 
The axrays show the outline of the viscus after ingestion of bismuth, 
hyperperistalsis, stasis, etc. (see Ulcer and Cancer), (b) Palpation con- 
firms the above findings and also elicits splashing (clapotage) of gas and 
water in the stomach; it occurs in healthy stomachs. The hand may 
palpate the final gush of gastric contents into the gut, or outline a tumor 
(adhesions, callus, pyloric spasm, cancer), (c) Percussion: The normal 
vertical dimension of the stomach is 10 to 14 cm. and its average capacity 
1600 c.c. Filling the stomach with water and percussing, with the patient 
standing, outlines both the lesser and greater curvatures, which may 
reach to the pubes. Siphoning the water and then distending the stomach 
with carbon dioxide, replaces the flatness by tympany, though distention 
is dangerous. When doubtful, the colon may be distended with gas or 
fluid. The greatest distention is at the fundus. The note changes with 
change of posture, the fluid being in the lower and the gas in the upper 
parts; the most experienced have confused enormously dilated stomachs 
with ascites and ovarian cysts and have introduced a trocar; in Jadon's 
case the stomach contained 45 quarts. Leube palpated the lower end 
of the stomach by means of a rigid sound; this practise is abandoned. 
(d) Auscultation elicits the splashing which may be heard by the patient, 



dilatation of the stomach 507 

and sometimes metallic heart tones, crepitation, hissing of gas or a drip- 
ping sound as the patient drinks. 

Complications. — (a) Constipation is the rule, because less fluid passes 
the pylorus; in the exceptional diarrhea, sarcinse may be found in the 
stools, (b) The urine is often alkaline, its chlorides lessened and its 
amount reduced as a result of acid vomiting; acetone and diacetic acid 
are occasional, (c) The skin is dry and emaciation common, even in 
benign forms because food is imperfectly absorbed or lost to the organism 
by fermentation and possibly by tissue-destroying toxins, (d) Auto- 
intoxication may develop, causing headache, vertigo, drowsiness, psy- 
choses, polyneuritis, tetany, slow pulse and dyspnea. Tetany (Neu- 
mann and Kussmaul) occurs oftenest in hypersecretion or stenosis from 
cancer or ulcer; 88 per cent, of cases die. 

Diagnosis. — The vomiting, impaired motility, as shown by Leube's test 
dinner, the visible outlines, x-rays, and the low lesser curvature which 
is not seen normally, distinguish gastrectasia easily; its cause may be 
determined with difficulty only. The stomach may be physiologically 
large (megalogastria) , but then there is no motor insufficiency, no vomiting 
and no stagnation. Gastroptosis will be considered later. Stenosis may 
be intermittent, latent and misinterpreted (stenose meconne du pylore) ; 
a test of the digesting or fasting stomach may reveal nothing between 
the attacks when muscular compensation is good. The degree of stasis 
is determined by washing out the stomach at varying times after the test 
dinner. Retention of food after twelve hours almost certainly indicates 
ulcer or cancer. In pyloric stenosis there is greater dilatation than in 
simple motor insufficiency (or atony) and marked peristalsis always 
indicates obstruction. The benign must be differentiated from the 
malignant type; benign pyloric obstruction runs a more remittent, longer 
course, over two years, even fifteen years; HO and the ferments are 
always present, often increased and sarcinge are often, and lactic acid 
seldom, present; there is more supernatant fluid and the total acidity 
runs 70 to 100 or over, and the free HC1 50 to 80; while in cancer the 
march of symptoms is progressive and achlorhydria, cachexia, anemia 
with leukocytosis, hydrops, pyloric tumor, the Oppler-Boas bacillus and 
metastases develop with relative rapidity. The spasmodic form runs 
an intermittent course. The prognosis depends on the etiology and 
amenability to treatment; spasmodic types are curable; relative stenosis 
may somewhat improve. In infants with spastic obstruction or hyper- 
trophied pylorus the onset within the first month of life is characteristic, 
with forcible vomiting, though the child be carefully fed, emaciation, 
visible peristalsis, constipation, and usually a palpable pylorus. The 
23 cases of volvulus of the stomach (Muhlf elder, 1911), showed gastric 
meteorism, difficulty in introducing the stomach-tube, singultus, symp- 
toms of ileus, sinistrocardia, dysphagia and thoracic pains. 

Treatment. — 1. Etiological factors should be treated. 

2. General measures, to give tone to the musculature are abdominal 
massage, only when ulceration and inflammation are excluded; drugs, 
especially strychnine and atropine, and an ice-bag to the epigastrium; 
hydrotherapy; faradization of the stomach; external is seemingly as 



508 DISEASES OF THE STOMACH 

efficacious as intragastric application; and abdominal binders or supports. 
This treatment avails only in atony. 

3. Gastric therapy, (a) Gastric lavage removes the fermenting contents, 
relieves the pressure exerted by accumulated food and fluid, cleans off 
the mucus, lessens vomiting and auto-intoxication, and may permanently 
help atony and temporarily mitigate stenosis. The stomach is washed 
with luke-warm water until it returns clear; salicylic acid and sodium 
bicarbonate may be added, as in chronic gastritis; the patient soon 
welcomes the relief afforded; washing two hours before the evening 
meal is preferable, to insure less stagnation through the night, (b) 
The food should be well divided, nourishing not voluminous, and given 
with moderate quantities of water, in small amounts and at intervals 
of four hours. The diet consists of meat, eggs, leguminous purees, 
thoroughly cooked rice, small amounts of butter (fats and carbohydrates 
are more prone to fermentation), and an ounce or two of olive oil in 
pylorospasm and moderate benign stenosis. A dry diet was advised by 
Van Swieten, but moderate amounts of fluid aid in propulsion of food 
into the gut. A fluid diet is indicated in great pyloric stenosis and when 
the HC1 is decreased ; meat may be given if the acid is not decreased and 
the pylorus is not greatly stenosed. Recently there has been a reversion 
in favor of two fair-sized meals a day, giving the stomach time to empty 
itself and rest. Water is not absorbed by the stomach; indeed, absorp- 
tion from the stomach of sugar, peptone, dextrin and alcohol is attended 
by actual excretion of water into the stomach. In pronounced cases 
peptonized milk and water are given by rectum to supplement gastric 
feeding. In all cases careful individualization is indicated; the degree 
of insufficiency, i. e., the time required for evacuation, should be tested 
by Leube's meal and the patient fed accordingly, (c) Posture: The 
patient should lie on his right side one or two hours after eating, thereby 
relieving pressure upon the greater curvature and directing the food 
toward the pylorus, (d) Medication: (See Chronic Gastritis, Ulcer, 
Hyperchlorhydria) . v (e) Thiosinamin: (see page 553). 

4. Surgical intervention is imperative in severe or malignant stenosis 
and when medical treatment fails. It embraces (a) pylorectomy, (6) 
pyloroplasty, (c) gastroenterostomy. In 153 operations for benign stenosis 
Moynihan had only two deaths. In the pyloric stenosis of infancy the 
mortality under medical treatment is 72 per cent., under surgical 17 
per cent. (10 per cent., H. M. Richter). In 24 operations for tetany 
with pyloric stenosis 21 recovered (McKendrick) . 

CHANGES IN FORM, SIZE AND LOCATION OF THE STOMACH. 

Form. — The antrum cardiacum is a congenital bulging of the esophagus 
just below the diaphragm and the fore-stomach is a congenital dilatation 
above the diaphragm. There also exists a congenital narrowness of the 
pylorus as well as hour-glass stomach. 

The acquired hour-glass deformity is more common and may result 
from spastic hypertrophic muscle, ulcer, especially cancer developing 
upon ulcer, adhesions, abdominal tumors, peritoneal tuberculosis, 



ULCER OF THE STOMACH AND DUODENUM 509 

twisting of the stomach or hernia of it through the mesocolon. It may 
coexist with pyloric stenosis. Randolph and Thomas observed 2 cases 
in one family. The pyloric sphincter normally contracts so vigorously 
as to give an hour-glass appearance in many x-ray plates. 

Symptoms may be lacking in the lesser degrees of deformity; in the 
higher grades they are those of stenosis. (1) Only a part of a given 
amount of water introduced into the stomach may be recovered (Wolfler's 
first symptom). (2) After the stomach has been washed till the water 
returns clear the fluid may suddenly become clouded (Wolfler's second 
symptom). (3) The stomach is apparently emptied by the stomach-tube 
and yet splashing is obtained, from the cavity nearest the pylorus 
(Jaboulay's paradoxical dilatation). (4) Inflation by carbon dioxide 
produces distention first of the left and later of the right half of the 
epigastrium (von Eiselsberg's first symptom). (5) Normally when the 
stomach is distended and the gas passes through the pylorus into the 
bowel, there is a sharp gurgle over the pylorus ; in the hour-glass stomach 
the gurgle is heard two to four inches to the left of the median line (von 
Eiselsberg's second symptom). (6) On distention by carbon dioxide 
Moynihan found tympany only over the upper part of the stomach and 
not over its lower half. (7) When the stomach is distended a furrow may 
appear (Eichhorst and Schmid-Monard). (8) Filling the stomach with 
water and illuminating it by a light introduced into the stomach, the 
cardiac portion appears translucent and the pyloric part dark (Ewald). 
(9) A rubber balloon, introduced into the stomach and then inflated 
through the stomach-tube,, fills or outlines a part only of the stomach 
(Hemmeter) . 

Treatment is surgical. Moynihan successfully operated on 23 cases 
by single or double gastro-enterostomy, gastroplasty, gastrogastrostomy, 
partial gastrectomy and dilatation of the stenosis. 

Size. — Megalogastria and microgastria are usually accidental findings 
if not associated with other gastric disease. Microgastria may be con- 
genital, or result from spasm, infiltrating cancer or chronic stenosing 
gastritis (linitis plastica). The latter condition is a diffuse or circum- 
scribed cirrhosis of the stomach. Many cases of carcinoma are brought 
under this caption, even after microscopic examination. The connective- 
tissue increase may be localized, as at the pylorus, or diffuse, involving 
the entire stomach, particularly in its submucous coat. The localized 
form gives the usual symptoms of pyloric stenosis. The generalized 
type is attended by pain, vomiting and the toleration, by the stomach, 
of small amounts of food; a rounded, or sausage-shaped tumor is felt 
in the epigastrium. The prognosis is grave unless surgery is invoked. 

Location. — The stomach at birth is vertical; in adult life three-quarters 
or the whole stomach is to the left of the median line. 

Gastroptosis. — (See Enteroptosts, page 555). 

N\ ULCER OF THE STOMACH AND DUODENUM. 

Definition. — Ulcer is characterized pathologically by a "punched out" 
funnel-like ulcer, oftenest near the pylorus, and clinically by localized pain 
and tenderness, hematemesis and hyperacidity. 



510 DISEASES OF THE STOMACH 

Frequency. — It is found in 2.5 to 5 per cent, of all autopsies. 

Etiology. — The causation is obscure, (a) Age. — Most ulcers occur 
between twenty and sixty years of age, with about equal frequency in 
each decade. (b) Anemia and chlorosis are predisposing factors. Anemia 
and (c) hyperacidity are usually regarded as important factors; the 
writer believes that hyperacidity is only a result, (d) As a normal 
access to the stomach of arterial blood prevents its autodigestion, it is 
thought that interruption in the local circulation is the cause of ulcera- 
tion (embolism and arterial spasm). Embolism and ulceration follow 
burns (13 per cent.). However, ulcer often occurs at an age when arterial 
changes are rare, though syphilis, alcoholism, arteriosclerosis, hard 
work, cardiac, renal and hepatic diseases apparently cause some of the 
cases in later life, (e) Occupation. Many cases occur in servant girls 
and in cooks ; (/) trauma in cooks, shoemakers and tailors is an accessory 
factor; the tasting of hot foods and pressure against the stomach; the 
pressure of corsets, the swallowing in certain trades of particles of iron, 
porcelain and glass; and imperfectly masticated or improper food, may 
be brought under this caption. External trauma is a distinct factor. 
(g) Bacterial necrosis may cause ulcer, as in Dieulafoy's cases of pneu- 
mococcic hemorrhagic ulceration of the stomach, (h) The idea was 
recently advanced that ulcer results from lack of anti-enzyme, which 
normally resists necrosis or digestion. Operative figures indicate that 
duodenal ulcers are twice as frequent as gastric, but these statistics 
represent a narrow group of cases; Mayo's figures give 64.5 per cent, 
duodenal, 32.5 per cent, gastric and 3 per cent. both. 

Pathology. — Scars indicating healed ulcers are three times as frequent 
at autopsy as open ulcers. The ulcer is known as ulcus simplex to 
distinguish it from malignant or syphilitic ulceration; ulcus rotundum, 
as the smaller ones especially are round; ulcus pepticum and perforans. 
The peptic ulcer occurs almost exclusively in the stomach, lower esophagus 
and upper duodenum. Its general morphology was first thoroughly 
described by Cruveilhier (1829) and Rokitansky (1839) ; it has a "punched 
out," clean-cut appearance; in contour it is round or oval in small, and 
irregular in large, ulcers; it is usually small, but may even measure four 
by seven and a half inches; it is funnel-shaped in old cases; its apex 
is eccentric and directed toward the serosa, its sides are terrace-shaped 
and its floor is clean. In 90 per cent, the ulcer is single; as many as 34 
ulcers have been reported. Extension is more common in acute than 
chronic types and more toward the peritoneum than laterally. Micro- 
scopically there is no infiltration with round cells. Its localization in 
90 per cent, is near the pylorus on the posterior wall or lesser curvature; 
its complications, as hemorrhage and perforation, and its sequel®, as 
pyloric stenosis and deformations, will be considered under clinical 
symptoms. 

Symptoms. — The general clinical picture varies, cases being typical, 
doubtful or latent. 

In the typical cases there is an epigastric pressure, which later becomes 
a cutting, localized pain; this is observed one and a half to two hours 
after eating, and ceases only with vomiting or passage of the food into 



ULCER OF THE STOMACH AND DUODENUM 



511 



the bowel. The appetite is usually good; hyperacidity and hypersecretion 
are noted in the test meal or the vomitus; tenderness occurs over the 
epigastrium, and in half the cases bleeding from the stomach or blood 
in the stools is observed. 

The typical triad of cardinal symptoms includes pain with localized 
tenderness, hematemesis and hyperacidity. 

1. Pain. — The most important, early, characteristic and constant 
symptom (in 90 per cent.) is pain, which is paroxysmal and is localized 
and occurs during digestion. It is boring or burning, seldom lancinating. 
The diet affects the pain greatly; milk is well tolerated, usually, but solid 
food and very hot or very cold foods or beverages cause discomfort. 
This disappears quickly with rectal feeding. The seat of the pain varies 
in different patients, but is the same 
in a given case. Generally it is epi- 
gastric and near the ensif orm or cramp- 
like in the right mammary line under 
the liver. Sometimes there is wide 
irradiation toward the sternum, ribs, 
shoulder, scapula, lower abdominal 
quadrants, and infrequently in the 
brachial plexus and pulmonary 
branches of the vagus, resembling 
angina pectoris or producing pain in 
the arms and legs. The pain may 
vary with change of position, depend- 
ing on the localization of the ulcer. 

In relation to eating, sometimes 
the pain occurs two to ten minutes 
after eating, the old "wound pain," 
supposedly due to contact of food 
with the eroded nerves in the ulcer. 
Typically, pain occurs at the height 
of digestion, i. e., one and one-half 
or two hours after ingestion of food, 
caused by the hyperacidity. Patients 
fear to eat because of the inevitable 

pain. Pain may increase at the time of the menses or cease during preg- 
nancy. Pain from the scars or adhesions of an ulcer is infrequent and is 
usually drawing or vague. In old ulcers pain may be atypical or absent. 
If pain comes on at once it may suggest esophageal or cardiac ulcer; or, 
if it occurs three hours or more after eating it is suggestive of ulcer of the 
duodenum. 

Moynihan describes the symptoms of duodenal ulcer as follows: "The 
patient tells you that he has certain definite attacks, and if you let the 
man tell his own story, he will give you the impression of having read 
something which has been written about duodenal ulcer, which he is 
recounting to the best of his recollection to please you. He says that his 
trouble comes on in attacks which are nearly always worse in winter than 
in summer and are very apt to be precipitated by a chill. He takes a 




Fig. 37. — Normal adult stomach, 
x-ray after bismuth meal. Note that 
the duodenal cap and pyloric part of 
the stomach are to the right of the 
spine, (x-ray by Dodd.) 



512 DISEASES OF THE STOMACH 

meal at eight in the morning and from two to two and one-half hours 
after it he is fairly comfortable; it is his best time. At the end of that 
time he has a feeling of discomfort in the epigastrium; he feels full and 
heavy and may get some relief from the belching of gas. Some of these 
patients develop a habit of belching. They may bring up a very sour 
fluid, which tastes very bitter and acid and makes the mouth dry and the 
teeth chalky. This pain gradually increases until the next meal-time 
comes. To this I applied the name of ' hungry pain.' At the next meal 
the patient almost instantly gets relief and that relief persists for two or 
three hours again. He probably eats a heavy dinner and will nearly 
always tell you he has something before he gets into bed, a glass of milk 
or a cup of cocoa and a biscuit. He sleeps comfortably, until he wakes 
about 2 a.m. He get relief from nibbling a biscuit, which he keeps at 
the bedside. The pain is found to be most relievable by something 
stodgy and indigestible. Taking an alkali relieves the pain; so will 
washing the stomach." 

Tenderness is most often found under the ensiform. It is usually 
circumscribed and is more often and advantageously found on the lightest 
touch rather than on deep palpation; rigidity is a protective reflex. 
Tenderness in the back (Cruveilhier) suggests ulcer on the posterior wall 
of the stomach, often with adhesions to the pancreas, and is found in 
30 per cent, of cases to the left of the tenth to twelfth dorsal or upper 
lumbar vertebrae. The abdomen, back and chest are often exquisitely 
hyperesthetic. 

2. Hematemesis. — The second cardinal symptom is hematemesis. Its 
average frequency is 50 per cent. Vomiting of blood in ulcer is most 
frequent in the pyloric ulcer (posterior wall and lesser curvature) or, less 
frequently, from ulceration reaching the liver, panrceas or spleen. Hemor- 
rhage when small may be overlooked (occult hemorrhage); melena 
alone is found in 11 per cent, of cases. The hemorrhage must amount to 
a pint to turn the stools black. It may be large and lethal; no blood 
may be vomited and the stomach and bowels are found filled with one 
massive clot. The usual signs of internal hemorrhage exist, as collapse, 
pallor, moderate fever, hemic murmurs, amaurosis and rarely optic 
atrophy or hemiplegia. If profuse it is voided bright red; if slow and 
moderate the acid turns it dark, "coffee-grounds" vomitus. If red blood 
cells cannot be found because of complete disintegration of the cells, 
blood can be detected by treating it with acetic acid, extracting with 
ether and then testing with the guaiac and turpentine reaction. Occult 
hemorrhage occurs in 25 to 50 per cent, of cases but is not as constantly 
present as in gastric cancer (see Hematemesis and Cancer). The tests 
for occult hemorrhage are valuable to determine the length of the medical 
treatment of ulcer and to detect bleeding in apparently normal vomitus. 
Profuse hemorrhage usually indicates deep ulceration. Hemorrhage 
complicates acute more than chronic cases. The hemorrhage is usually 
fairly profuse in ulcer; it may be spontaneous during sleep or rest or 
may result from excitement, exertion or improper diet. One or two 
hemorrhages are the average but they may recur many times. In a case 
of "chronic dyspepsia" with vague symptoms the writer inflated the 



ULCER OF THE STOMACH AND DUODENUM 513 

stomach with carbon dioxide; the patient collapsed in the office and 
vomited nearly a quart of blood. 

3. Hypek acidity. — This is the third cardinal finding. Leube finds 
it in 50 per cent. In old ulcers hyperchlorhydria is present in only 10 
per cent, and they explain most of the cases of decreased acidity; in fresh 
ulcers hyperacidity occurs in 70 per cent. Hyperchlorhydria is probably 
due to irritation of the vagus (Pawlow), and like hypersecretion, develops 
notably in ulcers near the pylorus and especially with stenosis. Compli- 
cating cancer, hypersecretion or catarrh may cause subacidity. 

Test meals should not be given when there is pain, tenderness and 
vomiting of blood, although some employ the stomach-tube for diagnosis 
in atypical cases, and also to relieve the vomiting and to introduce silver 
and bismuth. Organic acids, as lactic, are absent, the carbohydrates 
poorly digested and the albumins are rapidly converted into albumoses 
or peptones. The motility of the stomach is normal in one-quarter and 
slow in three-quarters of the cases. 

4. Other Symptoms. — Vomiting, present in 75 per cent., is a less 
valuable diagnostic than pain. It occurs at the height of the pain, 
two or three hours after eating, whereas in dilatation or hypersecretion 
it occurs much later. Vomiting and pain depend directly on the diet 
and localization, vomiting and hypersecretion denoting chiefly pyloric 
ulceration; vomiting usually relieves the pain. The vomitus consists 
of fine particles, is sour, grits the teeth and shows much acid and no 
fermentation. The appetite is frequently good or exaggerated. Acid 
eructations may cause a burning sensation back of the sternum or between 
the shoulder blades; much esophageal burning indicates incontinence 
of the cardiac orifice. Diarrhea is rare. Constipation is due to anemia, 
diet, rest, vomiting, possibly reflex inhibition of intestinal motility or to 
impeded peristalsis by scars and adhesions. Dysmenorrhea and amenor- 
rhea are not infrequent. Emaciation and anemia may become profound. 
The urinary findings are not characteristic; reduction of the chlorides 
does not differentiate from carcinoma; the urine is slightly acid or 
alkaline when the stomach is dilated; the phosphates are increased; 
with dilatation, indican and ethereal sulphates are increased. Acetonuria 
and diaceturia sometimes result from inanition. 

Clinical Forms of Lebert. — (a) In the hemorrhagic form bleeding may 
be acute or chronic, the first or the last and fatal symptom, (b) In the 
perforative form there may have been no previous symptoms, (c) In 
the dyspeptic type there are atypical symptoms, such as pain which is 
not sharp, vomiting which is infrequent and excess of hydrochloric acid, 
but no increase in mucus, (d) The cachectic form, in old ulcers with dilata- 
tion and hypersecretion, may be confused with carcinoma. Other types 
are (e) gastralgic or neuralgic form; (/) vomitive form; (g) latent ulcer 
(scars at autopsy); (h) a form with tumor; (i) recurrent type; (j) stenotic 
type; (k) secondary carcinomatous type. 

Clinical Course. — Ulceration is frequently long latent before diagnosis 

is possible and persists some time after all symptoms have disappeared. 

The course may be acute and rapid, especially under appropriate therapy, 

but averages three to five years (even twenty to thirty-five years, due to 

33 



514 DISEASES OF THE STOMACH 

pyloric obstruction, dilatation or adhesions.)- Very large ulcers probably 
never heal. They frequently remit with appropriate therapy, but recur, 
especially in the spring and fall, or with the resumption of the old diet. 
Ulceration can be considered cured only when all symptoms have been 
absent for six months. 

Localization. — Tenderness and tumor are indicative of ulcer on the 
anterior wall; hemorrhage and dorsal pain suggest posterior involvement. 
Pain in a lateral decubitus suggests localization in the fundus or pylorus ; 
dilatation, in the pylorus or duodenum; pain under the ensiform during 
the act of deglutition suggests cardiac ulcer. Ulcers are palpable in only 
0.1 per cent, of cases. The percentage of involvement of the cardia 
is 6; of the fundus 4; of the lesser curvature 36; of the posterior wall 
30; of the pylorus 12; of the anterior wall 9. In over 80 per cent, of 
cases it occurs in a small area about the pylorus, lesser curvature and 
posterior wall. 

Complications and Sequels. — (a) Perforation (3 per cent.) may occur 
into the peritoneum, usually with collapse, peritonitis and vomiting 
(in 33 to 66 per cent, of cases) . Perforation may be prevented by omental, 
peritoneal, pericardial and pleural adhesions. The danger of perforation 
in ulcer of the anterior wall is seven times greater than of other locations. 
Perforation of a latent ulcer maybe confused with rupturing appendicitis 
or salpingitis. Perforation may occur into the heart, colon, gall-bladder, 
portal vein, pericardium, thoracic or abdominal wall; or it may produce 
pneumothorax subphrenicus, which is suggested by pleurisy, epigastric 
and hypochondriac pain, stiffness in the back, painful eructations and swal- 
lowing, singultus or local edema. In 90 per cent, of all perforations there 
is a history of ulcer covering over three years (Brunner). (b) Simple 
peritonitis (perigastritis) may cause a friction murmur over the stomach. 
Perigastritis may invade all contiguous organs and cause the greatest 
gastric intolerance, (c) Adhesions develop in about 40 per cent, of ulcers; 
they are protective against perforation, but may impede cicatrization 
of the ulcer or lead to erosion of the pancreatic or hepatic bloodvessels; 
they may impede motility, deform the stomach (hour-glass stomach) or 
obstruct either orifice or even the bowels; 75 per cent, of adhesions are 
to the liver and pancreas. The dragging pain of adhesions is increased 
by exercise, standing and eating. Pain in the shoulder, back or chest, 
suggests adhesions to the liver, pancreas and diaphragm, respec- 
tively. Dilatation of the stomach indicates pyloric stenosis, or less 
often, pyloric spasm. Troublesome adhesions may finally so stretch 
as to relieve all symptoms, (d) According to Liebert (9 per cent.) or 
Zenger, the majority of cases of cancer develop from ulcer. The typical 
symptoms of ulcer are followed by loss of weight, occult bleeding, gradual 
lessening of hydrochloric acid and other evidences of carcinoma. Poly- 
neuritis is a rare complication. 

Diagnosis. — The diagnosis is determined by the cardinal symptoms 
and various clinical types enumerated. In general it is more easy in 
the young than in older individuals with chronic ulcer. 

Pain is often the only symptom; if it is atypical, hyperacidity may 
indicate ulcer; according to Riegel pain in simple hyperacidity is less 



ULCER OF THE STOMACH AND DUODENUM 515 

regular than in ulcer and localized tenderness is absent. Where pain 
alone exists, one must remember the gastric crises of tabes, small hernias 
in the linea alba, and pain in the transverse colon, which usually ceases 
on evacuation of the bowels. Without careful examination movable 
kidney may be confused. The pain in gall-stones is paroxysmal, but more 
irregular and independent of eating. The gall-bladder is tender and may 
be distended and palpable. The paroxysm in gall-stones is longer, far 
more violent and is often attended by fever and a chill. The pain more 
often radiates to the right side and to the shoulder and the vomiting 
is not that of ulcer, though hyperacidity and gastric dilatation may follow 
cholelithiasis. As to duodenal ulcer Graham states "There remains a 
certain proportion of cases that will mislead. Those cases of gall-stones 
in which the stomach symptoms of gas, distress, sour belching and dilata- 
tion predominate, and pain is only of a dull character, will usually be 
diagnosticated as ulcer; but the duodenal case, of which the chief symp- 
tom is the sudden, sharp, intense pain of perforative peritonitis, and in 
which, with no obstruction or hyperacidity, the other stomach symptoms 
are in abeyance, will be diagnosticated cholelithiasis. Differentiation 
in many cases must be made on the operating table." 

In differentiating ulcer, gall-stones and appendicitis, we consider the 
chronicity and periodicity of the symptoms, the "hunger" pain, vomiting 
and eructations of gas, which occur in all three; the time of the pain, its 
regularity and its relief by vomiting, eating or alkalies determine an 
ulcer. Even in "appendix dyspepsia" we may observe pain, vomiting 
and hematemesis. In gastric arteriosclerosis, pain may follow a full meal 
with or without exercise. Chronic poisoning, as by arsenic, may be sus- 
pected, as in the case of the Duchess of Orleans until Littre diagnosed 
ulcer. 

Hemorrhagic erosions and fissures of the stomach present no constant 
clinical picture. After eating there is a sense of burning over the entire 
stomach. The chemism and tender points of ulcer are lacking, though 
Cohnheim finds hyperchlorhydria and believes that solid food relieves 
the pain. Shreds of tissue are always found, according to Pariser, which 
cease with cessation of pain. 

Pyloric spasm may also occur in cardiac disease, appendicitis, tenia, 
ascaris, spastic* constipation or nicotinism. 

Differentiation from carcinoma is not often necessary. In Kraus's 
clinic the author saw 2 cases; 1 was an old man with cachexia, pyloric 
tumor and decreased hydrochloric acid, which was diagnosticated cancer; 
the other was a young girl with vomiting of blood, in whom the 
diagnosis of ulcer was made. The postmortem examination showed 
that the old man had a round ulcer and the girl had a cancer. The 
author has seen 15 cases of carcinoma under the age of thirty. (See 
table on page 517.) 

X-ray Findings. — (a) In gastric ulcer; the finding of bismuth in the 
stomach after six hours indicates atony, tumor or spasm or stenosis of 
the pylorus. The pylorus may be displaced upward to the left, by ulcer 
on the lesser curvature, bringing the pylorus and cardia nearer together. 
The last part of the greater curvature may be drawn up vertically, instead 



516 DISEASES OF THE STOMACH 

of curving upward to the right. Fluoroscopy may detect adhesions (caus- 
ing displacement), antiperistalsis (indicating organic disease, as cancer 
or ulcer), puckerings, indentations, filling defects, protrusions, partial 
or imminent perforation or an organic or spastic hour-glass stomach. 
(6) In duodenal ulcer, we may observe gastric hyperperistalsis ; residual 
bismuth in the duodenum or in the stomach if stenosis from scar con- 
traction occurs; hypermotility with early emptying of the stomach; 
tenderness over the ulcer; irregular outline of the cap or first portion, 
where 95 per cent, of postpyloric ulcers are found; and dilatation of the 
duodenum or diverticulum of a perforating ulcer. 

Prognosis. — The mortality averages 7 per cent., about equally divided 
between hemorrhage and perforation; in over one thousand cases, 
death occurred in 2 per cent. (Leube). Very deep, old ulcers rarely heal. 
The deeper the ulcer the greater the danger of hemorrhage and per- 
foration. Ulcers with hypersecretion give a relatively poor prognosis. 
Carcinomatous degeneration must be considered when treatment is not 
successful. 

Treatment. — 1. Absolute Rest. — Rest in bed for a month or more was 
recommended by Cruveilhier, in addition to which Leube advises hot 
fomentations to the epigastrium, which relieve pain within a few days. 
Women should remain in bed during menstruation, even after recovery. 

2. Absolute Rest of the Stomach. — The ingestion of even small 
quantities of food or water excites peristalsis and secretion and distends 
the ulcer. Rest permits the stomach to contract and the edges of the 
ulcer to come more completely in apposition. The more absolute the 
rest of the stomach the more rapidly the ulcer granulates and cicatrizes. 
Chronic ulcers show little tendency to cicatrize. In rectal feeding the 
usual rules should be followed; pancreatized milk, grape-sugar, baby 
foods, meat juice and eggs, should be given, in amounts not to exceed 
eight ounces, at eight-hour intervals; they should be injected slowly, 
with the patient on his left side and should be given warm, which pre- 
cautions obviate excessive peristalsis. A fountain syringe with a soft 
tube is always used. Nutrient rectal enemata can be retained invariably 
if the technique is carefully carried out. Wine or spirits irritate the bowel. 
Rectal tenesmus is obviated by administering, a short time before the 
enema, an opium suppository of one-half grain of the extract. A patient 
in bed can manage with 1800 calories; in rectal alimentation by milk 
only 300 calories are absorbed; enemata of 10 per cent, dextrose, by 
the drop method, increase the nutrition and lessen the acidosis of starva- 
tion. Peptonized milk is far inferior to milk pancreatized for twenty-four 
hours, in which amino-acids abound. Among 1000 gastric ulcers, parotitis 
developed in 4.5 per cent, on the strictest diet, but only in 0.4 per cent, 
when water was given by mouth (Rolleston and Oliver) . Water may be 
given by rectum or food by the duodenal tube. 

3. Pain. — Rest of the stomach relieves pain in most cases;, small 
doses of opium or atropine by rectum, may bo given, but there is danger 
of the habit. 

4. Superacidity. — Treatment should be initiated after one week of 
gastric rest. Massive doses of sod. bicarbonate 5ss-j in a starch wafer, 



PLATE XIV 

Fig. 1 Fig. 2 





Fig. t. — Uleer of Lesser Curvature, Retraction of Lesser Curvature, draw- 
ing Pylorus up and to the left. The so-called "snail-form," described by 
Haudek. (Radiologist, Dr. Learning.) 

Fig. 2. — Uleer of Lesser Curvature and Pylorus. The typical bowl- 
shaped bismuth residue is not as marked as is usual, although pyloric 
stenosis exists. (Radiologist, Dr. Busby.) 



Fig. S 



Fig. 4 





Fig. S. — Ulcer of Lesser Curvature. Spasmodic Incisure of Greater 
Curvature. (Radiologist, Dr. Busby.) 

Fig. -4. — Uleer of Pylorus vv^ith Adhesions and Distortion, Closely Resem- 
bling Carcinoma. (Radiologist, Dr. Busby.) 



(From Lockwood's Diseases of the Stomach.) 



ULCER OF THE STOMACH AND DUODENUM 



517 



Cancer. 



Ulcer. 



Chronic 

gastritis. 



Gastralgia. 



Hyperchlor- 
hydria. 



Etiology 

Tongue 

Appetite 

Pyrosis 
Belching 

Pain 



Vomiting 



Hema- 

temesis 



Test 
Meal. 



Tumor 



Collat- 
eral 
Symptoms 

Course 



75 per cent, over 40 
years. 

Heavily coated. 
Usually anorexia. 

Often pyrosis. 

Usually fetid 
belching. 

The pain is less in- 
tense, but more 
constant; sel- 
dom free in- 
termissions, dur- 
ing which no 
distress is felt in 
gastric region. 
Pain not in- 
creased at the 
height of diges- 
tion. Tenderness 
less frequent and 
intense. 



Usual. Hours after 
eating or once a 
day or alternate 
days, etc. Copious, 
coarse mucus, 
fermented. 

F r e q u e n t — small, 
dark, like coffee 
grounds, decom- 
posed, usually late 
in disease. 

Early reduction 
HC1 and later, 
total absence; fer- 
ments decreased 
or absent; lactic 
acid present; im- 
paired motility 
and absorption; 
abundant mucus, 
Oppler-Boas bacil- 
lus — yeast — pos- 
si'bly tumor 
shreds; coarse, un- 
digested particles 
of food. 

In 80 per cent. 



Cachexia— edema. 



Part of a year. 



75 per cent, un- 
der 40 years — 2 
to 4 times oft- 
ener in women. 

Usually clean 
and red. 

Good; only fears 
to eat. 

Water brash. 

Usually absent. 

Intense; appears 
shortly after 
meals; grows 
severer on pres- 
sure; disap- 
pears at the end 
of digestive 
period ; per- 
fectly free 
periods more 
frequent ; par- 
oxysmal. 



Frequent — at 
height of diges- 
tion — smaller 
amount, finely 
homogeneous, 
no mucus, acid. 

Frequent — co- 
pious, bright; 
may be early 
symptom. 

Hyper chlor- 
hy dria often ; 
ferments nor- 
mal or in- 
creased; no 
lactic acid or 
Oppler-Boas 
bacilli; food 
well digested. 
No mucus. 



In but one pro 
mille (from py- 
loric spasm, 
hypertrophy, 
cicatrix, etc.). 

Absent. 



Longer; helped 
by treatment — 
aggravated by 
arsenic. 



Males. 



Grayish-white 

fur. 
Poor. 

Frequent. 
Copious. 

May be present 
but not pro- 
nounced and 
rarely actual 
pain but ten- 
derness of 
diffuse char- 
acter. Lanci- 
nating pains 
in atrophic 
gastritis only. 



Frequent; mu- 
cus. 



None. 



Decreased HC1 
(rarely in- 
creased, gas- 
tritis acida) ; 
later may be 
achylia. Much 
mucus. 



None. 



Absent. 



Women. 



Normal. 

Variable. Some- 
times perverted. 
None. 
Variable. 

The pain appears 
without regu- 
larity, and not 
dependent upon 
meals ; may be 
relieved by pres- 
sure ; intervals 
of several days 
free from pain. 
Tenderness rare; 
conforms to out- 
lines of the 
stomach. Elec- 
trical test (Leube) 
during digestion ; 
if pain decreases, 
it is gastralgia ; 
if it does not, 
may be ulcer or 
gastralgia. 

Rare; no mucus. 



None. 



Normal or vari- 
able. If HC1 is 
decreased, the fer- 
ments are normal. 



Chronic ; helped 
by treatment 
— aggravated 
by arsenic. 



None. 



Absent. Nervous 
stigmata often. 

Arsenic helps. 



Males. 



Clean. 

Good, often 

increased. 
Present. 
Usual. 

The pain ap- 
pears about 
one or two 
hours after 
meals, disap- 
pears after 
eating, espe- 
cially meat, 
milk or eggs, 
or after the 
administra- 
tion of bicar- 
bonate of so- 
dium. Pain is 
less regular. 



Much less fre- 
quent, then 
acid and no 
mucus. 



None. 



As in ulcer. 



None (very 
rarely from 
pyloric spasm) . 



Absent. 



Like ulcer. 



followed by a swallow of water, give the best results. Then Carlsbad 
water should be given, in small quantities and in sips; it consists of sodium 
sulphate 50, sodium bicarbonate 6 and sodium chloride 3 parts ; it neutral- 
izes the acid, aids intestinal digestion and cleanses the stomach (half 
an ounce of the salts in a pint of water, taken in quarters every ten 
minutes, the last dose one-half hour before meals). Alkalies operate 
also on the duodenum relaxing the pylorus. Roberts prescribed a lozenge 



518 DISEASES OF THE STOMACH 

composed of magnesium carbonate grains 3|, chalk grains 2\, sodium 
chloride grain 1, which dissolved slowly in the mouth, increased the sali- 
vary flow and neutralized the excess of acid (v. i. 5 and 6). 

5. Diet. — After a week of rectal feeding, eight to ten meals daily of 
predigested milk with soda should be given in small quantities. Cooked 
milk is more easily digested and curds less. The casein engages and 
neutralizes the acid. If peptonized milk is distasteful or the stomach is 
irritable it may be administered as a thin gruel. Potato puree, arrow- 
root, wheat-meal, baby foods, buttermilk, soups with meal and alkalies 
which precipitate the casein in finer form and ice-cream may also be given ; 
but the milk diet, recommended by Cruveilhier is most efficacious. After 
the patient has been on the above-mentioned diet for ten days, soups, 
rice, sago, soft-boiled eggs, calves' brains and chicken may be adminis- 
tered. Slightly boiled or poached eggs are digested better than raw 
eggs and may be given with bread-crumbs from the inside of the loaf. 
Custards may be given. Tea and coffee should be forbidden. Strauss 
has found that sugar lessens the amount of acid. Cohnheim gives olive oil 
freely at all times to relieve spasm and inhibit hyperchlorhydria; it 
also protects the surface of the ulcer, promotes regurgitation of the alka- 
line duodenal contents into the stomach, increases nutrition and lessens 
constipation. After fifteen days Leube permits grated beef, and after 
about another week tender roast beef, chicken and pigeon, to which others 
would add lamb, macaroni, thymus gland and bread. After the fifth 
week roasts and souffles may be given. The Lenhartz diet, which allows 
ice-cold milk and eggs, sugar and egg, raw minced beef and ham, rice, 
etc., is of higher caloric value; it is given even at once after hematemesis 
on the ground that increased nutrition promotes cicatrization. The 
practitioner will find the first method superior, but the writer with^ 
holds meat, meat extractives (in soup) and salt for months after the 
ulcer course. 

6. Drugs. — Bismuth relieves pain and is taken most advantageously 
in olive oil, but it has no curative value. Fleiner, Kussmaul and others 
administer bismuth by means of the stomach-tube. Large doses may 
accumulate in the ulcer, the drug is expensive and the subnitrate may 
cause nitrite poisoning, methemoglobinemia, cyanosis, fever, salivation, 
vomiting, cramps, dyspnea, collapse and the black line on the gums, 
whence the subcarbonate is preferable. Belladonna relieves pain, relaxes 
the pylorus and lessens hyperacidity by its vagal action. Silver is used 
to wash the stomach before meals (Reichmann) ; it is readily precipitated 
and may produce nausea, diarrhea and even argyria. 

7. Symptomatic Treatment. — Pain is best relieved by rectal alimen- 
tation, as is vomiting, which sometimes may necessitate the adminis- 
tration of bismuth, belladonna or minute doses of phenol. Hemorrhage 
is treated by absolute rest of the stomach, intestine, mind and body; 
morphine quiets peristalsis and mental excitement. Styptics, astringents, 
fomentations and ergot are contra-indicated. Syncope promotes spon- 
taneous coagulation and stimulation should be avoided as long as possible. 
In severe hemorrhages adrenalin (gtt. x, 1 to 1000 solution) and horse 
serum are indicated; saline transfusion should be considered, but more 



CANCER OF THE STOMACH 519 

than one pint seldom should be given, for death has occurred from 
reaction and renewal of hemorrhage. 

8. Surgical Treatment. — Most cases heal absolutely or improve 
greatly under proper medical treatment; this is especially true of fresh 
ulcers. Leube's last series (v. s.) of 627 ulcers, gave 2.5 per cent, mortality 
in the cases of hemorrhage; in the cases without hemorrhage, the mor- 
tality was 0.3 per cent., the complete cures 90 per cent., the improved 
cases 8.5 per cent, and the failures 1 per cent. Clairmont, with gastro- 
enterostomy, obtained complete cures in but 52 per cent, and improve- 
ment in 15 per cent.; a comparison with Leube's figures is suggested; the 
average surgical mortality is 6 per cent., though the figures of Robson, 
Mayo and Moynihan are close to 1 per cent. ; 156 cases of sequential jejunal 
ulcer are recorded, and the gastric ulcer returned in 20 per cent, of 
gastroenterostomy cases. Excision of callous ulcers entails a 5 per 
cent, death-rate, not a high figure in consideration of the frequency of 
carcinomatous degeneration. Perigastric adhesions or abscess and col- 
lections of pus beneath the diaphragm, necessitate operation. In cases 
of perforation if operation is undertaken within twelve hours, 71 per cent, 
recover. 

Surgical interference is necessary in a limited number of cases. The 
writer's conclusions are that (i) fresh ulcers always and (ii) chronic ulcers 
in far over half the instances belong to internal medicine; (iii) half the 
"inveterate" cases respond to medical treatment; (iv) some of the cases 
with "chronic dyspepsia" and almost none of the cases with hemorrhage 
call for surgical interference; (v) the results of operation are disappoint- 
ing ; and (vi) no proof exists that ulcers heal better with gastroenteros- 
tomy than with medical treatment. 



CANCER OF THE STOMACH. 

Cancer of the stomach constitutes 33 to 50 per cent, of all cancers 
and is found in 1 per cent, of autopsies. 

Etiology. — This is as obscure as in other carcinomata. (a) Age: 
According to Lebert 1 per cent, occurs in persons under thirty years; 
18 per cent, between thirty and forty; 61 per cent, between forty and 
sixty and 20 per cent, in those over sixty years of age. Rare congenital 
cases are recorded. Of late years cancer is becoming more frequent in 
relatively young persons, (b) Heredity is noted as an etiological factor 
in 6 to 17 per cent, and in Broca's series there were 15 instances among 
a family of 26. (c) Ulcer of the stomach is a frequent antecedent; 
C. Graham found ulcer in 60 per cent, of his cases — a higher figure than 
is found in general practice (4 per cent.). Trauma, external pressure, 
as 'in shoemakers, or internal ulceration, pulmonary tuberculosis and 
alcoholism are slightly predisposing factors. 

Pathology. — (a) In origin it is an abnormal growth of the glandular 
epithelium (Waldeyer), which unlike mere adenomatous or papillomatous 
proliferations, extends beyond the mucosa into the other coats of the 
stomach and very often into other organs and tissues. Cancer may 



520 DISEASES OF THE STOMACH 

develop in the normal or atrophied mucosa or in open or cicatrized ulcers. 
(b) It is almost always primary and is very rarely metastatic or extends 
to the stomach by contiguity; secondary growths are usually from 
mammary or pancreatic cancer; Welch collected 37 cases. It is almost 
invariably single. 

Histology and Morphology. — A tumor, in the clinical sense, usually 
develops, although in some cases the cancer is infiltrative and flat (car- 
cinoma planum) . There are three main types : (a) Carcinoma fibrosum 
(scirrhus), the most frequent type, contains much poorly vascularized 
stroma and relatively little carcinomatous tissue; it is hard and, leading 
to much induration, is prone to stenose the pylorus, where it is especially 
frequent, or the cardia; if it is diffuse, it causes the stomach to shrink 
(carcinoma atrophicans); its onset is insidious; it grows slowly and 
ulcerates less than other types, (b) Carcinoma medullare is next in fre- 
quency; the cell elements preponderate; there is much soft, vascular 
tissue and the knife scrapes out much "cancer juice"; it may form 
cauliflower-like exuberances; early extensive degeneration, ulceration 
and metastases are common; this type includes the cylindrical-celled 
adenocarcinoma, epithelioma and the very vascular fungus forms, (c) 
Carcinoma gelatinosum (colloides) is least frequent; it produces nodular 
tumors or diffuse infiltrations, which contain colloid material; it inclines 
rather to extension by contiguity than to metastatic deposits. 

The gastric mucosa shows focal wasting of the peptic- and acid-secreting 
epithelium and substitution by cylindrical epithelium, round cells and 
connective tissue. This secondary atrophic gastritis explains the chemism 
of gastric cancer, viz., diminution in the secretion of acid, rennet and 
pepsin; in some cases after surgical extirpation of the tumor, the secretion 
of acid and pepsin has returned. 

Localization. — Cancer occurs (a) in the pylorus in about 60 per cent., 
(b) in the lesser curvature in 20 and (c) in the cardia in 10 per cent, of 
cases; i. e., about 90 per cent, of cancers occur in these sites; this is 
explained by their greater exposure to mechanical insult, their relative 
fixation and the greater muscular activity of the pylorus and cardia. 
Many tumors, apparently pyloric in origin, begin in the lesser curvature, 
whence a palpable pyloric tumor often means one of considerable exten- 
sion; this is an important surgical point. 

Complications. — (a) Ulceration results from inadequate vascularization; 
it is usually central and does not depend on the size of the tumor. The 
tumor may ulcerate almost completely and Ziegler observed total disap- 
pearance, though metastases declared the nature of the scar. (b) Hemor- 
rhage or slow seeping of blood is caused by ulceration, as is also (c) per- 
foration (3 per cent.) into the peritoneum or by adhesions into adjacent 
abdominal organs or Vessels, into the lung, pleura, pericardium or the 
abdominal wall, of which latter 25 cases are recorded (Taussig); per- 
foration is often prevented by adhesions, (d) Stenosis of the cardia 
or pylorus is common, sometimes causing hypertrophy of the muscle 
fibers, which on section of the stomach appear as red lines, (e) Dila- 
tation of the stomach follows pyloric obstruction; atrophy is observed 
in cardiac localization or in carcinoma atrophicans (diffuse cancer) and 



CANCER OF THE STOMACH 521 

hour-glass deformation may result when an annular scirrhus develops 
in the mid-stomach. (/) Local extension by contiguity occurs by the 
submucous lymphatics with early involvement along the lesser curva- 
ture ; the peritoneum is often involved and less often there is extension 
to the portal vein, spleen, esophagus or colon, (g) Metastases occur 
in 50 per cent., in the liver, peritoneum, lymphatics, pancreas and 
lungs. 

Symptoms. — Geneeal Clinical Picture. — Anorexia, distaste for 
meats, gastric oppression and eructations after eating, mark the usually 
insidious onset, and generally the dyspepsia develops in a patient pre- 
viously free of gastric symptoms. Less frequently the disease begins 
acutely or follows closely on symptoms of gastric ulcer. Vomiting occurs, 
and then distress after eating solid food and mechanical or secretory 
insufficiency. There is gradual loss of weight, strength and endurance. 
Examination reveals anemia, cachexia, emaciation, lax skin, flabby 
muscles and often a tumor near the pylorus. A test meal shows imper- 
fectly digested food and absence of free hydrochloric acid. The symp- 
toms progress steadily or remissions occur, especially early in the disease. 
The ankles become puffy and the prostration is profound. Ulceration 
may relieve pyloric or cardiac stenosis, but gradually within a year after 
the first marked symptoms death results from the exhaustion due to pain 
or vomiting, local complications or intercurrent disease. 

1. General Digestive Symptoms. — (a) The tongue is heavily coated, 
not being cleaned by mastication, and there is a bad taste in the mouth. 
The appetite is decreased or absent in 85 per cent., specially for meat 
and fats; the appetite may be normal when the motor power is good and 
cancer develops on an ulcer, (b) Pain, present in 90 per cent., is usually 
diffuse, dull, oppressive and less severe than in ulcer. Boas describes a 
grating sensation. It is increased several hours after eating or in the 
night, but is not wholly relieved by vomiting or dieting. Localized 
pain and tenderness are suggestive of circumscribed peritonitis. Pain 
may be reflected to the sternum, shoulders and acromion, (c) Vomiting 
(in 85 per cent.) is an obstinate and rather late symptom, resulting 
chiefly from pyloric stenosis. It appears late in the day or in the night, 
and may occur only on alternate days. There may be no vomiting in 
cancer of the curvatures, in diffuse cancerous infiltration involving the 
muscularis or in pyloric cancer when ulceration is marked. The fre- 
quently fetid vomitus contains much mucus, poorly digested food, 
little or no free hydrochloric acid, much lactic acid and often blood, 
which may be obvious or occult. Sudden vomiting may be the first 
symptom. Fecal vomiting usually indicates gastrocolic fistula (of 
which Voorhoeve in 1912 collected 104 cases) ; the stools in these cases 
may contain undigested meat (lientery) — "the patient vomiting into 
his own bowel." (d) Hematemesis, present in over 50 per cent, of 
cases, is due to parenchymatous oozing and is therefore moderate in 
amount; it is dark in color, as the blood stagnates in the stomach and is 
converted from oxyhemoglobin to hematin. Profuse bleeding occurs in 
1 per cent. The author has seen 4 cases with fatal, profuse, bright 
hematemesis. (e) Constipation is present in 75 and diarrhea in 25 per cent. 



522 DISEASES OF THE STOMACH 

of the cases; the writer has seen ichorous stools resulting from necrosis 
of the ileum. 

2. Special Gastric Symptoms. — (a) Tumor is felt in 80 and seen in 
40 per cent, of the cases, but is not an early symptom. It is most often 
missed in persons with wide thoraces and rigid abdominal muscles. It 
occupies the right epigastric area, as an ovoid, irregular mass, best de- 
termined when the knees are drawn up and the mouth is open, after the 
bowels have been flushed out and with the patient in several postures, 
as on the side, face, genupectoral position, etc. ; in some cases the tumor 
may be felt lower or even on the left side. The tumor may be palpable 
one day and not the next. Distention of the stomach by gas brings for- 
ward tumors of the anterior wall and greater curvature, obliterates tumors 
of the posterior wall and lesser curvature and pushes downward and to 
the right tumors of the pylorus; motility on distention excludes adhesions. 
Distention must be moderate lest the stomach rupture. If the pylorus 
is incontinent from ulceration or infiltration, the gas escapes rapidly into 
the gut. A visible peristaltic wave or gastric rigidity (Cruveilhier, 1852) 
suggests pyloric obstruction. Percussion is subordinate to palpation 
and inspection, and auscultation occasionally elicits friction or a stenotic 
murmur over the abdominal aorta. Respiratory excursion is often 
present, though less than the excursion of the liver or spleen; if adherent 
to the omentum there is no excursion. If non-adherent tumors of the 
stomach, intestine and omentum are grasped at the height of inspi- 
ration their ascent during expiration can be prevented (Minkowski's 
expiratory fixation); on the other hand, tumors of the liver, spleen 
or stomach (if adherent to the liver) must ascend during expiration. 
(b) Chemism: (i) Bird (1842) and Van der Velden (1879) noted the 
achlorhydria of gastric cancer. Absence or decrease of hydrochloric acid 
is not pathognomonic, as it is also absent in nervous dyspepsia, fevers, 
cardiac, renal or hepatic disease, pernicious anemia, cachectic states, 
gastric atrophy, amyloid degeneration and toxic gastritis; hydrochloric 
acid is absent in 66 per cent, and decreased in 33 per cent, of carcinoma 
involving other organs than the stomach; the writer has seen many cases 
of rectal cancer in which digestive symptoms and achlorhydria led to an 
erroneous diagnosis of gastric cancer. In cancer it is due to the secondary 
atrophic gastritis. An Ewald test breakfast is withdrawn in an hour 
and tested as described under Chronic Gastritis. If there is no stagnation 
the total acidity ranges from 6 to 8 ; in stagnation it is higher from lactic 
and other organic acids. The absence of free acid is observed early, 
while the total acidity remains normal; later the total acidity is decreased. 
Free acid may persist, both in those cases which develop from peptic 
ulcer and in those without this antecedent. The gastric contents are 
often fetid, (ii) The pepsin and rennet are decreased in 66 per cent, of 
cases, (hi) Lactic acid is present in 75 per cent, of cases (Croner and 
Riitimeyer), and though also present in atony, gastritis and pyloric 
obstruction, 85 per cent, of cases in which it is found are gastric cancer 
(Scruff) ; it does not develop early. The factors involved in its formation 
depend on the reduced hydrochloric acid, motor insufficiency, stagnation, 
pyloric obstruction, slow absorption and probably poor digestion of 



PLATE XV 




Oppler-Boas Bacillus in Vomitus. (Musser.) 



CANCER OF THE STOMACH 523 

proteids; in the normal stomach it is absorbed as fast as formed (Sticker). 1 
(c) Microscopically the thread-like, Gram-positive (Plate XV) Oppler- 
Boas bacilli appear in the test meal, feces, or in clumps, in the fenestras 
of the stomach-tube. They produce lactic acid in the presence of proteids 
which act like ferments and originate from the tissues or the cancer; 
the bacilli point strongly to the existence of cancer, but may occur in 
ulcer and atrophic gastritis (with hypertrophy of the pyloric musculature) . 
Small particles of tumor tissue or sarcinse are rarely observed. Occult 
hemorrhage, i. e., blood seen only with the microscope or detected chemic- 
ally or spectroscopically, has the same significance as in gastric ulcer, 
but is more frequent (95 per cent.) ; pus in the fasting and washed stomach 
is very important, (d) Motility: Aspiration of the fasting stomach 
demonstrates stagnation in over three-fourths of the cases; disturbed 
motility may appear very early in the disease. The stomach is usually 
much dilated in patients whose appetites persist and little dilated in those 
with anorexia. If the stomach is empty after seven hours, good motility 
alone is proved, not good digestion. Every case of stagnation should 
arouse suspicion of carcinoma. The recent tryptophan reaction has no 
great or early clinical value; it depends upon the fact that, in gastric 
carcinoma, the ingested proteins are split into more elaborate products, 
amino-acids, than in normal digestion. 

3. Other Symptoms and Complications. — (a) Cachexia is more 
than malnutrition; it is probably the result of toxins which break down 
the proteids. The body weight is usually greatly reduced; in exceptional 
cases it may temporarily increase, as in pyloric stenosis or from hope, 
as in a patient who gained 70 pounds after operation. The skin itches 
and is anemic or clay-colored, somewhat resembling the tint of pernicious 
anemia, though distinguished (i) by its later appearance, (ii) by its 
association with loss of weight, (iii) by the red cells being seldom lower 
than 2,000,000 (60 per cent, being between 2,000,000 and 4,000,000) 
and the hemoglobin seldom below 40 per cent.; and (iv) by the leuko- 
cytosis (see Pernicious Anemia). Schneyer described the absence of 
the digestive leukocytosis; it occurs in only half the cases. As in nephritis 
or chlorosis, the face may not show the real anemia; the wrinkling and 
wasting of the hands and face and the inelasticity of the skin may be far 
more significant, (b) The urine is decreased from poor absorption and 
vomiting, the physiological change in the acidity-curve after eating is 
absent, the urea is increased from increased toxemic catabolism, albu- 
minuria is present in 35 per cent, of cases and indicanuria is common, (c) 
Toxemic symptoms. Fever of a low, irregular or intermittent type results 
in half the cases, from the cancer products, from septic absorption through 
the ulcer or from complications. Coma closely resembling coma diabeti- 
cum may result from the cancer toxins or the breaking down of the 

1 As a test meal Boas employs 1.5 per cent, oatmeal to 100 parts of water, given at night 
after lavage; the gastric contents are tested the next morning; the Uffelmann method is 
employed as modified by Strauss, for phosphates, alcohol and sugar also give the reaction; 
5 c.c. of the gastric filtrate are added to 25 c.c. of ether and shaken in a burette; the lower 
25 c.c. are drained away and 25 c.c. of distilled water are added to what remains in the 
burette (the etheral extract). Two drops of a 10 per cent, solution of ferric chloride and 
20 c.c. of water are added; the blue solution turns to green if lactic acid is present. 



524 DISEASES OF THE STOMACH 

proteids; acetonuria has been noted. Phlebitis and the less common 
multiple neuritis, tetany and amaurosis are ' toxemic, (d) Metastases 
or extension by contiguity: Enlargement of Virchow's supraclavicular 
gland may result from any abdominal carcinoma, but 50 per cent, are due 
to cancer of the stomach (Troisier) ; enlargements of the para- and peri- 
umbilical glands or of the umbilicus itself (Quenu and Longuet) are 
late symptoms. Tansini remarks that the abdomen, sunken in pyloric 
stenosis, becomes distended in peritoneal diffusion. Liver deposits may 
appear before any stomach symptoms. Icterus occurs in 5 per cent. 
Schnitzler remarked metastasis in Douglas's cul-de-sac, stenosing the 
rectum but without ulceration in it; Boas rates its frequency at 25 per 
cent, (e) Ascites results from the cachexia and, like the swelling of the 
ankles, appears late in the malady. Some cases are due to carcinomatous 
peritonitis, the fluid often showing blood and cancer cells, with mitoses 
(Dock), and others result from glands or tumor compressing the porta 
hepatis. (f) Perforation may occur (a. Pathology). 

Cancer of the cardia presents symptoms like those of esophageal cancer 
(q. v.). Symptoms may be absent. The stomach is never distended. 
There may be tenderness under the xiphoid. The tumor when advanced 
may be palpated, as well as the perigastric lymph nodes. 

Diagnosis. — Diagnosis is easy in the typical case. No single finding, 
as achlorhydria or even tumor, is pathognomonic; only the grouping 
of symptoms and signs is final. Single analyses of the stomach contents 
are often deceptive; they should be repeated frequently and considered 
in connection with other findings. Vomiting in middle or advanced 
life is suspicious when accompanied by emaciation, anemia, pruritus 
and insomnia. With absence of hydrochloric acid and the ferments, 
the findings of tumor, blood, lactic acid, Oppler-Boas bacilli and dilated 
stomach are positive. The diagnosis may be doubtful, even in the presence 
of pyloric tumor, emaciation and gastric dilatation, when hydrochloric 
acid is present ; the tumor may then be due to peptic ulcer, hypertrophy 
of the pyloric musculature or pyloric spasm due to hyperchlorhydria ; 
in the last instance the tumor is alternately hard and then soft. The 
diagnosis between beginning cancer, nervous dyspepsia and atrophic 
gastritis must be reserved for a time. Atrophic gastritis is more chronic, 
often lasting years without emaciation. Youth and adolescence do not 
exclude cancer; in the young, gastric cancer is more rapid in evolution, 
and hydrops and peritonitis are more common. Abdominal atheroma 
may closely simulate cancer. Ulcer (q. v.). Early diagnosis may be 
possible when, in an ulcer cure, the patient still vomits and occult blood 
persists. Achylia and stagnation, in the fasting stomach, are particularly 
suggestive. The meiostagmin, isohemolytic and complement-deviation 
reactions may prove helpful. 

Xrray plates and fluoroscopy develop many decisive results — more 
often late than early in the disease. Holzknecht holds that residual 
bismuth after six hours with an achylia indicates cancer if the second 
bismuth meal shows a normally shaped stomach (thereby excluding 
atony) and if the first bismuth meal has reached the splenic flexure. 
Ragged edges may appear or indentations, like finger prints. Bismuth 



PLATE XVI 



Fig. 1 



Fig. 2 





Fig. 1. — Carcinoma of Body of Stomach. Rigid Patency of Pylorus. In- 
creased Motility of the Colon, Head of Bismuth Column in Six Hours 
being in the Descending Colon. Fluoroscopic examination of this ease 
shows duodenum filled with bismuth as far as the duodenojejunal angle 
within ten minutes after the ingestion of the bismuth meal. (Radiologist, 
Dr. Learning.) 

Fig. 2. — Carcinoma of the Lesser Curvature, not Involving the Pylorus. 
(Radiologist, Dr. Le Wald.) 



Fig. 3 



Fig. 4 








Carcinoma of Pyloric Half of the 
Stomach. (Radiologist, Dr. Learning.) 



Carcinoma of the Pars Media. 



(From Lockwood's Diseases of the Stomach.) 



CANCER OF THE STOMACH 525 

flowing early into the duodenum denotes pyloric insufficiency. The 
narrowing in ulcer is short, linear and sharply contoured, whereas in 
cancer it is longer, and its outlines more vague. The hook-shaped picture 
means an operable carcinoma, and the horn-shaped picture indicates 
inoperability. Gastrocolic fistula, adhesions, hour-glass deformity, 
perforation or metastases may be apparent. 

The so-called latent, dyspeptic, gastralgic, anasarcous and ascitic 
forms of cancer, and those causing early metastases (for example, in 
the liver, lungs or bones) and intestinal obstruction, show in what direc- 
tion error may occur. In some cases the general symptoms overshadow 
the local, as anemia, fever or inexplicable emaciation; in other instances, 
the local symptoms may mislead, as finding hypersecretion, or when the 
trouble begins acutely, as in one-quarter of cancer cases (Boas). 

Differentiation.— (a) Pancreatic tumors (q. v.) are deep, fixed, 
immobile and disappear on gaseous inflation of the stomach; the normal 
pancreas is sometimes palpable in meagre subjects, (b) Cancer of the 
gall-bladder has respiratory excursion but neither expiratory fixation nor 
lateral movement; the digestive symptoms, chemism and ectasia of 
gastric cancer are lacking, (c) In duodenal carcinoma the gastric chemism 
is lacking; occult blood and icterus are suggestive, (d) Cancer of the 
colon is usually distinguished by the intestinal signs and absence of 
stomach symptoms, (e) Enlarged aortic glands are distinguished by lack 
of altered chemism, and abdominal aneurysm by presence of expansile 
pulsation. (/) Omental and peritoneal tumors are more diffuse, (g) 
Foreign bodies (hair tumors), subserous lipoma, fibromyoma (62 cases 
reported), myxoma and other benign gastric tumors, and palpable round 
ulcers, are much rarer sources of error. Of sarcoma 171 cases are reported 
(Grosset, 1912); perforation occurs in 10 per cent.; 52 were successfully 
operated on. 

Prognosis. — The average duration is one year (three months to three 
years). Death results from exhaustion by pain or vomiting, hemorrhage, 
gangrene, perforation, portal pressure, intercurrent pneumonia, nephritis 
and tuberculosis. 

Treatment. — 1. Medical or Palliative. — (a) Condurango bark seems 
to increase the appetite, (b) Vomiting is treated as in gastritis, dilatation 
and ulcer, but with less success; lavage is indicated in pyloric stenosis; 
boric or salicylic acid may be added for fermentation; narcotics by 
rectum, rectal feeding, champagne and carbolic acid, as outlined before, 
are also useful, (c) Hemorrhage is rarely profuse and usually subsides 
on rectal feeding; iron, ergot and lead should be avoided, (d) Achylia 
is seldom helped by hydrochloric acid or pepsin, (e) Pain necessitates 
fomentations, lavage, chloroform (3 to 5 drops) with ice, and atropine 
or opium by rectum. (/) For constipation, cathartics are inferior to warm 
colonic flushings or salts, glycerin or olive oil by rectum, (g) Diarrhea 
is lessened by lavage; when due to pyloric insufficiency, salol, beta- 
naphtol (aa gr. x) and opiates are indicated, (h) Stenosis of the cardia 
may yield to dilatation, (i) Motor insufficiency necessitates lavage, 
which should be practised before supper, (j) The diet should be soft 
and small in bulk. Meats and fats are digested with difficulty. Vege- 



526 DISEASES OF THE STOMACH 

tables, cereals, small quantities of milk, koumyss, honey, pastries, tea, 
coffee, diluted wine, peptones and baby foods may be tolerated. 

2. Surgical Treatment. — Cases having good surgical prospects are 
few, but operation only can cure. When a tumor is found it usually 
has reached the pylorus from the lesser curvature, yet tumor does not 
contra-indicate operation (v. X-rays). For resection cases should reach 
the surgeon before the tumor is palpable, a condition possible only in 
private practice, for hospital cases are always advanced. Metastases, 
peritonitis, extreme anemia, nephritis and other visceral lesions and 
glandular invasion are contra-indications to operation. Pylorectomy 
results in an immediate mortality of under 30 per cent., half the death- 
rate in the time of Billroth, who did the first operation (1878). Recur- 
rence has been noted after five years. Leriche reports one case well after 
16, and Kocher, after 19 years. The Mayos report resections with a 
mortality of 10 per cent.; in one group of 25 cases only one case died; 
38 per cent, of their cases were living three years and 25 per cent, were 
well five years after resection. Gastrostomy in cardiac cancer and gastro- 
enterostomy in pyloric obstruction seldom prolong life. 



HEMATEMESIS. 

Definition. — Hematemesis is not synonymous with gastric hemor- 
rhage; it is the vomiting of blood, which may issue from the stomach 
or may reach it from the gums, nose, larynx, lungs, esophagus, or even 
the intestine. Gastrorrhagia designates profuse hemorrhage from the 
stomach. It may be arterial, venous or capillary. 

Etiology. — (a) Various forms of ulceration, as simple ulcer, carci- 
nomatous, tuberculous, diphtheritic, typhoid, syphilitic, uremic or 
phlegmonous ulcers, hemorrhagic erosions, and perforations into the 
stomach from without, as gall-stones, or aneurysm dissecting down 
from the arch of the aorta are etiological factors. Parrot described 
superficial ulcers in the newborn. Dieulafoy describes a pneumococcic 
hemorrhagic gastritis. Chiari, Murchison and Dieulafoy described 
small smple ulcers causing profuse, often repeated and fatal hemorrhage ; 
they dievelop in perfect health, with no previous stomach symptoms; 
they are easily overlooked at operation or autopsy because they involve 
only the mucosa or perhaps some of the muscularis. (b) Trauma, such 
as external violence, or internal trauma, as from foreign bodies, thermal 
or chemical injury, and violent vomiting, as sea-sickness and hyper- 
emesis, may be causal, (c) The cause may be vascular, such as amyloid 
degeneration which sometimes involves the stomach and bowels alone, 
aneurysm, embolism, vicarious congestion from suppressed menstruation, 
passive congestion of cardiac or hepatic origin; and esophageal varix 
(when due to cirrhosis of the liver, there is in 33 per cent, of cases no 
other evidence of cirrhosis) ; Welch and Powell found varices in the floor 
of peptic ulcers; malarial deposits in the liver; acute pylethrombosis, 
causing profuse hemorrhage; and parenchymatous oozing, where no 
postmortem changes are found (Hale White reports 36 cases of what he 



NEUROSES OF THE STOMACH 527 

terms gastrotaxis) . (d) Nervous causes are injuries to the central nervous 
system, vasomotor influences, hysteria in which the blood is small in 
amount and occurs usually in the morning vomit, tabetic crises, etc. 
(e) Acute infections may be etiological factors, as malaria, hemorrhagic 
exanthemata, yellow fever, sepsis, appendicitis and genito-urinary sepsis; 
Busse (1905) collected 96 cases following operations; they result from 
direct embolism (of which 35 per cent, were in the mesentery or omentum) 
or retrograde embolism; the hemorrhage occurred in the stomach or 
bowels; 55 per cent. died. (/) Blood diseases, as pernicious anemia, 
leukemia, hemophilia, purpura, scurvy and splenic anemia, may be 
causal, (g) Poisons, which early erode and later ulcerate, as acids and 
caustics, those causing fatty degeneration of the vessels, as arsenic and 
phosphorus, and uremia or cholemia, may cause hematemesis. 

Of all causes, round ulcer and liver cirrhosis are the first suggested. 

Symptoms. — The symptoms are (a) those of the antecedent disease, 
(b) In some cases no blood may be vomited, and the incident remains 
undiscovered, unless the stools are examined. In vomitus cruentus 
gastric uneasiness is common. The amount vomited varies from micro- 
scopic quantities to those sufficiently large to cause death. "Occult 
hemorrhage" has been particularly emphasized by Boas; the diet for days 
previously should contain no meat, blood, iron or chlorophyl, but solely 
eggs, fruit, starch or fat. In profuse gastrorrhagia the blood is bright 
red, if it remains in the stomach only a short while, as in most cases 
of peptic ulcer. In smaller hemorrhages it is black or rust-colored, as 
in cancer, uremia, cholemia and various poisonings; rust-colored blood 
may become bright on the edges or surface when it has stood for some 
time. Blood may issue in the fluid form, or as clots, in which case it is 
suggestive of valvular disease, vascular disease or the dangerous hema- 
temesis of cirrhosis; the author has seen large clots in typhoid and gastric 
carcinoma, (c) Melena may render the stools black, tarry and offensive. 
(d) Systemic signs. A gradual or sudden intense anemia may be noted, 
with the usual signs of secondary anemia (q. v.), vertigo, syncope, rapid 
pulse and some dyspnea, and later, amaurosis, slight fever, dicrotic 
pulse, hemic murmurs, moderate edema, albuminuria and sometimes 
hemiplegia or convulsions. 

Diagnosis. — Differentiation from hemoptysis (q. v.), from the swallow- 
ing of blood from the nipples in nurslings or from the vagina in the 
newborn, fracture of the skull, esophageal or throat disease and from 
simulation of blood in the stools from ingestion of bismuth, coffee, tea, 
claret, iron or blueberries, does not need particular elaboration, as the 
microscopic, chemical and spectroscopic examination determines doubt- 
ful cases. Treatment (v. Ulcer). 



NEUROSES OF THE STOMACH. 

Neuroses of the stomach occur as a part of a neurosis, as isolated 
nervous symptoms, to be considered under neurasthenia or as reflex 
affections. 



528 DISEASES OF THE STOMACH 



I. Secretory Neuroses. 

These affections have been described especially by Reichmann, Ross- 
bach, Sahli and Riegel. 

1. Hyperchlorhydria. — A qualitative anomaly of gastric secretion in 
which there is an excessive secretion of hydrochloric acid during digestion ; 
it is not solely a neurosis, though conveniently classified as such. 

Etiology. — (a) General etiological factors: (i) It is most frequent 
in youth and middle age, the better situated classes, Polish Jews and 
brain- workers ; (ii) a neurotic or psychopathic tendency is a predisposing 
factor, as is also (iii) chlorosis, (b) Local causes are (i) rapid eating, 
cold drinks and condiments; (ii) tobacco, alcohol and coffee; (iii) gall- 
stones, constipation and appendicitis. 

Symptoms. — (a) Pain, the chief symptom, varies from a sense of dis- 
comfort in mild cases to extreme gastralgia in severe cases; it is most 
marked in ulcer, pyloric stenosis and dietetic vices. It develops at the 
height of gastric digestion — i. e., one or two hours after eating — and is 
due to the excess of free hydrochloric acid; the more food, especially 
meat, ingested the later is the pain, for the food engages the free acid 
longer. Carbohydrates cause increased pain as they do not engage the 
acid and amylolysis is decreased. The patient often feels a cramping 
or spasm of the pylorus. Pain lasts one-half to several hours. It is re- 
lieved by vomiting and usually also by ingestion of more food or of alkalies. 
(b) Belching and pyrosis are frequent and the eructated hyperacid fluid 
causes a burning in the esophagus, (c) Vomiting of a burning sour fluid 
is not frequent, save in severe cases, (d) The appetite is usually good, 
and occasionally ravenous, (e) Tenderness over the stomach and gastric 
hyperesthesia are usually diffuse, moderate in degree, coincident with 
the pain and associated with some epigastric distention. (/) Stomach 
tests show a total acidity of 100, even 160; the proteids are well subdivided, 
amylolysis delayed, motility and absorption normal or increased in un- 
complicated cases and no lactic acid, no fermentation and no gas are 
present, (g) Constipation and headache are common; the gums may 
retract; the urine chlorides are decreased, the acidity lessened during 
digestion and an alkaline reaction and phosphaturia are present. 

Diagnosis. — The diagnosis is determined by hyperchlorhydria in the 
vomitus and test meal, by the relief of pain by vomiting or ingestion of 
more food or alkalies and by negative physical findings. 

Differentiation. — (a) Ulcer is marked by localized tenderness, hema- 
temesis or occult bleeding and more symptomatic regularity. (6) Gastritis 
is characterized by mucous formation and decreased secretion, (c) Gastro- 
succorrhea or continuous secretion (v. ?'.). (d) Gastrectasia and gastroptosis 
are excluded by the .r-rays. (e) In gall-stones pain has no relation to eating, 
occurs at longer, irregular intervals and is associated with tenderness 
of the gall-bladder. 

Course and Prognosis. — The disease begins slowly and may disappear, 
to recur after days to months, from irregular living, nervous strain, 
excesses, diet or without obvious cause. The nutrition is fairly well 



NEUROSES OF THE STOMACH 529 

maintained. The outlook is good if early treatment is instituted; com- 
plications modify the prognosis. 

Treatment. — 1. Prophylaxis. — Nervous factors, smoking, haste in 
eating, chlorosis, etc., should receive appropriate treatment. 

2. Diet. — (a) Proteids are most beneficial, for they take up the largest 
amount of hydrochloric acid, without increasing the HC1; veal, beefsteak, 
mutton and ham absorb twice as much hydrochloric acid as other pro- 
teids; fish fat and salt are avoided; milk and some kinds of cheese may 
be given. (6) Carbohydrates are restricted, because the early amylolytic 
digestion by the ptyalin is arrested; a slice of stale bread, biscuits, 
toast, zwieback or purees of aleuronat meal may be tried; Strauss 
allows six ounces of 2 per cent, grape-sugar solution, unless there is motor 
insufficiency. Potatoes, salads and most uncooked vegetables should 
be interdicted, (c) Fats may be given in limited quantities, including 
small amounts of cream or unsalted butter (one ounce); two drams of 
olive oil before meals inhibit the secretion of acid, (d) Condiments, 
mustard, pepper, vinegar, spices, lemon, horseradish, coffee, alcohol, 
cold foods and drinks should be forbidden. Cocoa or milk may be given. 
(e) Thorough mastication and small meals, at frequent intervals, are most 
efficacious. 

3. Medication. — (a) Sodium bicarbonate 3j\ in a starch wafer with 
but little water, at the height of digestion neutralizes the hyperchlor- 
hydria; alkalies not only act chemically but inhibit secretion by action 
on the glandular cells, (b) Extract of belladonna, i to J grain, given at 
meal-time, lessens secretion and mitigates pain; opiates should be 
avoided. Nux vomica is valuable, (c) Lavage with silver nitrate (1 to 
1000) solution is useful in obstinate types. 

2. Gastrosuccorrhea (Hypersecretion, Continuous Secretion). — This 
is a quantitative perversion of gastric secretion, in which secretion exceeds 
the needs of digestion; the lightest forms occur only when food is ingested 
(alimentary form) ; the severest occur without ingestion of food. Some 
gastric juice may be found in the normal stomach, due to secretion 
initiated by swallowed saliva or mucus, but over one ounce is rarely 
physiological, (a) The intermittent form occurs in attacks which last a 
day or two, is often called acute or nervous dyspepsia and has about 
the same etiology as hyperchlorhydria; it has been observed during 
tabetic crises. Colic-like pain develops, usually at night, followed by 
sour eructations and repeated vomiting, first of food, then of three ounces 
or more of yellowish-green fluid which contains hydrochloric acid and 
ferments; there is seldom blood. During the attack the pulse is small and 
rapid, the skin clammy, the urine scanty and alkaline, and headache 
is frequent. Thirst is great and drinking may give temporary relief, 
but is followed by increased vomiting. Between attacks the acidity 
is normal and the general health good; occasionally there is a constant 
sense of gastric discomfort, (b) The second form is continuous gastro- 
succorrhea. Its etiology in most instances is pyloric obstruction or 
pyloric spasm from ulcer, gall-bladder disease or appendicitis. 

Symptoms. — (a) Pain is more marked than in hyperchlorhydria, 
develops later after eating and very often from 11 p.m. to 2 a.m.; 
34 



530 DISEASES OF THE STOMACH 

it may occur before meals, for the gastric secretion is constant, or in 
severe cases, day and night; it is relieved by eating and vomiting, (b) 
Vomiting closely follows the pain and may occur at its height or during 
the night; the quantity of vomitus is large when there is dilatation (a 
frequent complication or a common cause of this type). It contains 
hydrochloric acid, ferments and little mucus; vomiting may be absent 
in light cases, (c) Other digestive symptoms. The tongue is often red 
and clean, sometimes coated. The teeth are often carious. The appetite 
is usually good, sometimes ravenous or in advanced cases poor. The 
marked thirst sometimes suggests diabetes. The bowels are sluggish. 
(d) The test meal and lavage show a total acidity up to 100 and free acid 
to 60. After a test dinner the fluid separates into three layers — the 
upper foamy, the middle consisting of yellowish fluid and the lower one 
of sediment of undigested carbohydrates; the proteids are found con- 
verted into peptones. When the stomach is washed out thoroughly at 
night, examination on the next morning of the fasting stomach reveals 
up to ten ounces (or even a pint) of hydrochloric acid and ferments, 
i. e., secretion without the stimulus of food; if the fasting stomach is washed 
out two or three hours later, gastric juice is again found, (e) The urine 
is the same as in hyperchlorhydria. Old cases show marked emaciation, 
even cachexia, lax muscles and dry, inelastic skin. 

Course and Prognosis. — The onset is slow and the course protracted. 
Death from exhaustion may result in untreated cases. Complications are 
frequent, especially (a) dilatation, for the stomach is never empty; the 
hydrochloric acid does not inhibit the growth of sarcina? or yeast and 
gases may generate. The dilatation is most often secondary. Dilatation 
may also result from (6) pyloric spasm; in health the pylorus relaxes 
intermittently and allows the acid chyme to reach the duodenum; the 
pylorus is reflexly contracted by the acid fluid in the duodenum until 
this is neutralized, when it again relaxes. When the secretion is con- 
tinuous, the passage of acid into the duodenum constantly contracts 
the pylorus, which may be felt as a tumor. In this case cancer may be 
simulated, especially when there is emaciation or blood in the stomach. 
(c) Tetany is a rare complication. 

Diagnosis. — The diagnostic features are pain at night, vomiting, and 
thirst, which are more common than in hyperchlorhydria; and continuous 
secretion after lavage and during fasting. 

Treatment. — Treatment is (a) that of hyperchlorhydria as to prophyl- 
axis, diet, mastication and stimulants, (b) Rectal feeding is a valuable 
accessory; water by rectum quenches the raging thirst, (c) Oral feeding 
is allowed at long intervals; overloading the stomach with fluids is 
carefully avoided, id) Lavage with silver nitrate (1 to 1000) relieves 
pain and hypersecretion, (e) Olive oil, alkalies and belladonna are indi- 
cated as in hyperchlorhydria. (/) Gastroenterostomy may be indicated 
by pyloric obstruction, never by hypersecretion per se. 

3. Hyposecretion. — Hypacidity (hypochlorhydria) and anacidity 
(achlorhydria) refer -respectively to reduction or absence of hydrochloric 
acid, which may occur from nervous or organic causes. When the 



NEUROSES OF THE STOMACH 531 

ferments and acid are absent, achylia gastrica nervosa is a more ap- 
propriate term; the condition may be transient or enduring. Suppressed 
secretion may occur in hysteria or tabetic crises. 

II. Motor Neuroses of the Stomach. 

1. Irritative Type. — (a) Hyperkinesis or hypermotility hurries the food 
into the intestine in three to five hours or less. It exists as a separate 
neurosis, or in the hasty digestion of hyperchlorhydria and in achylia, 
that the intestines may earlier digest the unaltered food. (b) Peri- 
staltic unrest or tormina ventriculi nervosa occurs particularly in neuras- 
thenia and organic pyloric stenosis. In some cases the unrest may be 
wholly subjective; in others, both neurotic and organic, the peristaltic 
movements from left to right may be seen, as well as antiperistalsis in 
the opposite direction. Treatment is that of the underlying neurosis. 
(c) Pyloric spasm occurs very seldom as an independent neurosis; it 
occurs usually in connection with ulcer, hyperacidity, hypersecretion, 
erosions, chronic stenosing gastritis, gall-stones, cancer of the stomach, 
poor mastication of food and drinking of cold fluids, (d) Spasm of the 
cardia occurs in organic disease or neuroses of the esophagus and stomach ; 
it is the cause of idiopathic dilatation of the esophagus and the spasm in 
tetanus and hydrophobia; it makes vomiting difficult. The treatment is 
causal, (e) Nervous eructation was first described by Dejardin (1814) . It 
occurs especially in sexual neuroses. The odorless ructus results from swal- 
lowing of air (aerophagia), which constitutes a most intractable habit. 
Bouveret thinks air is forced down by pharyngeal contractions, either un- 
consciously or during false eructations, in which the patient, in attempting 
to raise gas, swallows air; such large quantities could never generate in the 
stomach; Bardet estimated that one patient raised twenty quarts in 
an afternoon. Coincident cardiac and pyloric spasm causes distention 
(pneumatosis) . Treatment lies in the use of the sound, suggestive therapy, 
the difficult task of breaking the habit and asafetida which renders the 
ructus offensive. (/) Nervous vomiting occurs (i) only in the neuroses, 
as neurasthenia, migraine and exophthalmic goitre ; but under this caption 
we may bring for differential purposes (ii) cerebrospinal conditions, as 
compression of the brain, meningitis, tumor, tabes, etc., or toxic con- 
ditions, as uremia or cholemia. (iii) Most cases are reflex from the nose, 
as from disagreeable odors; the respiratory tract; pelvic or abdominal 
conditions, as pregnancy, menstruation, calculi, etc. The symptoms 
may present many incompatible elements; thus the patient may vomit 
without nausea, almost without effort like an eructation; it often occurs 
without pain or reference to the fulness or emptiness of the stomach; 
even though it is frequent, the nutrition may be remarkably good, the 
tongue clean and the appetite good. Periodic or cyclic vomiting, described 
by Gruere (1838), has some resemblance to tabetic crises; Edsall con- 
siders it an acidosis, for which 3$s-ij of sodium bicarbonate is indicated. 
In the 10 fatal cases on record there was fatty degeneration of the liver 
and sometimes appendicitis. 



532 DISEASES OF THE STOMACH 

Robert's conclusions are as follows: 

1. Vomiting of a chronic type, following a gradual epigastralgia, from 
one-half to three hours after eating, is attributable to ulcer. 

2. Chronic vomiting, soon after food ingestion is stenosis of the cardia, 
nervous abnormality, cerebral lesion or acute gastritis. 

3. Copious vomiting ten or more hours after eating indicates mus- 
cular insufficiency; frequent repetition indicates stenosis. 

4. Vomiting in the night occurs in cholelithiasis, hypersecretion, 
muscular insufficiency and nervous abnormality. 

5. Vomiting attempts when the stomach is empty indicate a cause 
other than gastric, e. g., reflex cause, toxemic, cerebral or nervous. 

6. Morning nausea and retching indicate pregnancy, alcoholism, 
pharyngitis, nephritis or a nervous abnormality. 

7. Periodic vomiting of clear gastric juice in considerable amounts 
indicates a secretory neurosis or ulcer. 

8. Vomiting as a sequel of headache, accompanied by severe nausea, 
but no gastric symptoms, characterizes migraine. 

9. Sudden vomiting with tinnitus, deafness and vertigo is attributable 
to disturbances of pressure in the internal or middle ear. 

10. Periodic sudden vomiting, with gastric pain and nausea, retraction 
of the abdomen, obstinate constipation during, but not preceding, the 
attack and freedom from abdominal tenderness are suggestive of the 
spinal crises, nervous vomiting and lead colic. 

11. Periodic attacks of vomiting with colic, constipation and tympany 
suggest chronic intestinal stenosis. 

2. Depressive Motor Neuroses (Lessened Motility). — There are 
three types: (a) Atony, which has been considered under dilatation; 
(b) pyloric insufficiency, which is seldom a neurotic condition, as compared 
with its frequency in cancer, ulcer and duodenal obstruction; inflating 
the stomach with carbon dioxide, it rapidly passes into the intestine with 
a gurgling gush, (c) Insufficiency of the cardia causes regurgitation of 
food and fluid; rumination (merycismus) is regurgitation in which the 
food is again chewed and reswallowed. These are generally involuntary 
processes, but some neurotic males, psychopaths or idiots can regurgitate 
at will. The affection is hereditary or imitative. Its mechanism is 
congenital weakness of the cardia, stimulation of the vagus or aspira- 
tion into the esophagus by the inspiratory act. It should be treated 
by giving small meals at frequent intervals; suggestive measures are 
indicated. 

III. Sensory Neuroses of the Stomach. 

1. Hyperesthesia. — A sensation of burning or weight usually occurs 
when the stomach is full, but at times also when it is empty. Carbo- 
hydrates, fats or spices may induce the condition. Silver nitrate, gr. 
| to J, or phenol, gr. \ to j, given on the empty stomach, often affords 
relief. 

2. Gastralgia. — Gastralgia (or cardialgia, a poor but widely used 
term) does not strictly include the pain of ulcer, hyperacidity or hyper- 
secretion. An etiological classification is as follows: (i) Cerebrospinal 



NEUROSES OF THE STOMACH 533 

causes, including various brain, cord (tabes), peripheral and functional 
nervous affections, (ii) Constitutional causes, including chlorosis and 
debility, (hi) Toxic causes (gout, nicotine and constipation), (iv) 
Reflex causes, from the genito-urinary and alimentary tracts, splanch- 
noptosis, uterine or ovarian disease or masturbation. Fliess holds that 
dysmenorrhea and gastralgia may arise from disease of the lower nasal 
turbinates. Most cases occur in women between fifteen and forty-five 
years of age. 

Symptoms. — Severe gastric pain begins suddenly, often at night, lasts 
for a few minutes to an hour or so and subsides, usually to recur after 
a variable interval. The pain may radiate widely. It bears no relation 
to eating. Diffuse superficial hyperesthesia over the stomach is not 
infrequent, but deeper pressure usually affords some relief. Vomiting, 
hiccough, hunger, headache, depression, polyuria, clammy sweats, rapid 
pulse or even collapse may attend the seizure. 

Diagnosis. — A diagnosis is made only by exclusion and usually after 
the seizure. Rheumatic myalgia is more constant. A tabetic crisis is 
at once recognized by the Argyll-Robertson pupil and the absent knee- 
jerks. Intercostal neuralgia gives Valleix's three tender points. In 
ulcer or circumscribed peritonitis the pain is associated with localized 
tenderness. Hyperacidity and hypersecretion should be excluded. A 
sharp thrust over the gall-bladder during deep inspiration nearly always 
elicits well-localized tenderness in biliary colic. 

Treatment. — Treatment is (a) etiological — neurasthenia, anemia or 
constipation. Fowler's solution Tflij before meals is excellent. (6) The 
attack. Morphine hypodermically affords the only certain immediate 
relief, but in these very cases may establish the habit. If given, it should 
be exhibited by mouth without the patient's knowledge. Heat and 
sinapisms may relieve or aggravate the attack. Silver, phenol, gelsemium, 
belladonna and Hoffmann's anodyne often give relief. 

3. Disturbances in the Sense of Hunger and Appetite. — Loss of 
appetite (anorexia) may be nervous, though more commonly gastric, 
tuberculous or toxic. Anorexia nervosa may be absolute and cause 
profound emaciation. Parorexia is a perversion, in which the patient 
craves for unusual foods. In polyphagia the appetite is enormous, 
but is capable of satiation; in boulimia (hyperorexia) the polyphagia 
is paroxysmal, sometimes with vertigo, palpitation, etc.; they are 
most frequent in hyperchlorhydria, hypersecretion and hypermotility, 
but also occur in diabetes, brain disease, intestinal parasites or 
from quinine, orexin or even opium. Acoria is loss of the sense of 
satiation. These anomalies probably result from changes in the bulbar 
hunger centre. 

IV. Mixed Neuroses of the Stomach. 

Dyspepsia nervosa or pseudodyspepsia may occur as a species of 
local neurosis, as a reflex from other organs, but much oftener a part of 
the neurasthenic symptom-complex. Leube's contention that digestion 
itself is normal must be modified, as the hydrochloric acid may be in- 
creased, normal or decreased, but perhaps in the majority of cases the 



534 Diseases of the intestines 

gastric functions are nearly normal. Two main groups of symptoms 
prevail: (a) the centric, neurasthenic or hysteric apathy, irritability and 
vertigo; (6) the gastric eructations, variations in appetite, oppression 
and diffuse tenderness, which are probably also cerebral in origin. The 
symptoms vary greatly in degree, often change their form with rapidity 
and the general nutrition is good. Organic disease must be carefully 
excluded by repeated examinations of the secretions and motility of the 
stomach. The treatment is rest, correction of worry and strain, self- 
control and suggestion. 



DISEASES OF THE INTESTINES. 

ACUTE ENTERITIS. 

It is difficult to draw a close distinction betweeu acute catarrhal 
enteritis, intestinal dyspepsia and simple diarrhea. Catarrhal enteritis 
is the most common intestinal disease. 

Etiology. — 1. Primary Forms. — (a) Errors in diet and ingestion of 
spoiled food containing ptomaines, unripe fruit and impure water are 
common causes, (b) Disturbance in intestinal secretion possibly occasions 
acute enteritis, (c) Cold, trauma, foreign bodies, fecal retention and 
toxins eliminated from the blood may initiate inflammation, (d) Some 
cases are infectious. Bacteria are an important factor; one-third of the 
weight of the normal stool is caused by bacteria, of which 48 species are 
normally present; inflammation may arise from pathogenic organisms or 
virulence attained by some inhabitant of the intestine, e. g., the Bac. coli 
and Gartner's Bacillus enteritidis. In a milk diet the Bacterium lactis 
aerogenes and in a meat diet the Proteus vulgaris may be possible factors. 

2. Symptomatic Forms. — (a) Enteritis is constant in some infections, 
as in typhoid; it is frequent in others, as in sepsis or influenza; and rare 
in others, as in measles, scarlatina, etc. (b) General diseases, as nephritis; 
burns; intestinal parasites, ulcers or tumors; and metallic or other poisons 
are etiological factors; (J) stasis is rarely by itself a potent cause. 

Pathology. — Redness, swelling, increased mucus secretion, parenchy- 
matous degeneration and interstitial infiltration, in the few cases coming 
to autopsy, may not be conspicuous, as they regress after death. Folli- 
cular swelling or even ulceration, ecchymoses, erosions or swelling of the 
mesenteric glands may be observed. 

Symptoms. — The chief symptom is diarrhea, due to increased peri- 
stalsis, secretion or exudation. The stools number two to fifteen daily 
and contain mucus; they are brownish-yellow and moderately frequent, 
or colorless, odorless and alkaline or neutral, and very frequent; they 
contain triple phosphates, calcium phosphate and oxalate crystals, 
sometimes cholesterin, Charcot-Leyden crystals, and few leuko- 
cytes. Thirst, colic pains, borborygmus, visible peristalsis, tympany 
and gurgling are frequent. Febrile forms with acute splenic tumor are 
recorded, which may at first resemble typhoid. Albuminuria, cylindruria 



Acute enteritis 535 

or even acute nephritis may develop exceptionally; the urine is scanty 
in proportion to the amount of fluid lost by the bowel; indican, ethereal 
sulphates and acetone may be present. In some few cases, gastritis, 
herpes or muscle and joint pains occur. Collapse is rare in adults, though 
there may be a close resemblance to cholera. In the vast majority of 
cases convalescence is established in a few days. 

Diagnosis. — (a) Duodenitis can seldom be diagnosticated, though sug- 
gested by pain, tenderness over the duodenum and catarrhal icterus. 
(b) Jejunoileitis seldom exists alone; diarrhea is absent if the colon is 
not affected ; the stools contain intimately mixed mucus, as small hyaline 
globules under the microscope, (c) In enterocolitis the bile is decomposed 
below the small intestine; when it is present in the stools it signifies 
increased peristalsis which moves the bile along before it can be disin- 
tegrated and indicates acute enterocolitis; bile may be found only in the 
globules of mucus. Many undigested food particles (lientery) are rather 
significant if fever, biliary or pancreatic obstruction and gastric atrophy 
are excluded; they consist of undigested meat, starch granules (which 
are more significant than muscle fibers) and fat particles, (d) Colitis 
is characterized by the absence of bile and lientery, by thin stools and 
by more or less mucus, obtained especially on washing out the bowel 
immediately after a movement, (e) Proctitis is marked by tenesmus, 
dysuria, evacuation of mucus alone and bloody mucus covering but not 
mixed with the solid stools; it is also diagnosticated by digital or procto- 
scopic examination. 

Treatment. — (a) In the early stage evacuation of the causal irritant 
indicates fractional doses of calomel, followed by castor oil; stronger 
evacuants irritate or inflame the intestine. Colonic flushings with pure 
water or injections of olive oil may be added, (b) Absolute rest in bed is 
always indicated, (c) The diet should be restricted to barley-water, or 
no food should be given for a day or two. (d) Heat is applied to the 
abdomen, (e) A dram each of paregoric and bismuth should be given 
after each bowel movement until the number is controlled. 

If bismuth is given in large amounts, the subcarbonate is preferable 
(v. page 518). 

!fy — Phenylis salicylates (salol) gr. xx 3J 

Sodii bicarbonatis 5ss 3J 

Cretse preparatse 5ss 5iss 

Bismuthi subnitratis 5J SJ 

M. et divide in pulveres x. For child; adult. 

S. — One powder in milk or thin arrow-root solution every three hours. 

Lack of tone is relieved by gambir (catechu), colic by belladonna 
and flatulency by ammonia and ginger: 

1$ — Tincturse gambir compositae 5J 

Fluidextracti belladonna? gtt. xij 

Spiritus ammonia? aromatici * . . 3ii 

Syrupi zingiberis 5ss 

Misturse cretse q. s. ad. §iv 

M. et S. — A tablespoonful every two or three hours. 

Betanaphtol gr. x p. c. in capsules, or tannigen gr. xv every three hours, 
are seldom indicated. (/) No laxatives are given for the resulting con- 



536 DISEASES OF THE INTESTINES 

stipation. (g) Opium suppositories relieve tenesmus (see Dysentery). 
(h) The diet may be increased in a few days to bouillon with raw egg, 
hashed beef or chicken, toast, zwieback, roast beef and milk; fruits 
and vegetables even when cooked should be given with caution, because 
recurrence predisposes to chronic enteritis, (i) Cramps, collapse, etc., 
are treated as in cholera (q. v.). 

CHRONIC ENTERITIS. 

Etiology and Pathology. — The etiology is that of acute enteritis, from 
repeated attacks of which the chronic type may develop. 

Chronic enteritis suggests a causative chronic gastritis, achylia gastrica 
and other gastric conditions; or intestinal catarrh may cause anorexia, 
eructations or abdominal distention. Hyperchlorhydria may disturb 
the intestines by the escape into them of more acid than they can neutral- 
ize, and hypo- or achlorhydria initiates bowel trouble because hydro- 
chloric acid bears an important relation to the intestinal and pancreatic 
secretions. 

The pylorus remains closed until the food in the stomach is ready 
for the intestinal juices and then it relaxes; the hydrochloric acid, 
reaching the duodenum, provokes a flow of bile (which arrests the action 
of the pepsin), and of the pancreatic secretion (which neutralizes the 
hydrochloric acid) by acting upon the duodenal mucosa, which gives 
off into the blood "secretin"; secretin acting upon the pancreas causes 
it to secrete; then the pylorus again relaxes. When the pancreatic juice 
is poured out it contains no active proteolytic ferment, but in the succus 
entericus there is an activating ferment (enterokinase) which converts 
trypsinogen into trypsin. The bile activates the fat-splitting pancreatic 
ferment. 

In chronic enteritis the mucous membrane is brownish-red or slate-gray 
and often thickened and the muscular is is sometimes hypertrophied. 
Polypoid hyperplasia, cystic degeneration, atrophic changes, catarrhal 
erosions and follicular ulcers may occur. 

Symptoms. — Constipation is more frequent than diarrhea; in some 
cases a single, soft, morning evacuation is noted, or perhaps several; in 
others constipation is broken occasionally by short attacks of colic and 
diarrhea; continuous diarrhea indicates inflammation of both the large 
and small gut. Constipation is due to alteration of the nerve fibers 
or inflammation in the muscular coat. Abdominal tension or colic is 
distinguished from gastric discomfort and pyloric spasm in that it occurs 
independently of eating. Diarrhea results from decomposition and fecal 
irritation. There may be pain, flatulency, borborygmus or occasionally 
tenderness over the bowels, but the sole diagnostic criterion is the presence 
of mucus; its intimate mixture with the stool indicates inflammation in 
the small gut; coating of the passages with mucus indicates colitis, 
and evacuations of mucopus alone, proctitis. Mucus globules when 
bile-stained indicate inflammation of the small gut, as do shreds of 
bile-stained mucus. Pus cells are rare except in proctitis. Mucus is 
always indicative of enteritis and never occurs from ulceration or carcinoma 



CHRONIC ENTERITIS 537 

alone (a slight coating of mucus over hard feces is not significant.) Blood 
always indicates a complication, such as piles, ulceration or cancer. The 
stools may contain much undigested meat, starch or fat. 

The functional examination of the feces does not give us as exact 
information as does the examination of the stomach contents. Schmidt's 
test diet includes 3 pints of milk, 3 ounces of zwieback, two eggs, 1.6 
ounces of butter, one-quarter pound of rare, tender steak, 6 ounces of 
boiled potatoes, 2 ounces of oatmeal and two-thirds ounce of sugar, 
distributed among the three meals. With the first meal a capsule of 
five grains of charcoal or carmine is given and the first examination is 
not made until the stools become colored black or red. In this way (i) 
the " period of passage" is established, the normal time being ten to twenty 
hours, (ii) Mucus, microscopically, appears as translucent, sago-like 
and often bile-stained flakes, which must not be confused with starch 
particles, (iii) Much connective tissue, recognized by its yellowish-white 
color and its toughness, indicates reduction of the hydrochloric acid. 
(iv) Muscle fibers, appearing as reddish threads or lumps, may indicate 
achylia gastrica, lack of trypsin, lack of the activating enterokinase or 
very active peristalsis, (v) Free starch granules indicate intestinal catarrh ; 
normally only starch enveloped in cellulose is present, (vi) The normal 
stools shows hydrobilirubin, detected by mixing fluid feces with an 
equal amount of a 5 per cent, solution of bichloride of mercury, which 
mixture turns yellowish-red after twenty-four hours; bilirubin, recognized 
by a green color in the above test, indicates catarrh of the small bowel 
(except in young children) . (vii) The fermentation test is made by mixing 
a dram of the feces with sterile water in a bottle which is connected 
above with a tube containing water; almost no gas results in normal 
cases; an acid reaction with fermentation is due to carbohydrate fer- 
mentation; if it becomes alkaline and foul in odor it is due to proteid 
fermentation, (viii) With experience, it can be readily determined 
whether the fat is increased. 

Nutrition is maintained in some cases; in others pallor, emaciation, 
slow pulse and cold extremities may be noted. Attacks of diarrhea and 
lientery suggest achylia gastrica. 

Prognosis. — Save in either extreme of age it is good as to life, but is 
doubtful at any age as to complete recovery. Improvement is tardy 
and often transient. Intestinal atrophy may develop, though less fre- 
quently than in puerile forms. 

Treatment. — (a) An hygienic conduct of life is most essential. A 
flannel band should be worn over the abdomen. (6) The diet must be 
carefully supervised; salads, alcohol, fruits and vegetables of every 
description, either raw, or cooked, sweets, pickles and acids are among 
the forbidden foods; eggs, fresh butter, lean meats, stale bread, rusks, 
thoroughly cooked rice or sago and potato puree are permissible; i. e., 
simple foods, in small amounts and at frequent intervals, controlled by 
frequent examination of the feces, (c) For constipation, often due to 
the careful diet, purgatives are avoided and the bowels moved by enemata 
of olive oil. For diarrhea, bismuth in dram doses and tannigen are most 
efficacious (see Acute Enteritis). Calcium carbonate and salicylate 



538 DISEASES OF THE INTESTINES 

are recommended (aa 5ss to a quart of charged water; one-half glass 
q. i. d.). Schmidt employs 10 per cent, hydrogen peroxide in agar, (d) 
Flatulency. As flatus results from stagnation plus catarrh, the indications 
are restriction of foods which ferment (v. s.) and the administration of 
aromatic remedies (see page 535). 

1$ — Mentholis .... . 3ss 

Phenylis salicylatis 5iij 

Extracti belladonna? gr. iv 

M. et fac capsulas xx. 

S. — One after meals. 

(e) Colitis (see Treatment of Dysentery). 

ENTERITIS (COLITIS) MUCOSA OR MEMBRANACEA. 

This disease was described by Mason Good (1825) and Da Costa 
(1871). The name implies inflammation, but most cases are neither 
enteritis nor colitis. Nothnagel named the non-inflammatory variety 
colica mucosa, which is a secretory neurosis. 

Etiology. — (a) Eighty to 90 per cent, occur in young, nervous women, 
40 per cent, of whom have uterine troubles; few cases are seen in nervous 
men or children. (6) Nearly all patients suffer from chronic constipation. 
Its pathology is unknown; in some autopsies no anatomical alteration is 
noted, in others that of enteritis. 

Symptoms. — (a) Mucous casts of the bowel, shreds or lumps are voided 
periodically ; the mucus may resemble a huge diphtheritic cast, is usually 
evacuated in large amounts, which often constitutes the entire bowel 
movement and contains very few leukocytes or other signs of inflamma- 
tion, (b) There is usually in the attack colic or pain and tenderness 
over the splenic flexure of the colon, sometimes diffuse and occasionally 
radiating into the leg. If the mucus firmly adheres to the bowel wall 
the pain is particularly severe and obstruction of the bowels may be 
simulated. Tenesmus in voiding the mucus is usual, as are formation 
of gas and increase of the original nervous symptoms, as palpitation, 
tremor or vertigo. There may also be coincident diarrhea, achylia 
gastrica and a periodic sand formation, (c) Constipation, distention 
and anorexia exist between the paroxysms, which last a day or even a 
week and are separated by weeks or months. It is said that death may 
occur during an attack. 

Treatment. — (a) The less the fundamental neurotic symptoms are in 
evidence the better are the results of therapy; education, the rest cure 
and other measures outlined under hysteria and neurasthenia are indi- 
cated, (b) Constipation (v. i.) is treated dietetically — Graham bread, 
leguminous vegetables, including the husks, vegetables with much 
cellulose (which seems to be the most important element) — fruits with 
small seeds and thick skins, as gooseberries, currants or grapes, large 
amounts of cream, butter and bacon, and olive oil. Von Noorden's 
results with this diet are: 79 per cent, partially or permanently cured, 
16 per cent, unknown result and 5 per cent, failure, (c) Local measures 
include colonic flushings with normal salt solution, or half a pint of 



INTESTINAL ULCERATION 539 

olive oil left in the rectum over night (Kussmaul) . (d) Narcotics, purga- 
tives, irrigation with alum, tannin and silver solutions, and operations 
are distinctly contra-indicated. The morphine habit may be readily con- 
tracted. Belladonna suppositories are very efficient for the pain. The 
patient in an attack is kept in bed and heat is applied to the abdomen. 

DIPHTHERITIC, CROUPOUS AND PHLEGMONOUS ENTERITIS. 

Klebs-Loeffler diphtheria is very rarely encountered, and practically 
all membranous enteritis is diphtheroid (v. page 78). 

Phlegmonous or purulent enteritis is extremely rare and chiefly of 
anatomical interest. Most cases develop in the duodenum. It may be 
primary, but more often is secondary to intestinal ulceration, carcinoma 
or intussusception. In a form due to the colon bacillus, multiple purulent 
foci are found in the intestinal wall, which frequently cause perforation. 

INTESTINAL ULCERATION. 

Ulceration in acute infections, as typhoid, dysentery, sepsis, diph- 
theria, etc., and chronic ulcers, 'as syphilitic, tuberculous and actinomy- 
cotic, are considered under General Infections. Rarely ulceration has 
been observed from favus and mucor corymbifer. Inflammatory ulcers 
as the catarrhal and follicular, usually occur in the colon; they may be 
simple or so-called dysenteric (q. v.) ; they are seen in enteritis, infantile 
diarrheas, etc. Stercoral (decubital) ulcers develop from the pressure of 
hard feces or foreign bodies, in the dilated pouches of the colon or above 
an intestinal stenosis. Constitutional affections, as leukemia, scurvy 
and amyloidosis, uremia and mercurial and arsenical poisoning are 
occasionally causes. 

Symptoms. — The symptoms are rarely distinctive without suggestive 
etiological factors; most ulcerations occur without symptoms or with 
ambiguous symptoms, (a) Diarrhea is frequent, particularly in ulcera- 
tion of the large gut; it is often absent with lesions of the small gut or 
upper colon; it results from decreased absorption and increased peris- 
talsis, due to exposure of the intestinal nerves. (6) Blood in the stools 
is mixed with them in lesions of the small gut, sometimes covers them 
in lesions of the large gut and is voided independently of the feces in 
rectal lesions. It is more often dark and tarry, especially in tuberculosis, 
than bright, except in low-situated lesions and in some profuse typhoid, 
dysenteric or duodenal hemorrhages. Blood is common in other diseases 
than ulceration, as in cancer, piles, stasis and blood diseases, (c) Pus 
is seen more frequently in colonic than in ileac ulceration; it is common 
in cancer, proctitis and croupous enteritis. Pure pus is rather indicative 
of rupture of extra-intestinal pockets into the intestine, as appendicitic 
and salpingitic abscesses, (d) Mucus indicates enteritis only, which may 
complicate ulceration, (e) Shreds of tissue are very rare, save in dysentery. 
(/) Local symptoms are ambiguous, as tenderness, pain and tympanites. 
(g) General symptoms depend on the basic disease ; fever is most frequent 
in cancerous, dysenteric or tuberculous ulcers, (h) Rupture causes 



540 DISEASES OF THE INTESTINES 

peritonitic adhesions, diffuse peritonitis, retroperitoneal cellulitis or 
subphrenic pyopneumothorax, (i) The x-ray may show total absence of 
a shadow where the ulcers lie or else a fine marbled appearance. 

Treatment. — Treatment is that of enteritis or colitis. In chronic 
ulcerative colitis colostomy may result favorably. 



INTESTINAL DISORDERS IN INFANTS. 

Etiology. — Classification of the etiological factors is difficult because 
of the numerous species of bacteria in the intestine and the impossibility 
of drawing any absolute line between chemical and bacterial factors 
and between functional and organic changes. Most cases occur in 
children between six and eighteen months old, in the summer months, 
July especially, in the poorer classes and in infants not fed at the 
breast, for two main reasons: cow's milk is prone to disturb digestion 
and there is a greater chance for bacterial infection. Toxins may form 
in milk, when it is long in transit, particularly in hot weather. The 
Bacterium lactis aerogenes causes inflammation in the small and the 
Bacterium coli in the large intestine; the proteus, pyocyaneus, gas bacil- 
lus, various saprophytes, and Bacillus dysenterise are also factors, but 
their relative importance is not clearly defined; the Streptococcus enter- 
itis can hardly be considered as a distinct type. The distinction between 
intoxication and infection is maintained with difficulty; intoxication 
causes symptoms as erythema, hemorrhagic diathesis, anemia, nervous 
disturbances and dyspnea; and infection produces complications, as 
lobular pneumonia, nephritis, phlegmon, arthritis, purulent pleurisy 
and necroses in the liver. In institutional epidemics infection may be 
carried from one individual to another by fecal contaminations. Insects 
may convey infection. 

Symptoms. — 1. The acute dyspeptic or fermental form cannot be sharply 
distinguished from other severer forms, though possibly caused by the 
same microorganisms. The pathological findings are often remarkably 
insignificant. The temperature usually rises suddenly to 103° or 104°, 
remains high for a few days and falls suddenly. The tongue is dry, the 
face red, the pulse rapid and the breathing sometimes dyspneic. There 
is restlessness — sometimes initial convulsions — anorexia and vomiting. 
The stools in infants are normally yellow from bilirubin, thick and slightly 
acid in reaction; they become green from bacterial action or reduction 
of the bilirubin into biliverdin, react alkaline from albuminous decom- 
position or acid from acid fermentation and become thin and offensive; 
the evacuations number six to ten daily. The microscopic findings are 
those of acute enteritis in adults, as mucus, leukocytes, triple phosphates 
in the alkaline stools or cholesterin in the acid stools; blood in any quan- 
tity is uncommon. Involvement of the small intestine is attended by 
gas, cramping, large movements, and tenderness. Marked nervous 
symptoms, extensive edema and emaciation may result. Albuminuria 
and cylindruria occur in 20 per cent. Recovery is usual and prompt 
after thorough intestinal evacuation. 



INTESTINAL DISORDERS IN INFANTS 



541 



2. Cholera infantum occurs in severe infections, usually in children 
already suffering from some intestinal disorder; it constitutes 2 per cent, 
of summer diarrheas. The bowel movements are copious, alkaline and 
flocculous; though at first they contain food and are perhaps offensive, 
they become watery and odorless. Both the stools and the general 
clinical aspect resemble the picture of cholera Asiatica and cholera nostras 
(q. v.). Though there is fever, the extremities are algid and cyanotic, the 
pulse small, the heart tones weak and all symptoms of collapse are present; 
there are the pinched pallid fades cholerica, the thirst and the incoercible 
vomiting. The skin is rigid, as though the fatty tissue had hardened 
{scleredema or sclerema adiposum), and nephritis is almost invariable. 
These symptoms result from loss of great quantities of fluid by purging 
and vomiting, and from intoxication which produces the convulsions, 
irregular and Cheyne-Stokes's breathing, retraction of the neck, stupor 
and other symptoms, termed the " hydrencephalic state." Oestreich 
holds that hypostasis, resulting from compression of the lungs by the 
tympany, causes more deaths than does the toxemia. 

3. Acute enterocolitis (ileocolitis) may follow the dyspeptic form or 
the various specific infections in children, or may begin as an indepen- 
dent form. Pathologically it includes types which cannot be separated 
clinically, as simple enterocolitis, follicular ulceration and diphtheroid 
enteritis. In Rotch's cases of infantile diarrhea the Bacillus dysenterise 
was found in 16 per cent., sometimes in the dyspeptic type, but most 
often in the ileocolitic type (78 per cent.). In one collection of 412 cases 
Shiga's bacillus was found in 63 per cent.; Geo. Weaver never found it, 
though the Flexner-H arris type occurred in 25 per cent. (v. Bacillary 
Dysentery) . 

The symptoms resemble those of dysentery in the adult. The stools 
are small, yellow, green or brown and very frequent. Rotch tabulates • 
the differential features as follows: 



Acute fermental diarrhea. 


Acute ileocolitis. 


(a) 


Small intestine, mostly. 




Large intestine, mostly. 


(6) 


10 to 12 discharges; often large. 




10, 15 to 50 discharges, usually small. 


(c) 


No or little blood. 




Blood and sometimes shreds of tissue or 
membrane. 


H) 


Mucus. 




Mucus. 


(e) 


No tenesmus. 




Tenesmus. 


(/) 


Not much abdominal tenderness 
pain. 


and 


Abdominal tenderness and pain. 


is) 


No or slight lesions. 




Lesions marked. 


(h) 


Tempeiature high — 104° F. for one or 


Temperature may be high at first (103° F. 




two days, and then falling sharply by 


to 104° F.) but usually soon moderates 




crisis. 




(99° to 101° F.) and falls gradually by 




- 




lysis to normal after some weeks. 



The severity of the symptoms varies greatly; the catarrhal form may 
cause mild symptoms or result in death, with or without gastric symp- 
toms. The ulcerative and diphtheroid types are less often attended by 
vomiting, but run a fatal course of days or weeks. 



542 DISEASES OF THE INTESTINES 

4. Chronic dyspeptic disturbances often occur with gastric dilatation. 
The onset is gradual or it may directly follow the acute forms. The 
stools are green or gray, contain mucus, gas, sometimes pus and tissue 
shreds. Food and fluid are poorly absorbed; undigested food particles 
and fatty stools are observed; mucus is not common in marked cases 
of intestinal atrophy. Vomiting is rather frequent. There is usually 
little general disturbance, no fever and little or no colic. In some cases 
the emaciation may become extreme (pediatrophy, athrepsia), the 
muscles becoming weak, the voice faint, the eyes lustreless, the face of 
the "Voltaire type," and the abdomen distended. Death results from 
marasmus or intercurrent infections. 

Preventive Treatment. — Children should, if possible, be taken to the 
country in the hot months. Excessive swaddling is to be avoided. 

Diet. — (a) If the mother cannot nurse her child, a wet-nurse should 
be procured, as few stomach and bowel diseases occur in breast-fed 
infants. The wet-nurse must be carefully examined for syphilis and 
tuberculosis. The milk from the breast should spurt freely in several 
streams. A weak child may become dyspeptic even at the breast; 
calomel irritates but magnesium carbonate gives the most rapid relief; 
other children thrive, even when the stools are green. Sometimes colic 
and dyspepsia in the child are due to menstruation, beginning preg- 
nancy, excitement, lack of exercise or alcoholic indulgence in the nurse 
or mother. If a wet-nurse cannot be obtained, (6) cow's milk or some 
prepared food must be used, but most of the latter are objectionable 
because their carbohydrates are not dextrinized. Cow's milk differs 
from human milk in many details; its contamination is far more likely, 
whence the importance of pure milk and sterilized nipples and bottles. 
Human milk contains about 1 per cent, of proteids, 4 per cent, fats and 
7 per cent, of milk-sugar, but in cow's milk the percentages are respec- 
tively about 3.5, 3.5 and 5 per cent.; in cow's milk the casein constitutes 
80 per cent, of the proteids, which are physically and chemically different 
and contain more whey proteid and more of certain relatively uninves- 
tigated substances. In cow's milk the ferments and fats are different 
and the mineral salts, especially phosphates, are increased, which impede 
digestion. The first objection is the high percentage of proteid (casein), 
which must be predigested or the milk diluted. Simple dilution, however, 
necessitates giving too much water or reducing the fat and milk-sugar. 
In substitute feeding, the proteid of coivs milk must be reduced, fat added 
in the form of cream, and milk-sugar added to attain the normal percen- 
tage. The milk may be diluted with thin oatmeal-water, as a diastase 
ferment is present earlier and in larger amounts than previously admitted, 
though nature doubtless has her designs in withholding starches from 
mother's milk. Low dilutions should be given at first and gradually 
increased, regarding digestion and nutrition, as determined by regular 
weighing. Sterilization of milk destroys ferments and protective sub- 
stances. 

Treatment of Acute Dyspepsia. — (a) The stomach is tvashed out, if 
toxic symptoms are marked, with plain water or a 1 to 3000 resorcinol 
solution. (b) Calomel gr. J and magnesium carbonate gr. j every three 



INTESTINAL DISORDERS IN INFANTS 543 

hours for three doses, or one dose of castor oil (5ss-j) are usually 
administered, but cathartics congest or even erode the mucosa, (c) 
The bowel should be flushed with one pint of warm water, (d) Food 
should be ivithheld for two days, and plenty of boiled water should be 
given. Albumen-water (the whites of two eggs beaten in a pint of water) 
may then be given, and thin arrow-root-water, beef -juice and peptonized 
milk, may gradually be administered until the green color of the stools 
changes to a normal yellowish-brown. In one type, fat is not assimilated; 
the fatty acids, uniting with alkali, form soapy stools and withdrawing 
alkali, lead to alkali-penia and acidosis. In another type, starch is the 
injurious factor and in another, there is sugar-injury, as in gas-bacillus 
infections. The dysentery bacillus works least injury with lactose 
administration, which minimizes the nitrogenous waste (Kendall). 
Milk proteid seems the least injurious, particularly if the whey is removed 
from skimmed milk, (e) Other medication is usually superfluous. Lesage 
recommends lactic acid for alkaline green stools, 5 j of a 2 per cent, 
solution (p. a). Resorcinol J grain and dilute hydrochloric acid TTLv 
may be given after meals. 

Treatment of Enteritis. — If the case is seen early the stomach is washed 
out and feeding suspended as outlined above. The child should have 
plenty of boiled water and cool applications to the skin are indicated 
unless the extremities are blue and cool. Tannigen may be given, 10 
grains, several times daily, even in the very young. As in enteritis of 
adults, bismuth subnitrate, 3ss, bismuth salicylate, J to 1 grain and if 
these are ineffective, opium may be administered. (See page 269 for 
dosage.) 

Treatment of Cholera Infantum. — Lavage is ineffective, unless it is done 
in the earliest stages. There are three main indications: (a) fluid must 
be restored to the tissues, by subcutaneous saline transfusions which 
support the heart, fill the vessels, stimulate the kidneys and eliminate 
the toxins; 2.5 per cent, dextrose infusions are valuable; (b) cardiac 
stimulation, by hypodermics of strychnine and camphor and local heat; 
champagne quiets vomiting and supports the heart; brandy and whisky 
are given as in bronchopneumonia (q. v.), though perhaps alcohol further 
injures the intestinal epithelium; and (c) secretion must be checked by 
paregoric every four hours, small enemas of starch and laudanum or, 
which is more effectual, morphine. (See page 269.) In the fortunate 
cases which rally, nourishment is resumed only with the greatest 
caution. 

The Treatment of Colitis. — This is like that of dysentery and includes 
the measures above indicated, flushings with salt solution, 1 per cent, 
tannin or 1 to 1000 salicylic acid. 

The Treatment of Chronic Dyspepsia. — Treatment in institutional cases 
begins with nursing; one wet-nurse can nurse several children. Gastric 
lavage with two ounces of plain water, normal salt or 1 per cent. Carlsbad 
salts solution, increases functional activity. The extract of mix vomica 
stimulates secretion. Food is given in the smallest amounts compatible 
with maintenance of weight and energy. 



544 DISEASES OF THE INTESTINES 



APPENDICITIS. 



Definition. — Appendicitis, the chief abdominal malady, is an inflam- 
mation of the vermiform appendix. 

History. — Fitz in 1886 drew attention to the subject and coined the 
name, and Willard Parker first (1867) advocated operation. Appen- 
dicitis was previously confused with typhlitis, inflammation of the 
cecum; the term "perityphlitis" should be discarded. Our knowledge 
is largely due to the work of American surgeons. 

Etiology. — 1. Predisposing Factors. — (a) The appendix, a function- 
less vestige of the cecum, is inherently less resistant. (b) Its lumen 
is smallest at its cecal end, which favors retention of foreign bodies, pro- 
motes microbic growth and decreases or suspends drainage into the 
bowel, (c) The meso-appendix, which conveys the blood to the appendix, 
is shorter than the appendix, which therefore curls; the blood supply is 
easily altered by appendiceal edema and infiltration. (d) Foreign 
bodies and fecal concretions may produce erosions which apparently 
promote microbic access and therefore inflammation; Aschoff combats 
this view. J. F. Mitchell found foreign bodies in 7 per cent, of 1400 
cases of appendicitis and Louis J. Mitchell in 1600 autopsies, 1 per cent.; 
they include seeds, capsules, gall-stones, pins, nails, shot, fish-bones, 
etc. (e) Age. — Over 50 per cent, occur under twenty years of age and 
30 per cent, between twenty and thirty. It is rare in infancy and with 
advancing years obliteration and atrophy lessen its frequency. (/) 
Sex. There is a slight preponderance in males. 

2. Bacteriology. — The colon bacillus is found in 80 per cent, of cases, 
though probably in some of them it has overgrown another causal 
organism. Next is the staphylococcus, the virulent streptococcus, then 
the pneumococcus, proteus and pyocyaneus. In symbiosis with these 
organisms, or possibly operating without them as in gangrene, the 
anaerobes (gas bacillus, fusiform bacilli and anaerobe streptococcus) 
are factors in the necrosis, peritonitis and toxemia. Less frequently 
the typhoid, tubercle, influenza or actinomycosis organism is found; of 
the last 150 cases exist; Fenwick, in 1120 tuberculous ulcerations in the 
bowel, found but 0.8 per cent, in the appendix. 

Symptomatology and Pathology. — 1. The Early Clinical Course.— 
The onset is precipitate and characterized by four main symptoms, (a) 
Sudden, severe abdominal pain, the intensity of which ranges between 
colic and agony, is due to acute retention within the appendix caused 
by the occlusion of the cecal end. It is felt over the right lower abdomi- 
nal quadrant or over the pit of the stomach, and may even radiate along 
the genitocrural nerve to the testis, which is sometimes retracted. Reach- 
ing its greatest severity in a few hours, the pain persists until the pressure 
of the pus is relieved by drainage into the bowel, perforation or gangrene. 
Sudden relief from pain often indicates gangrene, (b) Nausea and' 
vomiting result reflexly from occlusion and follow within a few hours 
after the pain, (c) Abdominal tenderness is general at first and is often 
associated with a cutaneous hyperesthesia, which covers like half a 
girdle the right lower abdomen from the spine to the mid-line. The 



APPENDICITIS 



545 



right rectus muscle resists palpation, which explains most cases of early 
apparent tumor. A little later the general tenderness disappears, leaving 
well-localized tenderness over the appendix; McBurney's point is in the 
right lower quadrant of the abdomen (about two inches from the anterior 
superior iliac spine in a line drawn between it and the navel) or a little 



Fig. 38 



Fig. 42 




Fig. 39 





Fig. 40 



Fig. 43 




Fig. 45 




Figs. 38 and 39. — Obliterating appendicitis. Fig. 40. — Obliterating appendicitis, with 
distal enlargement. Fig. 41. — Obliterating appendicitis (at R), with calculi (C). Fig. 42. 
— Appendicitis with bending, obliteration and. distal distention. Fig. 43. — Appendicitis 
with curling around its mesentery. Fig. 44. — Strangulation by a band. Fig. 45. — Calcu- 
lous obstruction. (Dieulafoy.) 

below it in adults or above it in children ; less frequently the tender point 
may be found near the loin, pelvis (5 per cent.), bladder, rectum or 
uterus on rectal or vaginal examination, gall-bladder or very exceptionally 
on the left side of the abdomen or in hernial sacs, all of which correspond 
to possible variations in appendicular location. Pressure with the hand 
on the left half of the abdomen causes pain in the right side when the 
35 



546 DISEASES OF THE INTESTINES 

pressure is relieved. Palpation must be made gently, lest rupture occur. 
(d) Fever generally develops in a few hours to a day, according to the 
severity of the infection, rarely with a chill, reaching 101°-102°, or higher 
in some virulent types or in children. It signifies septic absorption and 
may cease suddenly in gangrene or gradually in rupture and may slowly 
recur from extension; abscess or peritonitis may coexist with low tem- 
perature. The pulse usually follows the temperature curve, though the 
author has seen it remain normal in cases of early gangrene. The leuko- 
cytosis parallels the fever, and often measures the sepsis; no reliance 
can be placed on its absence as an assuring sign nor on its presence as 
an indication for operation; extremely high counts (over 100,000) are 
ominous; counts of 900 or 600 are reported. The urine is often febrile, 
scanty and usually contains indican and sometimes albumin or even 
blood; dysuria may result from appendicitis in the pelvis; renal colic 
may be closely simulated. Profuse bowel hemorrhage is recorded. 
Constipation is usual. In Dieulafoy's toxemic type toxemia may obscure 
the local symptoms. 

2. The Later Clinical Course. — (a) The inflammation subsides 
gradually by drainage into the cecum. Though the inflammation may 
be circumscribed, the appendix rarely returns to normal; it suffers 
necrosis and ulceration which leave the appendix infiltrated, thickened, 
and more or less constricted at some point or the lumen is obliterated. 
The mucous membrane may be wholly substituted by granulation tissue. 
Occlusion at its intestinal end causes a cyst-like swelling as large as the 
thumb or even as a sausage. Adhesions to the abdominal wall and gut 
are common, (b) After a few days a localized peritonitic abscess fre- 
quently forms, usually over the psoas muscle at the angle between the 
ileum and cecum, but occasionally in some unusual localization of the 
appendix (v. s.), from perforation, generally near its mesenteric attach- 
ment, from necrosis or gangrene; when the abscess is well demarked, 
the pain, fever and pulse-rate decrease. A well-defined tumor may develop, 
over which no peristalsis occurs; dulness or tympany is elicited according 
to the depth of the tumor or its fluid or gaseous contents; fluctuation 
is present only in large abscesses; in infections due to the colon bacillus 
the tumor is more largely infiltration than pus. In the incised abscess 
the green or black and totally gangrenous appendix usually may be 
seen. The abscess may form without any symptoms other than those 
of the onset. The result of the abscess varies greatly : (i) it may rupture 
into the intestine which forms its wall (2 per cent.), and possibly carry 
the appendix with it; (ii) it may rupture into the urinary tract, of which 
cases nearly one-half are fatal; (iii) it may cause purulent thrombophlebitis, 
and any manifestations of septicopyemia, as secondary fever, suppurative 
pylephlebitis, pulmonary embolism, liver abscess, or subphrenic abscess; 
(iv) it may rupture into the retroperitoneal tissue, followed by high 
temperature; and all possible extensions may occur, as into the groin, 
scrotum, pelvis, pararenal tissue, pleura (84 per cent, are right-sided), 
lung, gluteal region, back, hip-joint, etc.; and (v) it may rupture into 
the free peritoneal cavity, (c) The third cardinal issue is diffuse septic 
peritonitis; its unfortunate and unmistakable symptoms are a sudden 



APPENDICITIS 547 

fall of temperature followed by a secondary fever, diffuse replacing 
localized tenderness and rigidity, leukocytosis, persistent projectile 
vomiting, rapid pulse, Hippocratic facies and collapse from profound 
intoxication. It most often follows the localized abscess, but may occur 
directly after a gangrene which is so sudden as to allow of no protective 
adhesions, or after perforation from a foreign body in the appendix. 
Variations, due to the type of infecting organism are as follows: (i) 
The staphylococcic peritonitis generally produces but little pus, or, if 
any, a seropurulent fluid; plastic lymph prevents absorption for a short 
time, but, as the peritoneum becomes abraded, leads to intoxication, 
collapse and diarrhea, (ii) The streptococcic form produces no pus, 
but causes a granular, blistered, dry peritonitis, rapid pulse, delirium 
and tympany, (iii) Colon infection produces an abundant, creamy, 
thick, offensive pus and slowly causes death after great depression, 
delirium and low arterial pressure. 

3. Remote Sequences. — Intestinal strangulation by adhesions and 
from chronic changes in the appendix reflex disturbances may result. 

In children the onset is very abrupt, the vomiting repeated, pain greater, 
the appendix more palpable and diarrhea and diffuse peritonitis more 
common than in adults, because the omentum is less able to envelop 
the appendix. In aged persons gangrene is more frequent. 

Diagnosis. — The diagnosis depends on the four cardinal symptoms of 
onset, followed by leukocytosis and other secondary developments. 
If all these symptoms are considered separately an analysis is necessary 
of every abdominal lesion causing pain alone, vomiting alone, tempera- 
ture, sensitiveness, abscess, tumor, disease in the right lower abdominal 
quadrant, perforation or peritonitis. 

Pain occurs in gall-stones, renal calculi, tabetic crises, internal incar- 
cerated hernias, epigastric hernia, intussusception, gastric or duodenal 
ulcer, tuberculous peritonitis, stone or torsion of the ureter, Dietl's 
crisis in floating kidney, uremia, colica mucosa, acute pancreatitis, the 
crises of angioneurotic edema, herpes zoster, pelvic peritonitis, ruptured 
extra-uterine pregnancy, twisted pedicles, pyosalpinx, dysmenorrhea 
and the reflected pain of vertebral disease, pleurisy and pneumonia. 
Fever in typhoid precedes the local symptoms. These affections, as well 
as gravitating abscesses, infected urachus, lesions of the abdominal wall, 
cancer, hysteria and hypochondriacal fear of appendicitis, are almost 
invariably excluded by the sequence of symptoms and careful general 
examination. Appendicitis, chronic ab initio, causes flatulency, constipa- 
tion alternating with diarrhea and a dragging discomfort in the right 
lower abdomen; appendicitis may cause hypersecretion, hyperchlor- 
hydria, gastralgia, epigastric tenderness or pain (also experienced there 
when pressure is made upon the appendix) and pylorospasm (v. page 
515). Confusion is possible with a mobile cecum. 

Prognosis. — The prognosis is most uncertain, because (a) there is no 
safe criterion for early diagnosis of the type; (b) the symptoms and 
signs are not proportionate to the actual lesions, 'e. g., light cases clini- 
cally may prove to be the most severe anatomically; (c) apparent 
improvement is often to the experienced observer the onset of alarming 



548 ' DISEASES OF THE INTESTINES 

complications; Dieulafoy well calls them " treacherous lulls" (accal- 
mies traitresses); (d) recovery is seldom complete anatomically, whence 
chronic, relapsing or residual appendicitis occurs in a more severe form 
in a full third of the cases. 

Treatment. — Cases may recover, temporarily (70 to 80 per cent.), 
but it is impossible to predict which ones will do so. After testing and 
seeing tested the so-called medical treatment, consisting of rest, starva- 
tion, laxatives and other placebos, and seeing gangrene, peritonitis with 
low temperature and death occur in "mild" cases, the conviction was 
inevitable that appendicitis is always surgical, regardless of type, time or 
tendencies. A surgeon at once should be associated with the practitioner. 
Recovery under medical treatment is due to good fortune alone. The 
so-called indications for operation are too often signs of irreparable 
damage. Early operation within one or two days of onset is attended 
by the least danger. Many operators dislike to operate between the 
second and eighth days or other arbitrary limits, but this position implies 
that the clinician can diagnosticate the anatomical changes which are 
present; gangrene, thrombophlebitis, imminent rupture, etc., cannot 
be excluded; in this period simple drainage is indicated — possibly, too, 
appendicectomy, if the appendix obtrudes in the field of incision; lavage, 
exploration and protracted operation are dangerous. In later cases, when 
there is apparent regression, treatment may be more conservative; com- 
plete demarkation may be waited for, but even in such cases thrombo- 
phlebitis or rupture into the general peritoneum may intervene. In 
diffuse peritonitis incision and simple drainage are indicated. The patient 
is placed in the semisitting posture (Fowler) and given constant normal 
salt enemas (Murphy). Many cases recover (see Pekitonitis) . (e) 
After the attack. After one attack of appendicitis the patient is prone 
to recurrence. In cases in which there was only incision and drainage 
of the abscess the attacks recur. Adhesions, flexions and stenoses favor 
a recurrence and digestive disturbances. 

INTESTINAL OBSTRUCTION. 

Etiology. — Obstruction arises from: 

I. Intussusception (Invagination). — In this most frequent form of 
acute obstruction (40 per cent.), the external part (the intussuscipiens 
or vagina) receives into it the intestine just above (the intussusceptum 
or invaginatum) . It develops in perfect health, in various acute and 
chronic affections, tumors, strictures of the gut, diarrhea and contusion. 
Two theories are advanced: (a) that the gut is spastically contracted 
and enters the gut below, and (b) that the gut below is paretic. The 
author saw, with Dr. Walls, a case in lead colic. In acute intussusception 
Wiggin found 50 per cent, in the fourth, fifth and sixth months of life, 
when the long mesentery of fetal life persists. In chronic intussuscep- 
tion 50 per cent, occur between twenty and forty years of age and 66 
per cent, in males. Pathologically only the vital form is of clinical impor- 
tance, in which the mesentery and its vessels are also invaginated; the 
"agonal" form occurs during the death agony, chiefly in children, in 



INTESTINAL OBSTRUCTION 549 

the small gut, is often multiple and does not involve the mesentery. 
The vital form is usually single, descending (in 99 per cent.) and com- 
plete; incomplete forms may result from polyps or other tumors, usually 
benign, which drag down the gut. There are three main forms : (a) 
the enteric, the small gut invaginating into the small gut, 30 per cent.; 
(6) the ileocecal, the small gut entering the large gut, 52 per cent.; and 
(c) the colonic, the large gut invaginating into the large gut (18 per 
cent.) or rectum; in rare cases Meckel's diverticulum may invaginate 
into the small gut. 

Symptoms. — (a) There is sudden, severe, reflex pain, which is usually 
umbilical in children but sometimes occurs elsewhere in adults, is con- 
tinuous or in chronic forms of intussusception, paroxysmal, (b) Early 
reflex vomiting may occur, in children, though in adults it is less frequent 
than in Other forms of obstruction; the later vomiting is fecal in 13 per 
cent.; vomiting is more marked in high than in low invagination and 
depends considerably on the degree of mesenteric invagination (vascular 
disturbance) . (c) The stools are 'characteristic, showing blood and mucus 
in 97 per cent, of acute and in 50 per cent, of chronic cases; the move- 
ments may not stop at once but only after several evacuations, and 
severe tenesmus (50 per cent.), (d) A sausage- or egg-like movable firm 
tumor (55 per cent.) may be palpated, most often over the ascending or 
transverse colon, sometimes by the rectum or vagina, and is occasionally 
visible at the anus, where it has been mistaken for prolapse or polyp, and 
extirpated. It is most common in children, in the ileocecal form, and 
nearly always to be felt during paroxysms of pain, (e) Meteorism and 
a depression in the right flank are infrequent. 

Clubbe's description is excellent: "The very sudden onset in a pre- 
viously healthy baby is a peculiarity of intussusception. The child is 
seized suddenly, screams, turns pale, vomits and in a short time seems to 
recover itself, only to cry again at intervals as if in pain. Soon after the 
first scream it may pass a normal motion. In from two to ten hours, in 
97 per cent, of cases, blood will be passed by rectum. The mass, which 
varies much in size and position, can nearly always be made out by careful 
palpation when the child is under an anesthetic. The child may not 
look ill, its pulse-rate may be hardly raised and its temperature may 
be normal." 

Issues. — Peritonitis results in 50 per cent, of acute and in nearly 100 
per cent, of chronic cases; perforation occurs in chronic (15 per cent.) 
more often than in acute cases; sloughing off of the gangrenous bowel 
occurs in 42 per cent, of adult cases, but seldom in children; in Cruveil- 
hier's case three yards of dead gut were discharged. Spontaneous reposi- 
tion and fistula are very uncommon. 

II. Strangulation. — This causes 35 per cent, of intestinal obstructions. 
Its mechanisms are innumerable; it is generally due to bands or isolated 
peritonitic adhesions; Meckel's diverticulum, the remains of the omphalo- 
mesenteric duct, which lies within a yard of the ileocecal valve and is 
sometimes continuous as a cord to the navel, caused strangulation in 
183 cases (Hilgenreiner, 1902); omental strands under which the gut 
is caught; holding of the gut in abnormal positions; and binding of coils 



550 DISEASES OF THE INTESTINES 

to each other. Incarceration may occur in congenital or acquired orifices 
and clefts in the omentum or mesentery or under the suspensory ligament 
of the liver, lig. teres or lig. latum uteri. Hernias include strangulations 
in the femoral, inguinal, umbilical locations or in the less frequent types, 
as the obturator, sciatic, lumbar, intersigmoid, retrocecal, foramen of 
Winslow, duodenojejunal (Treitz's retroperitoneal form) or diaphrag- 
matic. Seventy per cent, of cases occur in males, 40 per cent, between 
fifteen and thirty years of age, 90 per cent, in the small intestine, 67 per 
cent, in the right iliac fossa and 83 per cent, in the lower abdomen (Fitz). 

Symptoms. — The symptoms are urgent, (a) Early reflex vomiting, 
from shock, voiding in succession gastric contents, bile and fecal matter 
which usually consists of yellow, brown or black fluid, or very rarely solid 
feces, is strongly indicative of organic strangulation and lasts from the 
beginning to the end of the disease, (b) There is early severe reflex 
pain, which is greatest at the navel and lasts until collapse, peritonitis 
or paralysis of the gut develops, (c) Collapse, with Hippocratic expres- 
sion, weak pulse and hurried breathing, results reflexly and may occur 
early from the disturbed local circulation in the gut or later from peri- 
tonitis, (d) Complete, sadden stoppage of the boivels may result, in which 
no feces or flatus can pass; some feces from the lower gut may pass 
with enemata, but no gas. Meteorism of two kinds occurs: (i) the 
static variety in which gas accumulates above the obstruction and (ii) 
the local variety, in which the strangulated loop becomes distended, 
because its circulation is impaired; it may be seen or felt as an immovable, 
tense mass, showing no peristalsis and corresponding to the thick, edema- 
tous, hemorrhagically infiltrated and finally gangrenous gut. (e) The 
urine is decreased because of the vomiting and collapse; it contains 
indican if the obstruction lies in the small gut. Sometimes casts, albumin 
or nephritis are observed. (/) Strangulation sometimes may be found in 
the usual hernia locations. 

Diaphragmatic hernia is left-sided in 88 per cent., is congenital or 
acquired (from trauma especially) and is recognized in but 3 per cent, of 
the reported cases; it closely resembles pneumothorax (q. v.). The 
axray differentiates. 

In obstruction the mucosa in the occluded area may become ulcerated, 
easily penetrated by bacteria and hemorrhagically infarcted, leading to 
necrosis, perforation and peritonitis. 

III. Volvulus and Knots. — Volvulus is a twisting of the intestine 
around its mesenteric axis; twisting of the gut on itself is rare; volvulus 
occurs in 14 per cent, of obstructions (Fitz); 68 per cent, of the cases 
are males, usually between forty and sixty years old; it occurs in the 
sigmoid flexure in 66 per cent., less frequently in the cecum, colon ascen- 
dens, small gut and stomach. Predisposing causes are a vegetable diet, 
constipation, a long sigmoid flexure with a long, narrow mesentery, and 
mesenteritis. The twist may occur through 180 to 360 degrees or more. 

Symptoms. — The symptoms closely resemble those of the forms 
described, especially when knots form between coils of the small intestine. 
In volvulus of the sigmoid there is pain and vomiting, which are less marked 
than in strangulation or invagination and emesis is seldom fecal; the local 



INTESTINAL OBSTRUCTION 551 

meteor ism is more pronounced than in any other type of obstruction, for 
the huge coil of obstructed gut passes upward, in extreme cases pushes 
up the diaphragm to the third or fourth rib and seldom exhibits peris- 
talsis, since its circulation is disturbed. But little water can be injected 
into the rectum. Hemorrhagic peritoneal exudate is common. 

IV. Strictures. — Enterostenosis more often causes chronic than acute 
obstruction, (a) Congenital stricture is even rarer than congenital 
atresia, of which Helmholz collected 199 cases in the small bowel, (b) 
Cicatricial stricture results from healing of tuberculous, syphilitic, dysen- 
teric, duodenal and very rarely typhoid ulcers. Arbuson collated 129 
cases of tuberculous stricture, (c) Annular cancer, (d) compression by 
tumors (80 per cent, of which are pelvic) and (e) traction are other 
causes. (/) Inflammatory hypertrophy of the mucosa and muscularis is 
exceedingly uncommon. 

Symptoms. — The symptoms of chronic obstruction vary with the 
location of the stenosis. (1) Stenosis of the small intestine may occur 
(a) above the duodenal papilla, as a result of gall-stones or duodenal 
ulcer and closely resembles pyloric stenosis; (6) stenosis in the duodenum 
below the papilla results from gall-bladder adhesions, ulcer, tumors or 
pancreatic disease; icterus is frequent, as well as vomiting of bile and 
pancreatic juice which digests starch and fibrin in an alkaline medium; 
other symptoms are dilatation of the stomach, pale stools, very slight 
abdominal meteorism, except over the epigastrium, and the absence of 
indicanuria. (c) Jejuno-ileac stricture may result from healed ulcers, 
inflammation in replaced hernias and adhesions to the internal genitalia; 
the ulcer stricture may be multiple, twelve being recorded in one case; 
extreme stenosis may cause no symptoms. There is constipation, which 
sometimes alternates with diarrhea, colic, meteorism and visible pal- 
pable peristalsis, causing "intestinal stiffness" until the obstruction is 
finally overcome by the hypertrophied muscle above the stricture, when 
a gurgling sound is sometimes heard. The colon is collapsed. (2) 
Stricture of the large gut is marked by constipation, which is significant 
in a person not previously constipated or when cathartics have no effect 
in chronic constipation; by colicky pain, even more than in stricture of 
the small gut, because the stools are harder; eventually by nausea and 
vomiting, which are successively gastric, bilious and stercoraceous; -by 
meteorism along the colon and in the lumbar region behind, which is 
normally dull; by increased, even tetanic, peristalsis above the stricture, 
which possesses a localizing value; and by the ribbon-like or sheep-stools, 
which also occur in tumors, colica mucosa and constipation. Fluoroscopic 
results are often invaluable. 

V. Tumors. — (See page 553.) 

VI. Foreign Bodies. — Foreign bodies caused obstruction in 12 per 
cent, of Fitz's series, (a) Gall-stones — of which 250 obstruction cases 
are on record — lodge in the duodenum or lower ileum, ulcerating through 
the gall-bladder into the duodenum or less often the colon, or compres- 
sing the duodenum through a dilated pouch of the cystic duct. In but 50 
per cent, is there a history of colic or of icterus. Collapse is usually not 
marked, a tumor is seldom felt and the constipation is often only rela- 



552 DISEASES OF THE INTESTINES 

tive or alternates with diarrhea. (6) Fecal masses constitute the chief 
obstruction of the large gut, especially in the sigmoid. The writer saw 
absolute obstruction develop after a Thanksgiving dinner; there was 
fecal vomiting, collapse and a mass of hard food, measuring two inches 
in diameter, (c) Enteroliths form slowly of phosphates, sometimes of 
bismuth, chalk, iron or magnesia, usually with an organic nucleus. 
They measure one to nine inches in diameter and one enterolith weighed 
four pounds. Most common in the large intestine, they may develop 
in diverticula of the small intestine, (d) Hair tumors, twisted masses 
of ascarides, fruit seeds, oatmeal husks, stones and foreign bodies (in 
insane subjects) are possible causes. 

VII. Dynamic Heus. — Under dynamic ileus (paralytic or spastic ob- 
struction) may be included obstruction following mesenteric embolism, 
trauma, abdominal operations or inflammation in an undescended tes- 
ticle; it is largely associated with acute peritonitis. Spasmodic obstruc- 
tion may develop in gall-stone occlusion,* ulceration, hysteria and intes- 
tinal crises of tabes; it rarely produces fecal vomiting. 

Diagnosis of Intestinal Obstruction. — 1. Of the Fact of Obstruction. 
— The symptoms are generally unmistakable and consist of constipation, 
cessation of flatus, local distention, compensatory peristalsis and fre- 
quently collapse. The hernial sites, rectum and vagina must be carefully 
examined. 

2. Of the Location. — The uncertainties are manifold: 

Obstruction of the Small. vs. Of the Large Intestine. 

General Condition. — Earlier and more pro- Later and less impressed, 
foundly impressed. 

Symptoms more marked, more stormy onset, Signs more marked, as meteorism, less water 

more vomiting, more pain. Fluoroscopic can be injected, more peristaltic effort and 

tests. palpable rigid coils, more results by rectal 

or vaginal examination, more tenesmus. 

Indicanuria. — Earlier and marked. Develops later or not at all. 

Urine. — Much decreased. Little decreased. 

3. Of its Nature. — (a) It is practically impossible to recognize 
obstruction by bands, adhesions, Meckel's diverticulum, clefts and 
internal hernias (except diaphragmatic), (b) Invagination is not only 
the most frequent but also most characteristic in its clinical picture. 

(c) Strangulation is differentiated by its greater and earlier collapse, 
pain and vomiting, local meteorism and hemorrhagic peritoneal effusion. 

(d) Volvulus is suggested by advanced age, constipation, slower course, 
infrequent fecal vomiting and meteorism, which is greater than in any 
other form and is accompanied by little peristalsis. The small amount 
of fluid which can be injected, the hemorrhagic peritoneal fluid, tenesmus 
and slightness, lateness or absence of indicanuria are also suggestive. 

(e) In some instances of gall-stones, the lack of shock, of increased pulse 
and of meteorism, and the paradoxical intermittent release of flatus and 
feces, fecal vomiting, combined with the passage of flatus and feces, may 
be suggestive. 

4. Differentiation.— Flatulent colic, gall- or kidney-stones and incar- 
ceration of the kidney, uterus or testis are excluded by rapid stoppage 



INTESTINAL TUMORS 553 

of the bowels. Acute pancreatitis must be considered. Peritonitis 
is characterized by early fever, tenderness, meteorism, cessation of 
peristalsis, abdominal rigidity, fluid in the peritoneum and late collapse, 
fecal vomiting, later and less complete obstruction. 

Treatment. — In stenosis, typified by ulcer cicatrices, a concentrated 
fluid or semifluid diet is given and thorough mastication of solid food 
and avoidance of food chaff, skins, stone or gristle should be insisted on. 
Cathartics are inferior to enemata of oil. 

Thiosinamin, recommended to dissolve cicatricial stenosis, is given in 
10-drop doses, every other day, hypodermically (1 to 6 of alcohol). 

Operative measures may be instituted for foreign bodies or malignancy; 
the outlook is best in lesions of the colon and ileum. 

1. Medical Treatment of Obstruction. — In every case the physi- 
cian at once should divide responsibility with a surgeon. In acute cases 
food causes aggravation. Early gastric lavage affords transitory relief. 
Chronic fecal obstruction should be eliminated by colonic flushings, given 
with the body inverted; hard, desiccated feces must be dug out with 
the finger, with enemata to bring away fragments. High enemata, 
colonic inflation with air, laxatives, massage and puncture of the gut 
with an exploring needle, are always contra-indicated. Opium is useful 
only in the early stage to relieve shock. Stimulants are frequently 
indicated. Atropine, eserine and physostigmine sometimes help. 

2. Operative Treatment. — Medical treatment of strangulation, 
intussusception or volvulus is of little value. A most convincing statis- 
tical argument for early operation is Naunyn's series of 288 cases, in which 
75 per cent, of recoveries were obtained by operation in the first two 
days, while each successive day lowered the patient's chances to 40 
per cent., 30 per cent., etc. In 1074 recent cases, Wiltner reports recovery 
in 53 per cent. In 100 cases of intussusception in children 63 per cent. 
of operated recoveries are reported by Clubbe; 40 per cent, of adults 
and 80 per cent, of children die under medical treatment. Fifty-two 
per cent, of obstruction by gall-stones recover under expectant and 33 
per cent, under surgical treatment. 

INTESTINAL TUMORS. 

Carcinoma, the only neoplasm of clinical importance, constitutes 22 
per cent, of all cancers. Previous ulceration is predisposing. It is most 
frequent in males over forty years of age; 17 per cent, occur between 
thirty and forty ,and 14 per cent, under thirty years of age. 

Pathology. — According to Leube, 80 per cent, occur in the rectum, 15 
per cent, in the ceoum and colon and 5 per cent, in the small intestine. 
Hausmann, in 268 cancers of the bowel (excluding the rectum), found 
91 per cent, in the large and 9 per cent, in the small bowel; if figured 
more in detail, 37 per cent, occur in the sigmoid, 18 per cent, in the 
cecum, 11 in the descending colon, 9 in the transverse and 8 per cent, 
in the ascending colon, 8 per cent, in the ileum, 4 in the splenic and 3 in 
the hepatic flexure and 2 per cent, in the jejunum. The sigmoid, splenic 
and hepatic flexures are especially predisposed, probably because more 



554 DISEASES OF THE INTESTINES 

fixed and exposed to irritation. It is usually primary, sometimes second- 
ary by contiguity, but very rarely metastatic. Originating in the 
intestinal glands, it is usually annular in form and causes stenosis and 
ultimate occlusion of the bowel; it is less often nodular and very rarely 
diffuse and flat. Histologically it may be an adenocarcinoma (especially 
in the duodenum), scirrhus (in the sigmoid), medullary, cylindrical- 
celled (in the cecum and sigmoid), colloid or flat-celled (in the rectum). 
Beginning in the mucosa, early involvement of the other coats and lymph 
vessels is followed by later involvement of the peritoneum and metas- 
tasis, especially in the liver. McWilliams finds in the literature 105 
appendiceal cancers, but many reports are indecisive. 

Symptoms. — 1. Disturbance of the Intestinal Function. — (a) 
There is usually constipation, resulting from narrowing of the intestinal 
lumen; it is most marked in tumors of the large intestine. Ulceration 
frequently causes diarrhea. (6) The stools are irregular and band-like 
or sheep-like, to which, however, undue importance has been attached. 
(c) Blood, mucus and pus are common in the feces, though equally 
frequent in other ulcerations and in enteritis. The evacuations may be 
stinking, (d) Fragments of tissue are uncommon and are diagnostic 
only when showing carcinomatous arrangement of the cells, (e) Pain, 
due to enterostenosis, is usual; it may be sacral when due to sigmoid 
cancer. (/) Sudden complete occlusion of the bowel may follow previous 
gradual narrowing of the lumen, (g) The lower the tumor in the intes- 
tinal tract the greater is the tympany and fecal retention and the purer 
the pus and blood (i. e., the less mixed with the feces). Above the stric- 
ture the bowel is dilated and its muscle is hypertrophied (visible peris- 
talsis), (h) Bismuth, given by mouth and by rectum may localize the 
digitated markings of the stenosis in axray plates. 

2. Cachexia and marasmus are most suggestive. 

3. Tumor. — A tumor is best felt if the bowel is empty; it may be 
confused with a normal contracted colon, the edge of the ileopsoas or 
with fecal masses; it is irregularly oval in clear cases; annular forms 
escape detection, for they merely constrict the bowel. It is usually 
tender and is movable or immovable accordingly as the bowel involved 
is naturally free or fixed, or is adherent to other structures by adhesions 
or extension by contiguity. Whether free or fixed, the tumor is generally 
below the navel. Gas and fluid are sometimes felt or heard to escape 
through the stenotic point and distention of the large bowel by introduc- 
tion of air or fluid per rectum may aid in localization. If the tumor grows 
from movable gut it may disappear and reappear from time to time. 
A rectal and vaginal examination always should be made. 

4. Complications. — The malignancy of primarily ambiguous symp- 
toms may be declared by (a) icterus, especially in duodenal cancer; (b) 
hemorrhage from the bowels; (c) rupture into the bladder or vagina 
or into the stomach, with fecal vomiting and diarrhea from partially 
digested food entering the colon. 

Diagnosis. — Diagnosis is often difficult, except in rectal localization, 
for many symptoms indicate stenosis without declaring its nature. 
Differentiation is required from: 



ENTEROPTOSIS 555 

1. Movable Tumors. — (a) These may be pyloric, requiring differ- 
entiation from duodenal cancers, (b) The corset liver, movable spleen 
and kidney, (c) Omental and mesenteric tumors produce less entero- 
stenosis. (d) Scybala may coexist with malignancy. 

2. Immovable Tumors 1 . — (a) Renal and retroperitoneal tumors lie 
beyond the colon, on its inflation, and rarely cause the same degree of 
obstruction, (b) Encapsulated peritoneal exudate; the author has seen 
chronic appendicitic abscesses in individuals over sixty years of age 
diagnosticated as tumor, (c) Ovarian or uterine tumors are less obstruc- 
tive, (d) Localized inflammatory infiltration of the intestinal wall and 
circumscribed inflammation of the sigmoid flexure and colon. 

Rectal cancer demands special consideration. It is usually annular and 
when developed is rigid, frequently resembles an inverted funnel, becom- 
ing narrow upward. The colloid form extends upward and downward, 
is often tubular and causes much regional invasion. Digital or procto- 
scopic examination — unaccountably neglected more often than any 
other simple method of physical examination — saves many lamentable 
errors. The early stricture may yield when ulceration develops, with 
discharge of blood, often ichorous pus and sometimes malignant tissue. 
Tenesmus, piles, morning diarrhea, sacral pain, and abdominal pain 
before and during the movement are common. Cachexia usually 
develops with great rapidity; death may result from acute obstruction 
with preservation of color, nutrition and energy. Intoxication symptoms, 
as stupor, are frequent. 

Syphilitic strictures are slower and subject to greater variations; 
tuberculous ulcers are flatter, softer and more undermined. 

Sarcoma, of which Corner and Fairbanks collected 175 cases involving 
the small bowel, is more rapid and seldom stenoses the lumen. Hells- 
trom found 45 lipomata and Stetten 74 myomata recorded. 

Prognosis. — Marasmus, coma, anasarca, thrombosis, secondary infec- 
tions, stenosis or perforation causes death. 

Treatment. — Treatment is that of enterostenosis, in regard to diet. 
Opium must be used toward the end. Operation, either palliative 
enterostomy, colostomy or curative enterectomy, may be indicated. 
Hochenegg (1902) in 194 radical operations, reports a mortality of but 
12 per cent, and estimates his recoveries at 16 per cent. 

ENTEROPTOSIS. 

Enteroptosis is not a disease, but only a condition in which the 
abdominal viscera prolapse in the abdomen, as the stomach (gastrop- 
tosis), intestine (enteroptosis), colon (coloptosis) or solid viscera (splanch- 
noptosis), as the liver, kidney or spleen. The condition, first described 
by Morgagni, is known as Glenard's disease. Whatever causes relaxa- 
tion of the abdominal wall or of the intra-abdominal suspensory struct- 
ures may induce prolapse, as trauma, coughing, loss of weight, pregnancy, 
tumors of the liver, spleen or kidney, spinal deformity and corsets. 
Seventy-five per cent, of the cases occur in women. Stiller maintains 
that splanchnoptosis is a congenital asthenic condition whose most 



556 DISEASES OF THE INTESTINES 

frequent stigmata are a floating tenth rib (costa fluctuans decima), found 
in 80 per cent, of cases, and a habitus enteroptoticus, somewhat resembling 
the habitus phthisicus; in the normal chest the vertical line drawn from 
the ensiform to the navel is short, compared with the distance from the 
median line, horizontally, to the tips of the floating ribs; in the habitus 
enteroptoticus the vertical line is much longer and the horizontal line is 
shorter than normal and shorter compared with the vertical line. 

Symptoms. — 1. Stomach Findings. — Gastroptosis is characterized by 
falling of the organ to a lower point in the abdomen, whereby both 
its upper and lower limits are abnormally low, the epigastrium is flat- 
tened and the hypogastrium is distended. Eichhorst finds it in 35 per 
cent, of women and in 5 per cent, of men. Dilatation of the stomach 
is excluded by finding the lesser curvature at a lower point than normal. 
Gastric symptoms may be noted, as pain in the left hypochondrium from 
tension and increased by heavy meals, eructations, nausea and gastric 
or intestinal hyperesthesia, or as complications, vomiting, hyperacidity 
or motor insufficiency. In many cases gastric and other symptoms are 
entirely lacking. Radiographs demonstrate the ptosis, showing sagging 
of the middle portion of the stomach and pyloroptosis. 

2. Intestinal Findings. — Enteroptosis or coloptosis is frequently 
found with gastroptosis. The transverse colon sinks in its central seg- 
ment so as to assume the form of the letter U or V, as shown by radi- 
ography. Constipation is frequent. 

3. Floating kidney, liver and spleen will be described separately. 

4. Nervous symptoms occur in 50 per cent, of cases. Many subjects 
are nervous, slight and delicate women, who exhibit depression, cephalic 
pressure, backache, throbbing of the abdominal aorta, emaciation, con- 
stipation and anemia. 

Treatment. — (a) The treatment outlined under Neurasthenia (q. v.) 
is indicated. The diagnosis should not be disclosed to the patient, for 
suggestion initiates a long train of additional symptoms, (b) Increase 
in weight is effected by full feeding and the rest cure, (c) Supports to 
press upward and inward and maintain the viscera in their normal loca- 
tion often give considerable relief. Operations shortening the mesentery, 
resecting parts of the recti, suture of the liver, stomach and other organs 
to fixed tissues can as yet receive no general commendation. 

DILATATION OF THE COLON. 

Colectasia may be classified as follows: (a) Gaseous distention^ which 
may occur in acute toxemias; death resulted from heart paralysis (v. 
Typhoid and Enteritis), (b) Cases which are due to obstruction by 
feces, foreign bodies, volvulus, (c) Hirschsprung's disease or idiopathic 
colectasia, which occurs in children (in 80 per cent, of cases) as a con- 
genital lesion or in male adults over fifty years. It is due to obstruction, 
spasm, abnormal valves or long colon; in Formad's case there was 
great hypertrophy of the muscularis; the circumference of the colon 
was 30 inches and its Weight, with the contained feces, was 47 pounds. 
The leading symptoms are obstinate constipation and meteorism. Of 



PILES 557 

223 reported cases about 25 per cent, recovered under medical treatment 
and 57 per cent, after resection. Death results from marasmus, auto- 
intoxication, obstruction, perforation or peritonitis. 

INTESTINAL HEMORRHAGE. 

Etiology. — There are five groups: (a) Abnormal intestinal contents, 
as hard feces, foreign bodies, gall-stones, caustic poisons or parasites. 

(b) Intestinal lesions, as the various ulcerations, inflammation, invagina- 
tion, etc. (c) General affections; stasis, amyloidosis, mesenteric infarc- 
tion, aneurysmal rupture, scurvy, uremia and cholemia. (d) Infections, 
including typhoid, dysentery, hemorrhagic exanthemata and sepsis 
(see Hemorrhagic Diseases of the Newborn), (e) Blood from the 
stomach. 

Symptoms. — (a) Blood in the feces may be manifest, or "occult" i. e., 
found only microscopically, chemically or spectroscopically (generally 
present hours before it is seen by the naked eye). It is mixed with feces 
and dark, tarry and offensive when it comes from the small gut; it may 
coat the movements and be bright in color when it comes from the lower 
intestine, (b) Acute anemia follows profuse hemorrhage, evidenced by 
pallor, syncope and slight fever. 

Diagnosis. — The diagnosis of enterorrhagia concerns (a) the detection 
of blood, which may be simulated by bismuth or blueberries; (b) the 
question whether the blood comes from the bowel, mouth or stomach; 

(c) whether it comes from the large or small gut (v. s.); and (d) its cause, 
most often hemorrhoids, typhoid, dysentery or cancer of the lower 
bowel. No extended examination of the abdomen is permissible at the 
time of the hemorrhage. 

Prognosis and Treatment. — The prognosis and treatment are involved 
in the basic lesion (v. page 55). 

PILES. 

Etiology. — Hemorrhoids result from (a) stasis; portal stasis operates 
through the superior hemorrhoidal and inferior mesenteric veins and is 
more potent than cardiac stasis, which congests the middle hemorrhoidal 
and internal iliac veins; (6) from constipation, pregnancy and obstruc- 
tive lesions, as cancer of the rectum. Vigorous contraction of the abdom- 
inal muscles is a more potent cause than constipation (Duret). Usually 
spoken of as varices, piles are cavernous angiomata. 

Symptoms. — External piles appear as tender, painful, purple swellings 
outside the sphincter ani, singly or in a circle around the anus; they may 
be soft or hard. The pain is throbbing and often severe. Itching is very 
common. They may bleed, atrophy, ulcerate or suppurate. Piles which 
bleed are called "open" and those which do not, "blind." Internal 
piles occur above the sphincter, below which they may prolapse and 
strangulate. Tenesmus, mucus secretion and dull pain sometimes referred 
to the back and the sacro-iliac articulation, may be noted. 

Diagnosis. — Inspection excludes prolapse, condylomata, papillomata, 
etc. Causal carcinoma should be borne in mind. 



558 DISEASES OF THE INTESTINES 

Treatment. — (a) General factors, sedentary habits, and constipation 
are considered. (6) Local treatment: a small injection of cold water 
before each movement softens the irritating hard passage, constricts 
the piles and favors their reduction. Cleanliness relieves itching, for 
which also a 1 per cent, phenol salve is of value. The following formula 
is astringent and anodyne, but must be given w T ith reserve, (c) Surgical 
treatment is indicated when local measures fail. Boas lauds Bier's 
stasis, till edema appears; atrophy ensues. 

1$ — Extracti opii . gr. ij 

Extracti belladonnse gr. ij 

Cocainse (alkaloid) gr. iij 

Acidi tannici 5ss 

Olei theobromatis q. s. 

M. et ft. in suppositoria no. x. 

S. — One at bedtime. 

DIARRHEA. 

Definition. — Increased frequency of the stools with decreased con- 
sistence. Diarrhea is not synonymous with intestinal catarrh. In 
some individuals two or three movements a day are physiological. 

Etiology. — (a) Irritation; cathartics (some, as the aromatics, increase 
peristalsis and others, as salts, cause increased transudation); diarrhea 
dyspeptica; diarrhea stercoralis; diarrhea entozoica. In general there 
are two mechanisms: (i) the stools are hurried through the bowel by 
increased peristalsis, in which case bile is found in them; and (ii) there 
is increased serum transudation into the intestine when little or no bile 
is found, (b) Nervous diarrhea causes from two to fifteen thin move- 
ments, containing no increased mucus; it is attended by peristaltic 
unrest and is chiefly observed after excitement or in neurotics; some 
cases are reflex, as from uterine irritation, (c) Toxic substances in the 
blood may irritate the ganglia or brain, e. g., in uremia, typhoid or 
sepsis. 

Treatment. — Opium is the most valuable remedy, except in stercoral 
and dyspeptic types; it acts less by checking secretion than by sus- 
pending peristalsis and mitigating spasm; the crude drug is superior 
to its alkaloids, as its absorption from the bowel is slower and its effect 
more marked; f of a grain of the extract or a dram of the camphorated 
tincture should be given with bismuth in massive doses as in enteritis. 
Important adjuncts are local heat, rest and a spare diet, as in enteritis. 
In nervous diarrhea two drops of Fowler's solution before meals is 
advantageous. 

CONSTIPATION. 

Constipation is insufficient or unsatisfactory defecation. 

Etiology. — (1) "Physiological" constipation results from irregularity 
in going to stool, as in travel, from obesity, insufficient exercise or water, 
loss of fluid by sweating, a dietary rich in proteids, as milk, and from 
overmedication. (2) Constipation may be symptomatic of other affec- 



CONSTIPATION 559 

tions, as gastric ulcer, cancer, dilatation or hyperacidity; intestinal 
obstruction, cancer, adhesions, catarrh, passive congestion or enterop- 
tosis; pelvic conditions, as pregnancy, ovarian or uterine disease or 
enlarged prostate; injections which stimulate the inhibitory nerves; 
nervous disease, as meningitis, tumors, myelitis, the neuroses; diabetes 
and old age. (3) Habitual constipation may be familial. It may result 
from insufficient nervous energy in the large intestine; atony of the 
intestinal muscle may result from general debility, neurasthenia, etc., 
but seldom from atrophy or degeneration. Nervous constipation may 
be due to a spastic condition of the bowels. 

Symptoms. — Symptoms other than constipation are often absent, 
and when present are less often general than local (anorexia, coated 
tongue, bad taste in the mouth or abdominal uneasiness). 

Two or three movements in one day or a movement every two or three 
days come within physiological limits. The stools normally accumulate 
in the sigmoid and pass each day into the rectum, causing a desire to 
defecate, usually at the same hour. The constipated stool accumulates 
in the haustra of the colon or ampullae of the rectum. It is difficult to 
state the quantity of the normal passage, which does not depend wholly 
on the amount of food ingested; feces consist largely of mucus and 
bacteria and form even during starvation. The stools may resemble 
sheep's dung, probably due to intestinal muscular spasm. Retained 
feces are usually voided spontaneously in a few days with a serous 
diarrhea or as scybala covered with mucus which results from irritation. 
Fecal colic is due to peristalsis above the obstruction; there may be 
stercoral fever and meteorism. Marked obstruction rarely simulates 
enterostenosis, being marked by collapse, vomiting and great vesical 
or rectal tenesmus, which should always excite suspicion. Neglected 
cases may result fatally, especially in the old, debilitated or insane or 
when defecation causes great pain, as from fistula or piles. 

Fecal concrements (coproliths) occur in the large intestine, even simu- 
lating tumors of the intestine, omentum, kidney or spleen, from which 
differentiation may be possible only after thorough purging and flushing. 
They may be soft and easily indented with the finger, or hard, nodular 
and tender from the bowel ulceration they incite. Fecal tumors may 
develop with daily, though inadequate, movements. On pressure the 
bowel may at first seem to adhere to the fecal masses and then become 
free (Gersuny's sign). 

General symptoms are uncommon. Nervous symptoms are causal 
rather than coprostatic, as in the neurasthenic who believes he would 
be well if his bowels would move and who has most unpleasant sensations 
when they do. Vertigo, pressure in the head and mild dyspnea are 
always neurotic. Copropsychiatry is grossly exaggerated. Intoxication 
is rare, but has been considered causal of neuralgia, marasmus, chlorosis 
and numerous other concomitant conditions. The aromatic sulphates 
of the urine may be increased, due to formation of indol, skatol and 
pyrocatechin. 

Lane's Kink. Lane places great stress upon the development of 
accessory peritoneal bands, which produce kinks at the pylorus, lower 



560 DISEASES OF THE INTESTINES 

ileum, hepatic and splenic flexures and sigmoid. It is claimed that 
profound intestinal toxemia and constipation result, which induce dila- 
tation of the duodenum, vomiting and even gall-stones, gastric ulcers, 
changes in the breasts, arthritic changes and tuberculosis. To avert 
these disasters, he recommends ileosigmoidostomy or excision of the 
colon. 

The x-rays determine the rate of passage of bismuth; leaving the 
stomach, it should reach the cecum in four hours, the hepatic flexure 
in six and the splenic flexure in nine hours; visceroptosis and kinks are 
apparent; intestinal constipation and dyschesia (difficult evacuation 
of the rectum) are differentiated (v. i.). 

Treatment. — Treatment of causal factors (v. s.) is important. 

1. Diet. — (a) Coarse foods, as whole wheat, Graham, rye, cornmeal 
and bran breads, act less mechanically than chemically by the produc- 
tion of lactic or oleic acid, (b) Fruits relax the bowels, because of the 
malic, tartaric and citric acids they contain, as plums, raisins, apples, 
peaches, pears and prunes; grapes sometimes and bananas and per- 
simmons usually cause constipation. Fruits operate best when eaten 
at bedtime; it may be best to remove the excess of seeds or skins, (c) 
Vegetables act by the acids and gases they form; melons, sprouts, cabbage, 
cauliflower, cucumbers, turnips, carrots, spinach, tomatoes, asparagus, 
onions, cress, celery and squash should be given freely; excessive amounts 
may cause fatigue of the bowel, fermentation and constipation. Agar- 
agar, 3ij daily, may be given in mashed potatoes or apple sauce, (d) 
Sweets are laxative; if they do not cause indigestion, sugars, syrup, candy, 
sauces, molasses, jellies, jams, marmalades and honey are valuable laxa- 
tives, (e) Fats. — Moderate amounts of butter and olive oil are superior 
to animal fats, which tend to derange digestion. (/) Cold or charged 
ivater, taken on rising and through the day, excites peristalsis. Hard 
water constipates, (g) The following are to be avoided: red wines (con- 
taining tannic acid), excess of meat, eggs or rice, buckwheat, macaroni 
and other carbohydrates containing little water, tea, milk (sometimes 
laxative when not taken in sips but swallowed in larger quantities), 
chocolate and cocoa. The diet recommended affords material for bac- 
terial action, which follows the idea advanced by Schmidt, Strassburger 
and Lohrisch, that constipation results from too complete utilization 
of the average diet by the intestinal bacteria. Some individuals digest 
all kinds of vegetables; others pass unchanged even cooked vegetables. 
Hydrochloric acid partly digests and loosens the middle sheath of the 
cellulose, so that the duodenal and pancreatic juices operate more readily 
on it. This explains the constipation of hyperchlorhydria. Diet and 
copious drinking of water cure most cases. 

2. Punctuality at Stool. — The best time is immediately after break- 
fast; piles or prolapse may come down during the day, whence in these 
cases the bowels should be moved at bedtime. 

3. Posture at Stool. — Squatting, the natural posture, may be approx- 
imated by leaning forward or by placing the feet on a foot-stool; the 
thighs support and compress the abdomen, a matter of importance when 
it is relaxed. 



CONSTIPATION 561 

4. Massage. — Gentle massage along the course of the colon for a 
quarter of an hour, before breakfast, may give relief if continued for 
months. Sahli rolled over the abdomen a 7-pound cannon-ball. Massage 
is contra- indicated in spastic constipation. 

5. Mild Faradization. — Weak applications arouse short contrac- 
tions in the colon and are given with a moist sponge. The cold compress 
to the abdomen is a good adjunct. 

6. Exercise. — Exercise to develop and contract the abdominal 
muscles, as in tennis or rowing or by lifting the legs while lying on the 
back or lifting the rigid body from the lying to the erect posture solely 
by the abdominal muscles, is superior to walking, bicycle and horse-back 
riding. In ovarian and uterine disease exercise increases constipation, 
due to reflex inhibition of peristalsis, as shown by the laxative effect of 
narcotics. It is claimed that constipation is spastic (not atonic) in 25 
per cent, of female cases, as evidenced by colic, palpable or visible knots 
in the intestine and sometimes by ribbon-like passages; in these cases 
an irritating, coarse diet, massage, cold and electricity are to be avoided. 
The radiograph may show the spastic sigmoid or colonic flexures, etc. 
Hot baths or hot compresses to the abdomen for colic are indicated; an 
enema of warm oil is given each evening; extract of belladonna gr J in 
a suppository relieves spasm and tenesmus; the diet should consist of 
fine carbohydrates, butter and cooked fruit. 

7. Enemata. — Enemata excite peristalsis, lessen intestinal hyperemia 
and apparently benefit the hepatic circulation. They do not derange 
digestion as do cathartics, but may lose their effect by dilating the colon, 
whence the indication for their intermittent use. Water and olive or 
linseed oil may be used; oil enemata (five to eight ounces) are especially 
indicated in spastic constipation and colica mucosa, in which the oil 
may be left in the bowel over night. Antiperistaltic movements in the 
colon carry the oil to the cecum, in the low as well as in the "high" 
enema. In ordinary constipation, the passage of feces through the 
intestines is delayed, while defecation is normal; in dyschesia, there is 
no delay in the arrival of feces in the pelvic colon, though their final 
expulsion is not adequately performed; diet, abdominal massage and 
aperients, appropriate for intestinal constipation, are useless in dyschesia, 
attention to the hygiene of the bowels and reeducation of the defecation 
reflex by means of graduated enemata being the correct treatment. 
Dyschesia leads to secondary retention of feces in the pelvic colon, and 
in severe cases in still higher parts of the large intestine; unless enemata 
are given, the rectum is never empty, and in spite of its dilated condition 
there is insufficient room for all the retained feces. Glycerin supposi- 
tories are valuable, if used alternately with other methods. Fecal impac- 
tion indicates enemata, cathartics and digital evacuation of the hardened 
masses. 

8. Cathartics. — (a) Cathartics should be administered only after 
failure of the measures enumerated above; (b) their most successful em- 
ployment is intermittent and alternating; (c) drastics, hydragogues and 
cathartics producing secondary constipation are avoided, save in extreme 
cases. Every new remedy is the best for a short while. 

36 



562 DISEASES OF THE INTESTINES 

Varieties. — Aloes, found in nearly all proprietary and official pills, 
should be avoided in piles and uterine hemorrhage, because it congests 
the pelvic vessels; it is given in combination, e. g. — 

T\ — Extr. aloes . . . . gr. ss Acting in 15 to 20 hours, on the large bowel 

chiefly, increasing tonus. 
Extr. rhei gr. ij-v Actively purgative in 4 to 8 hours; stom- 

achic and tonic. 
Extr. nucis vomicae . . gr. | Acting on peristalsis and combating atony. 

Resinse podophylli .. . gr. xV Acting in 10 hours, producing "bilious 

stools." 
Extr. belladonna? ... gr. \ Relieving spasm (griping) and operating on 

(or extr. hyoscyami) ■ the intestinal nerves. 

Extr. taraxaci .... gr. j 
M. et f,t. pil. i. 

Rhubarb gripes and produces secondary constipation, caused by its 
tannic acid, whence it should never be given alone: 

1$ — Pulveris rhei compositi 5iv 

Sodii sulphatis . . . . . . . 5iv 

Sodii bicarbonatis 5J 

M. et S. — One teaspoonful at bedtime. 

Cascara sagrada improves digestion and produces little constipation 
afterward; the fluidextractum rhamni purshianse, Tfl,xv, is very bitter; 
the extractum is given in doses of from two to eight grains. Licorice 
is given as pulvis glycyrrhizse compositus, 5ss-j. Castor oil is a 
soothing laxative, relieving irritation and spasm, in nervous or lead 
constipation, in the latter combined with opium gr. J; its offensive 
taste may be partly overcome as follows: 

1$ — Olei ricini 5ij 

Olei gaultherise gtt. xl 

Glycerini 3ij 

M. et S. — One teaspoonful to one tablespoonful. 

In anemic patients the following formula is recommended: 

1$ — Ferri sulphatis gr. x 

Extracti aloes gr. v 

Extracti rhamni purshianse gr. xx 

Extracti belladonnse gr. iij 

Extracti nucis vomica? gr. iij 

M. et ft. pilulge no. x. 

S. — One after meals. 

Calomel should be given in the evening in fractional doses, combined 
with podophyllin, which also acts in eight hours, and followed the next 
morning by half an ounce of magnesium sulphate; calomel increases the 
peristalsis of the large and small intestines. Senna easily deranges diges- 
tion; it acts upon the large bowel; a small amount may be cooked with 
prunes; confectio sennce is given in dram doses. Cathartics often cause 
blood in the stools. Tobacco smoking and coffee in the morning are bene- 
ficial, but tea promotes flatulency and constipation. Consideration of 
the salines and drastics (v. Nephritis) is omitted, as their use is contra- 



NERVOUS AFFECTIONS OF THE BOWEL 563 

indicated except for emergencies; table salt, 3ss, well diluted and taken 
on rising frequently moves the bowels. Hormonal, a peristalsis hormone 
discovered by Zuelzer in the intestines, spleen, etc., promotes peristalsis, 
given intramuscularly or intravenously; it is prone to lower blood-pressure, 
even to the point of collapse. 



INTESTINAL DIVERTICULA. 

Telling tabulated 105 cases (1908). They may be congenital or acquired, 
false or true, in type. They may be the site of inflammation or malig- 
nancy. Occurring in the colon or sigmoid, the symptoms may resemble 
those of left-sided appendicitis. Infection, ulceration or gangrene may 
lead to peritoneal disasters. Pain, leukocytosis, fever, vomiting, diarrhea 
or constipation, blood in the stools and a low, perhaps pelvic, tumor 
which appears and disappears, are suggestive symptoms. 



NERVOUS AFFECTIONS OF THE BOWEL. 

1. Neuroses of Motility. — (a) Nervous diarrhea has been considered. 
It may occur in the neuroses, reflex irritation during dentition or in the 
crises of tabes; it is usually transient and is marked by absence of inflam- 
matory symptoms, as mucus, pus or blood. Nervous diarrhea may be 
confused with organic disease, (b) Enterospasm is caused by simulta- 
neous contraction of the circular and longitudinal muscles, which normally 
contract alternately. (See Dynamic Ileus, Spastic Constipation and 
Colica Mucosa.) (c) Sphincter spasm, aside from local rectal or anal 
lesions, results from sensory hyperirritability or decreased cerebral inhibi- 
tion; it is most common in hysteria and tabes, (d) Peristaltic unrest 
may be associated with diarrhea if the colon is involved, but more com- 
monly affects the small bowel only, when constipation or normal move- 
ments are usual, (e) Nervous constipation (atony) may result from the 
neuroses, intoxication from carbon dioxide and organic cerebrospinal 
diseases, in which conditions (/) sphincter paralysis may also result. 

2. Neuroses of Sensation. — Neuralgia mesenterica (enteralgia, entero- 
dynia) is most important; strictly speaking, it is always nervous, i. e., 
not due to organic causes; practically, other forms of abdominal pain 
are frequently included under enteralgia. The chief symptom is the 
abdominal pain, which is usually umbilical, sometimes relieved by press- 
ure and sometimes not; the abdominal wall may be hyperesthetic. 
Reflex disturbances in other organs may aid in establishing its functional 
character, as hiccough, vomiting, dyspnea, palpitation, rectal or vesical 
tenesmus, muscular twitchings, etc. The diagnosis necessitates exclusion 
of innumerable affections, chiefly abdominal but also general: (a) rheuma- 
tism of the abdominal muscles which is superficial; (b) lumbo-abdominal 
neuralgia, in which Valleix's three tender points are found (see Neu- 
ralcia); (c) hysteria, distinguishable by its stigmata; (d) tabetic crises; 
(e) intestinal affections, as appendicitis, peritonitis, coprostasis, para- 



564 DISEASES OF THE INTESTINES 

sites, flatulent colic, excessive catharsis, lead colic or colica mucosa; 
(./) gout; malaria and typhoid; renal and bilary calculi. 

Its treatment and that of the motor disturbances is of the fundamental 
nervous state. Symptomatically, hypodermics of narcotics produce the 
quickest but most dangerous relief; atropine is much safer. 

1$ — Spiritus chloroformi 3ij 

Tincturae opii camphoratse 5iv 

Tincturae asafcetidse 5iv 

M. et S. — One tablespoonful in hot water every fifteen minutes for three or four doses. 

3. Neuroses of Secretion. — The secretion neuroses are important. 
The chief types are serous nervous diarrhea and colica mucosa (v. s.). 



AFFECTIONS OF THE MESENTERY. 

I. Inflammation. — Mesenteritis is chiefly important in its relation to 
ascites, tuberculous peritonitis and other peritonitides (q. v.). 

II. Hemorrhage. — Primary hemorrhage is most rare. It is generally 
secondary to acute hemorrhagic pancreatitis, retroperitoneal hematoma, 
aneurysmal extravasation or the hemorrhagic fevers. 

III. Diseases of the Mesenteric Vessels. — (a) Infarction by embolism 
or thrombosis involves chiefly the arteria mesenterica superior, essentially 
a terminal vessel. Most cases develop in men past middle life; 360 
cases are reported. Its onset is sudden, with intense abdominal pain, 
collapse, vomiting (usually bloody and perhaps fecal, due to intestinal 
obstruction), diarrhea (40 per cent.) and bloody stools (40 per cent.). 
Unless there is an apparent cause for embolism, as valvular disease, the 
diagnosis is rarely made, for peritonitis or obstruction is usually suspected. 
The usual outcome is early death from collapse, but if the patient lives 
long enough acute peritonitis sets in, with distended abdomen and diffuse 
tenderness. In very rare cases collateral circulation allows of recovery; 
94 per cent, are fatal. The treatment is purely symptomatic and suppor- 
tive, but operation was successful in 46 per cent, of Boinet's series, (b) 
Periarteritis nodosa (v. page 410). (c) Dilatation of the mesenteric veins 
and phlebosclerosis occur, especially in liver cirrhosis, (d) Suppuration 
(thrombophlebitis suppurativa) may mark umbilical pyemia of the new- 
born or may carry infection from the appendix or rectum, (e) Of simple 
thrombosis of the mesenteric veins, Kraft collected 16 cases; in over half 
of the cases syphilis or liver cirrhosis was the cause. 

IV. Affections of the Chyle Vessels. — These vessels may become 
varicose or even hyperplastic (chylangioma). Cysts containing chyle 
may cause tumors and, by rupture, may result in chylous extravasation 
in the mesentery or chylous ascites (q. v.). Twenty-four chylous cysts 
are described by Broca. 

V. Mesenteric Tumors. — These may be dermoid, hydatid, serous, 
sanguineous, chylous or malignant, and may fill the abdomen. Their 
symptoms are those of an abdominal tumor, which is centrally located, 
movable and covered with a zone of resonant intestine. 



ACUTE YELLOW ATROPHY 565 



DISEASES OF THE LIVER. 

ACUTE YELLOW ATROPHY. 

Definition. — An acute degeneration of the liver cells, accompanied by 
shrinking of the liver, icterus and fatal nervous toxemia. Ballonius 
(1600) reported the first case. Best collected 500 cases. 

Etiology. — (a) Sixty-six per cent, occur in women and 50 per cent, 
between the years of twenty and thirty-; but 22 cases occurred under 10 
years of age. (b) Thirty-three per cent, of women with the disease were 
in the last half of pregnancy; it is infrequent in the first three months and 
the puerperium. (c) Ten soldiers were affected in Arnould's epidemic 
series, (d) Infections, as osteomyelitis, diphtheria, sepsis, erysipelas, 
typhoid, recurrent fever and secondary syphilis (in about 50 cases) ; or 
(e) poisoning, as from phosphorus, alcohol and chloroform narcosis, may 
antedate the disease, which may occur primarily in a sound or secondarily 
in a diseased liver. Worry is a predisposing factor in pregnancy or 
syphilis. 

Pathology. — The liver is small, the minimum record being 400 grams; 
it is often so lax that it can be rolled up ; the capsule is wrinkled, the color 
yellow (atrophia hepatis fusca) and the lobular markings obscure. The 
liver cells are granular, fatty, or tinged with bile; some are necrotic and 
others show regeneration. Foci of red tissue represent an advanced 
stage in which the fatty necrotic cells have been absorbed; the left lobe 
is often red, homogeneous and composed of detritus, showing the most 
advanced process, and the right lobe is yellow, showing more recent 
changes. Crystals of tyrosin are found. The apparent increase of the 
connective tissue is relative only. Icteric staining, small hemorrhages 
and fatty degeneration are found in the heart, kidneys, muscles, lungs 
and digestive tract. 

The disease is rather a necrotic process than an acute parenchymatous 
hepatitis. It is not determined whether the disease is an infection, to 
which it has some resemblance, or an intoxication, which initiates auto- 
lysis of the liver. 

General Clinical Picture. — Acute yellow atrophy begins with a prodromal 
stage in which gastric disturbance predominates; icterus develops in a 
few days when the second stage suddenly begins with cerebral symp- 
toms, delirium, vomiting and convulsions; shrinking of the liver, hepatic 
tenderness, enlarged spleen, hemorrhages, and abortion, if pregnancy 
exist; urinary symptoms, as bile, albumin, leucin, tyrosin and other 
unusual products in the urine; and subnormal or normal temperature. 
The issue is fatal. 

Individual Symptoms. — The prodromal stage lasts a few days (to three 
weeks or more) and is not characteristic. In the latter half of gestation, 
icterus and hepatic tenderness or enlargement are suspicious symptoms. 
Gastric irritability prevails. Icterus, absent only in extremely rapid 
cases, is obstructive from intrahepatic changes and increases with the 
second stage; the stools are acholic. 



566 DISEASES OF THE LIVER 

In the second stage (a) the hepatic dulness shrinks first in the left lobe, 
to one-half or one-quarter of its former dimensions, or the liver falls back 
toward the spine so that there is no liver dulness. The liver dulness may 
remain normal if death is rapid, as from hematemesis, or if the liver is 
cirrhotic or adherent to the abdominal wall. The liver is tender and pain- 
ful, and may feel flabby or pit to the finger. The liver region may appear 
sunken, (b) The spleen is enlarged in 66 per cent.; it is not enlarged 
when profuse hemorrhage or diarrhea is present, (c) Vomiting is almost 
invariable, the vomitus consisting of mucus, bile and finally blood; it is 
accompanied by hiccough, dry tongue, sordes and constipated, uncolored 
stools, (d) Nervous symptoms come on gradually with headache, or abruptly 
with delirium, anxiety, meningeal symptoms, trismus, wide pupils, amau- 
rosis, cerebral vomiting and convulsions (in 33 per cent, of adults and 
almost constantly in children). The nervous symptoms are due to hepatic 
insufficiency (hepatargia), the degenerated liver being unable to protect 
the nervous system, as it does in health, against various toxic products. 
(e) The urine is decreased or even suppressed. Bile pigment, albumin, 
casts and epithelial cells are found. Unusual products are found in the 
urine, due to the autolysis of the liver cells; leucin and ty rosin occur most 
frequently, though neither constant nor pathognomonic; sarcolactic 
acid, oxyamygdalic acid, peptone and albumose are also found. The 
urea is decreased, perhaps absent. The ammonium compounds, normally 
2 to 5 per cent, of the nitrogen excretion, are increased, even to 17 to 
20 per cent., to neutralize the acidosis. The uric acid and xanthin are 
increased. Indicanuria may be noted. Glycosuria is rare, though the 
glycogenic function of the liver can hardly be normal. (/) The temperature 
is usually normal or subnormal at the height of the process. The pulse 
at first may be slow, but later becomes very rapid and dyspnea develops. 
(g) Hemorrhages occur in the majority of cases, largely from the stomach 
and into the skin. Hemorrhages from the bowel, nose, mouth and genitals 
are less frequent. Uterine hemorrhages occur if pregnancy exist. Hemor- 
rhages in the retina are frequent, together with white flecks due to 
tyrosin deposit and fatty change. Erythematous eruptions, muscular 
pain, articular swellings and herpes may occur. 

Course. — Fifty per cent, of cases die between the fifth and fourteenth 
day and 30 per cent, between the third and fifth week. The more abrupt 
and severe the cerebral symptoms the more rapid is the course. Preg- 
nancy hastens the issue. Remissions may be observed. The pulse 
becomes rapid, the breathing difficult and irregular and nervous excitation 
is followed by paralysis of the brain centres. 

Diagnosis. — Diagnosis is based upon the icterus, nervous symptoms 
and shrinkage of the liver. Diminution of the liver may be simulated by 
tympanites or by the colon lying over the liver. The urinary findings 
are valuable with the above symptoms. Confusion may occur in icterus 
gravis or in the so-called bilious typhoid, pneumonia, recurrent fever, 
puerperal fever, yellow fever, or Weil's disease, most of which affections 
are febrile, while yellow atrophy is afebrile; the intensity of the icterus, 
shrinking of the liver, severe cerebral symptoms and the urinary findings 
are diagnostic. The greatest difficulty in diagnosis is acute phosphorus 
poisoning, for which the etiology alone is distinctive. 



PORTAL CIRRHOSIS 567 

Recovery usually indicates error in diagnosis. Ascites in acute yellow 
atrophy occurred in but eight instances (Tileston) (v. page 587). 

Treatment. — Treatment is directed to the heart depression, vomiting 
and nervous excitement (v. Typhoid). Two recoveries under salvarsan 
are alleged. 

PORTAL CIRRHOSIS. 

Synonyms. — Laennec's cirrhosis, alcoholic or atrophic cirrhosis. 

Definition. — Portal cirrhosis is a fibrosis of the liver, characterized 
(a) etiologically by alcoholism; (b) anatomically by induration around 
the portal vein radicles enclosing numbers of liver lobules, whose cells 
degenerate; and (c) clinically by portal obstruction (dyspepsia, hema- 
temesis, enlarged spleen and ascites) and often by signs of hepatic 
insufficiency. 

Classification. — Cirrhosis may be classified as follows: 



, n r^ / Portal vein syphilis. 

1. Capsular or Glissonian. < -,, • -r ,-,- 

[ Chronic perihepatitis. 



2. Vascular. 



Portal vein cirrhosis, first in clinical importance; 
its leading type is the alcoholic, atrophic type 
of Laennec. (A subtype is a hypertrophic 
cirrhosis, like the atrophic save that the liver 
remains large.) 

Hepatic vein cirrhosis, occurring in stasis (cy- 
anotic induration), and, according to French 
authors, with portal vein cirrhosis. 

3. Biliary Cirrhosis. Hanot's disease. 

4. Mixed Cirrhosis. (Portal vein and biliary cirrhoses combined.) 

Of these, two main forms are conspicuous — the portal and biliary. 

Etiology. — (a) Sixty to 75 per cent, of cases are found in men between 
forty and fifty years of age. Musser collected 685 cases in children, (b) 
Alcoholism is the chief cause; cirrhosis may be due to whisky, wine, beer 
or absinthe, especially in sedentary individuals; alcohol is absorbed by 
the gastro-intestinal veins and conveyed to the portal vein radicles, 
where its toxic effects are expended on the liver cells or interstitial tissue, 
but in what sequence it is not known, (c) Syphilis is a cause, especially 
in the young, in whom the spirochetes are conveyed by the umbilical 
vein to the liver, (d) Other infections, as malaria, typhoid, tuberculosis, 
etc., are possible causes; experimentally cirrhosis has been induced by 
the Bacillus pyocyaneus, B. coli and staphylococcus; and lactic, acetic 
and butyric acids; local mycotic necrosis is thought to be followed by 
fibrosis, the toxins probably entering by the hepatic artery, (e) Unknotvn 
toxemias. Spices, drastics, lead, phosphorus, arsenic, hemochromatosis, 
anthracosis, silicosis, repeated protein intoxication and possibly gastro- 
enteric auto-intoxication are exceptional etiological factors. It may be 
associated with gout, diabetes or other constitutional affections. There 
may be multiple causes, e. g., syphilis plus malaria or alcoholism. 

Pathology. — The essential change is fibrosis around the branches of 
the portal vein; either the connective-tissue growth is primary, causing, 
as it contracts, atrophic or fatty alteration of the liver cells, sometimes 



568 DISEASES OF THE LIVER 

with pigmentation; or the cells are first injured and are replaced by fibrous 
tissue. The connective tissue surrounds several lobules at a time (multi- 
lobular cirrhosis). Histologically the cirrhosis is atrophic, and this point 
is emphasized first, because some clinicians maintain that the liver is 
first large (the so-called hypertrophic stage) and later is shrunken; and 
a normal-sized or enlarged cirrhotic liver is histologically atrophic. 
An atrophic liver may be large from fat deposit, congestion or compen- 
satory parenchymatous hyperplasia. The iveight is as often increased 
as decreased, ranging from 2000 gm. to 1000 gm. or less. Its edge is 
rough, i. .e., granulations can be felt which represent the remaining 
relatively normal liver tissue. Regeneration of the parenchymatous 
cells is active but somewhat disorderly, irregular and unstable, the cells 
again wasting. The surface is sometimes smooth, and cirrhosis may 
appear only on microscopic examination. Granulations also occur 
in fatty liver, pylephlebitis and passive congestion. Its consistence is 
increased. The liver is gritty to the knife; its color is yellow (cirrhosis), 
perhaps green or brown. The connective tissue is increased and prominent, 
encroaching on the parenchyma. Injections of the organ through the 
portal vein are not successful, i. e., there is portal obstruction; there 
is a narrowing of the capillary vessels; these and the increased arterial 
pressure in the organ account for many of the clinical symptoms 
(v. page 574). 

General Clinical Picture. — The disease often exists for years without 
symptoms; this latency is marked by enlargement of the liver, and is 
due to compensatory cellular hyperplasia. In the minority of cases, 
transient swelling, pain or active hyperemia of the liver, dyspepsia and 
fever or icterus are observed; they are not characteristic. With marked 
shrinking there are symptoms (a) of disturbance of nutrition, as emaciation, 
which is often not noticed because the abdomen remains obese and a 
sallow skin, in which dilatation of the small arterioles (toxemia or alco- 
holism), dryness and hemorrhages are also observed; (6) of portal con- 
gestion, as early hematemesis, epigastric pressure, ascites, large spleen 
and disturbed breathing, circulation and digestion; (c) of intoxication, 
resulting from functional failure of the heart, liver and kidneys; and 
(d) of complications, as hemorrhage, diarrhea or cholemia. 

Symptoms. — 1. The Liver. — The liver is enlarged as often as it is 
decreased in size; the left lobe suffers greater and earlier contraction. 
Its edge is hard, but often cannot be felt, even after tapping, on account 
of its shrinkage or because the bowels cover it. The edge is uneven; 
its granulations may be confused with the small islets of fatty tissue 
in the abdominal wall, due to unequal wasting of the adipose tissue. 
Palpation of the liver is the only certain way of determining its lower limit, 
the results of percussion being unreliable. In infantile forms of portal 
cirrhosis the liver and spleen are larger than in adult types (v. i. for 
symptoms of impaired hepatic function). 

2. Portal Stasis. — Obstruction to the portal circulation causes: (a) 
The peritoneum is thickened, edematous and the seat of transudation, 
i. e., ascites, which occurs in 85 per cent, when the patient dies of the 
cirrhosis itself and in 50 per cent, when he dies from other causes. 



PORTAL CIRRHOSIS 569 

It is more common in small than in large livers. Ascites appears first 
without general edema, though later the legs may become swollen as the 
ascites compresses the inferior cava; pre-ascitic edema of the legs or 
abdominal wall may develop from cardiac or renal complications, involve- 
ment of the cava by perihepatitis or from thrombosis of the iliac veins. 
Under ascites its physical signs will be more closely considered. The 
amount of fluid may be enormous (nine gallons.) 

The fluid is usually amber-colored, seldom red from admixture of blood 
or very rarely turbid from fat (adipose ascites) or lecithin (chyliform 
ascites). The specific gravity is 1.008 to 1.015, with 0.6 to 1 per cent, 
albumin. The patient may die before ascites develops. A slowly develop- 
ing collateral circulation may permanently relieve an earlier ascites. It 
may disappear after hemorrhage or diarrhea, (b) The spleen is enlarged 
two- to sixfold, due to the early toxemia and the later stasis, in 75 per 
cent, of cases; it is a fair measure of the degree of liver cirrhosis. Its 
capsule and trabecular are hard and thickened (sometimes preventing 
splenic enlargement), and a systolic murmur is sometimes heard, (c) 
G astro-intestinal catarrh is due to stasis and alcoholism. Pain after eating, 
a coated tongue, vomiting, achylia, constipation, piles, diarrhea toward 
the end of the course and meteorism also occur, (d) A collateral circula- 
tion may be evidenced by enlargement of the veins about the navel 
(cirsomphalos or caput Medusa?). Prominence of the epigastric veins 
results from compression of the inferior cava. Anastomoses occur (i) 
between the middle and inferior hemorrhoidal veins (passing by the 
hypogastric to the cava) on the one hand, and the superior hemorrhoidal 
(passing by the superior mesenteric to the portal vein) on the other hand ; 
(ii) between the coronary veins of the stomach on the one hand and the 
esophageal and phrenic veins on the other, which empty into the vena 
azygos; (iii) between the veins in the ligaments of the liver and new 
adhesions and the phrenic veins; between the veins of the ligamentum 
teres and the veins of the abdominal wall and epigastric veins, which 
may sometimes be felt and may produce murmurs; (iv) the mesenteric, 
peritoneal and parumbilical veins also communicate with those of the 
abdominal wall. A well-developed collateral circulation is both a favor- 
able and an unfavorable symptom; it relieves the portal stagnation and 
helps the overtaxed liver to perform its functions; on the other hand, 
the dilated collateral vessels are likely to rupture and they convey directly 
into the general circulation toxic substances which the liver normally 
destroys or alters; this failure of detoxication causes the frequent arterio- 
sclerosis, granular kidneys and more acute toxemia, which resembles 
uremia, (e) The kidneys are congested, degenerated and often show hyper- 
trophy. The urine is decreased in amount, darker and of higher specific 
gravity, because the arterial tension is low in cirrhosis. More urine is 
often secreted during fasting than during digestion (opsiuria), which is 
the converse of normal conditions. The urobilin may be increased two- 
fold, indicating failure of hepatic function, if there is lessened urobilin 
in the stools (and hemolysis is excluded). The chlorides are decreased, 
as they accumulate in the ascitic transudate. The urea is often decreased, 
but the ammonium compounds are often increased, less from interference 



570 . DISEASES OF THE LIVER 

with the liver functions than from increase of acid products in the blood 
(acidosis), which the ammonium salts seek to neutralize. The amino- 
acids are regularly increased. Glycosuria* is uncommon save in the pig- 
mentary cirrhosis (see Diagnosis). Alimentary glycosuria may be pro- 
duced by administration of 100 gm. of grape-sugar or of levulose and 
galactose (in 50-86 per cent, of cases). In the writer's experience, 
physical signs are far more weighty than functional tests. Albuminuria 
may result from stasis or nephritis (v.i.). Blood may be found in the 
urine as a result of stasis in the bladder. 

3. General Symptoms. — Loss in loeight, anemia and an earth-like 
color are explained (a) by the inability of the liver to handle the carbo- 
hydrates, proteids, etc., (6) by the diversion of toxins through the col- 
lateral circulation into the general circulation, and (c) stasis catarrh. 
In 4 cases with well-developed collateral circulation, scurvy developed 
which the writer interpreted as toxemic. It was once thought that bile 
salts entered the blood and produced -'"cholemia" or that substances 
were retained which the bile normally excreted, producing " acholia;' 
now liver insufficiency (hepatargia) is considered responsible for toxemic 
symptoms (adynamia, headache, itching, delirium, stupor, convulsions, 
paralysis, contractures or coma); the writer twice observed Kussmaul's 
breathing. Much depends upon the integrity of the kidneys, which 
may for a time maintain adequate excretion. 

Complications. — 1. Hemorrhage. — (a) Cachectic capillary hemorrhage 
from the nose, mouth, lungs or stomach is less frequent than in biliary 
cirrhosis. Epistaxis occurs from dilatation of the vessels on the anterior 
part of the septum, (b) Of mechanical congestive hemorrhages from 
the esophagus, stomach, bowels, kidneys, bladder or uterus, those from 
the esophagus are most important. Their rupture causes hematemesis 
(which occurs in 23 per cent, of cirrhosis cases), chiefly in adults; if 
very profuse, blood may come up without vomiting; one of Osier's 
cases bled 10 pounds; it often causes blood in the stools. It may form 
dark clots; it is usually attended by less collapse than in hemorrhage 
from gastric ulcer. In 33 per cent, the first hemorrhage is fatal; in 66 
per cent, hemorrhages occur over a period of months to even eleven 
years. Varices are present in 80 per cent, and in over half, macroscopic 
rupture is detected; fatal hemorrhage may occur solely from capillary 
rupture. Hemorrhage may be the first symptom of cirrhosis. 

2. Peritonitis. — (a) Chronic peritonitis (15 per cent.) may occur 
with retraction of the mesentery and intestines; it prevents absorption 
of the ascites, (b) Tuberculous peritonitis (20 per cent.), often with an 
hemorrhagic exudate,^ follows the ascites of cirrhosis and hastens the 
fatal outcome. One would think that stasis would prevent the develop- 
ment of tuberculosis. 

3. Nephritis. — Nephritis occurs in 33 per cent, of cases. 

4. Heart. — The heart is "arteriosclerotic" in 60 per cent.; chronic 
myocarditis, endocarditis, fatty degeneration and dilatation of the 
right ventricle often occur. The arterial tension is low in cirrhosis. 

5. Lungs. — Bronchitis, emphysema and in 28 per cent, pulmonary 
tuberculosis occur. Right-sided hydrothorax occurs from stasis in the 



PORTAL CIRRHOSIS 571 

vena azygos and right intercostal veins; right-sided pleurisy, due to 
extension of perihepatitis through the diaphragm, occurs in 10 per cent, 
of cases. 

6. Brain. — Pachymeningitis, or progressive degeneration of the corpus 
striatum (see diagnosis of cerebral thrombosis) occasionally occurs. 

7. Fever. — "Intermittent hepatic fever" may result from hepatargia 
or perihepatitis. The temperature is usually subnormal in advanced 
cases, though fever and leukocytosis are observed in terminal infections. 

8. Icterus. — In atrophic cirrhosis jaundice is a genuine complication, 
due to duodenal catarrh or a radicular cholangitis; few pass through 
the disease without a muddy, yellow areola under the eyes. If present 
it is incomplete. Its frequency is 15 per cent. 

9. Anasarca. — Anasarca results from pressure on the cava by an 
extensive ascites, from perihepatitis with cicatricial involvement of the 
cava and from complicating cardiac or renal disease and marasmus. 

10. Other Complications. — These are rarer, pylethrombosis, clubbed 
fingers, multiple neuritis or delirium tremens. 

Course and Prognosis. — The clinical course seldom exceeds two or three 
years, but more often months than years; the maximum is fifteen years. 
There is no acute cirrhosis. Compensatory factors include (a) the col- 
lateral circulation, though this may throw toxins directly on the nervous 
centres and produce symptoms like uremia; (b) hyperplasia of the liver 
cells, which may produce veritable adenomata. As Hanot puts it, the 
diagnosis is based on the condition of the connective tissue, but the prog- 
nosis depends on that of the liver cells, (c) The kidneys may compen- 
sate to a small degree. Hale White holds that ascites is ominous, the 
patient rarely surviving the second tapping; though ascites is a late 
symptom, the author has seen numerous cases which survived frequent 
tappings, excluding perihepatitis, which White considers explanatory 
of these cases. The prognosis is relatively favorable in subjects under 
forty years with large livers and small spleens. Recovery is possible. 
In advanced stages death is the usual outcome. 

Death results from hepatargia (cholemia), marasmus, hemorrhage, 
ascites or intercurrent terminal infections; exhausting diarrhea or vomit- 
ing; cardiac, renal or other complications (v. s.). 

Differential Diagnosis. — Two classes of conditions require differen- 
tiation: those in which the liver is large and those in which it is small. 

1. When the Liver is Large. — (a) The fatty, amyloid, congested, 
cancerous and luetic livers are differentiated on page 587. (b) Leukemic 
deposits cause hepatic intumescence, but the blood examination is deci- 
sive, (c) Pericarditic pseudocirrhosis, described by Pick (1896), occurs 
in young, rheumatic and cardiac subjects and is characterized by symp- 
toms which on the one hand resemble disproportionately extreme passive 
congestion of the liver and on the other a capsular cirrhosis; the liver is 
large and firm, there is recurrent ascites without edema of the extremities 
and little or no icterus; contracting pericarditic adhesions may perhaps 
cause dilatation of the right auricle and vena cava inferior, thereby dis- 
tending the hepatic vein system; or possibly the inflammation extends 
down the cava inferior to the liver, (d) In Banti's disease the spleen is 



572 DISEASES OF THE LIVER 

enlarged first and there is early icterus and splenic anemia, while the 
cirrhosis and hematemesis occur later. 

2. When the Liver is Small. — The following possibilities should be 
considered: (a) Syphilis, characterized by stellate scars, nodes, pain and 
a positive Wassermann. (6) Passive congestion; the nutmeg liver may 
atrophy, but anasarca is observed first and there are primary character- 
istic heart findings, (c) In simple marantic atrophy the liver is small, 
there is no portal stasis and arteriosclerosis is found, id) Pylethrombosis 
is characterized by a rapid onset with swelling of the spleen, severe or 
repeated hematemesis, dilated veins and rapid recurrence of the ascites 
after tapping; it is due to tumor, nearby ulcers, suppuration or gall- 
stones, (e) Perihepatitis has a very much slower course than has cirrhosis 
and often results from pericarditis. (/) In chronic peritonitis the fluid 
is turbid, often hemorrhagic, with high specific gravity and many leuko- 
cytes; for differentiation see pages 615 and 616. (g) The peculiar pig- 
mentary cirrhosis of hemochromatosis (diabete bronze) was described by 
Troisier (1871), named by Recklinghausen and elaborated by Hanot, 
Chauffard and Letulle. Some toxic substance destroys the red blood 
cells (hemolysis), and so operates on the cells of the liver, pancreas and 
other organs that they transform the soluble blood pigment into insoluble 
hemosiderin and iron-free hemofuscin. These pigments are found in the 
muscles, intestine, heart, liver and pancreas, whose cells become pig- 
mented, degenerated and necrotic; the pigment passes into the connective 
tissue of the liver, skin and pancreas, with these sequels — cutaneous 
pigmentation like Addison's disease; cirrhosis of the liver and of the 
islands of Langerhans in the pancreas, causing the diabetes, which 
occurred in all but five of the French cases, but less commonly in this 
country; 94 per cent, are males. 

Treatment. — 1. Causal Therapy and Prophylaxis. — These have but 
limited application, save in preventing further injury by syphilis and 
liquors or medicinal tinctures. Antisyphilitic treatment may help all 
forms of cirrhosis. 

2. Medicinal Treatment. — Cirrhosis cases come under observation 
only after contracting connective tissue has formed. Naunyn and Rol- 
leston advocate potassium iodide and ammonium chloride. 

3. Diet. — Meat is tolerated not as well as skimmed milk. Rich or 
highly seasoned foods are to be avoided. 

4. Symptomatic Treatment. — The treatment instituted in chronic 
gastritis or alcoholism (q. v.) may be indicated. Flatulence is met by 
calomel in fractional doses, and salol 10 grains p. c, though it may cause 
renal irritation. Diarrhea should not be checked until the bowels have 
been cleansed, for it is eliminative. Unusual splenic intumescence may 
be treated by purging, for it is often a forerunner of hematemesis. Hema- 
temesis indicates absolute rest, horse serum and rectal feeding, as in 
gastric ulcer. Pain is controlled by local heat, calomel and salines. 
Nervous symptoms necessitate the same treatment as uremia, with 
sodium bicarbonate for the acidosis. 

5. Ascites. — Ascites is seldom benefited by the cardiants, sweats, 
diuretics or purges. Early repeated punctures may induce adhesions 
and consequent collateral circulation (see page 616). 



BILIARY CIRRHOSIS 573 

6. Operation. — Talma and Van der Meulen (1889) recommended 
operative measures, which were later amplified in various ways, to induce 
a collateral circulation; these consist of sewing the omentum to the 
abdominal wall, abrading the surface of the liver to promote adhesions 
and Widal reports a successful Eck's fistula. Bircher collected (1908) 
343 operations; the immediate mortality was 6 per cent.; of the sur- 
viving cases, 13 per cent, were improved, 33 per cent, recovered and 48 
per cent, were not improved. The ascites and collateral circulation 
involve vital as well as mechanical considerations; perhaps lessening 
of venous tension in the portal circuit helps the liver function. 



BILIARY CIRRHOSIS. 

Definition. — A cirrhosis characterized by fibrosis of an intralobular 
type, enlargement of the liver without contraction, splenic enlargement, 
chronic icterus without gross obstruction of the bile vessels, paroxysmal 
fever and absence of portal stasis. It is known as Hanofs disease (1876). 
The term hypertrophic cirrhosis is unfortunately ambiguous. 

Etiology. — Its etiology is obscure. Alcoholism is not a factor. Some- 
times it apparently results from (a) infection, either hematogenous, or 
an ascending cholangitis, (b) Age. Most cases develop between the 
twentieth and thirtieth years; it is rare after forty; a considerable 
percentage occurs in the young, especially in India, (c) Sex. Over 80 
per cent, of adult cases are males. 

Symptoms. — The onset is characterized by early icterus, less often by 
asthenia, fever, dyspepsia, diarrhea, splenic or abdominal pain. 

Cardinal Symptoms. — 1. The liver is uniformly enlarged and may 
weigh 2000 to 4000 gm. Its surface is smooth and its edge even, though 
somewhat blunt. Its pathology is considered under diagnosis. Its dul- 
ness extends from the fourth rib in the nipple line to the umbilicus or 
even to the iliac crest; it visibly bows outward the right costal arch and 
its weight drags down the right shoulder. The gall-bladder is not 
enlarged. The liver progressively increases, often paroxysmally with 
fever, pain and increased icterus. It never shrinks, except when com- 
bined with portal cirrhosis. 

2. Icterus develops early and is constant, permanent and characteristic. 
It is usually intense. It is due to obstruction of the smaller bile vessels; 
perhaps also to oversecretion of bile (polycholia) or bile pigments 
(polychromia) . The skin may become green or brown, frequently with 
itching, xanthelasma and eczema. 

3. The spleen is hypertrophied, usually relatively more than the liver, 
averaging 400 to 1000 gm. in weight, but sometimes actually outweighs 
it (2600 gm.), especially in infantile forms. It is hard, smooth and 
evenly increased in all its elements and dimensions. It is distinctly 
palpable and often clearly visible. 

Other Symptoms. — Digestive. — Nausea, vomiting, dyspepsia and tym- 
panites are uncommon. Diarrhea is frequent. The normal or diarrheal 
movements contain bile in over 90 per cent, of cases. 



574 DISEASES OF THE LIVER 

Nutritive. — Nutrition is maintained for years, but wasting subse- 
quently appears. Infantilism may be as marked as in cretinism or con- 
genital syphilis. Gilbert and Lereboullet collected 40 cases of clubbed 
fingers from hyperplasia of the soft tissues. 

Urinary. — The urine is highly colored, bile-stained, increased in 
amount, and may contain urobilin, indican or albumin. 

Circulatory. — The pulse is not slow; the often dilated heart may 
reveal a systolic murmur; dyspnea is frequent from pressure on the 
diaphragm by the swollen liver and spleen; the blood shows secondary 
anemia, decreased coagulability and moderate leukocytosis. Arthritis 
and neuritis are rare complications. 

Diagnosis. — The following table shows the essential pathological and 
clinical points of contrast with the portal type: 

Portal (Atrophic) Cirrhosis. vs. Biliary (Hypertrophic) Cirrhosis. 

1. Etiology; alcoholism; over forty years Infection; under forty years. 

of age. 

2. Liver, large or small (possibly both in Always large and to greater degree. Never 

succession) ; often shrinks. shrinks in pure forms. 

Granulations; larger. Small; very fine. 

Yellow. • Dark, icteric, green. 

3. Connective tissue ensnaring several Begins in lobule (monolobular or insular) 

lobules (multilobular or annular), around smaller bile radicles (cholangitis), 

and around portal radicles. in early stages at least. 

Distinction between connective tissue Not sharp, 
and lobules sharp. 

Connective tissue firmer, more fibrous; More delicate, reticular, richer in cells, em- 
more elastic tissue. bryonal. 

Contracts. No contraction (elephantiasis hepatis.) 

4. Liver cells, early fatty, degenerate, dis- Seldom fatty, normal for long time, regen- 

appear. erate, pigmented. 

5. Portal system cannot be injected Easily injected. 

6. Bile vessels. (Proliferating bile vessels in biliary form are not characteristic, and are 

probably merely compressed rows of liver cells.) 

7. Icterus infrequent, a complication ; when Constant throughout course, though the 

present, usually catarrhal. stools contain bile. 

8. Ascites rarely absent in advanced cases. Absent in all (except mixed forms). 

9. Collateral circulation — usual. Never. 

10. Hematemesis, frequent, early, mechanical. Very rare, late, cachectic or toxemic. 

11. Constipation usual. Diarrhea frequent. 

12. Duration of two or three years. Five to ten years. 

13. Death results from hematemesis, neph- Rare; death from hepatargia (cholemia) 

ritis, tuberculosis, peritonitis. with fever, delirium, typhoid state. 

It is a rare affection and a diagnosis of biliary cirrhosis is too often 
made. If the cardinal features under its definition are borne in mind 
it is differentiated with ease from hepatic cancer, echinococcns (q. v.), fatty 
and amyloid liver and Band's disease (see diagnosis of portal cirrhosis). 
Obstruction of the bile ducts may produce an enlarged gall-bladder (v. 
Icterus) ; the stools are usually but not necessarily acholic (e. g., in stone 
of the common duct). The spleen is not large. (It may be stated that 
some recognize a biliary cirrhosis due to chronic obstruction of the duct; 
simple mechanical obstruction never causes fibrosis, though it may follow 
ascending cholangitis. The liver is far less large in this obstructive type 
and is seldom hard.) Jn hemochromatosis and pigmentary cirrhosis 
icterus is absent and glycosuria is present jn about 85 per cent, of cases. 
(See Differentiation, page 587). 



ABSCESS OF THE LIVER 575 

Treatment. — The treatment is that of portal cirrhosis; no known 
means stops the formation of connective tissue. A generous diet may be 
given. Cold and dampness are especially to be avoided. Calomel in small 
doses (grain -^V~ Tir t- i- d.) may be given for weeks at a time and the 
salicylates and simple salines are sometimes beneficial. Operative 
relief by drainage of the gall-bladder is unwarranted and in the reported 
cases the true biliary cirrhosis is often confused with obstructive icterus. 

ABSCESS OF THE LIVER. 

Suppurative hepatitis occurs in 1.5 per cent, of autopsies; 97 per cent, 
occur in males. 

Varieties. — 1. In the septic type (55 per cent, of cases) the hepatic 
artery is the usual carrier of infection; the primary focus is usually in 
the external parts, especially the skull (Hippocrates), osteomyelitis, 
pulmonary abscess or gangrene, putrid bronchitis and, less often, from 
ulcerative endocarditis. Liver abscess occurs in 15 per cent, of surgical 
septicopyemias. Infected thrombi in the peripheral veins may become 
detached, infarct the lungs and thence reach the arterial circulation. In 
rare cases infective material may fall back from the cava into the hepatic 
vein, known as retrograde embolism. The bacteria are those enumerated 
under sepsis — the pyogenic organisms, pneumococcus, colon and typhoid 
or paratyphoid bacilli. 

The symptoms are obscured by the general toxemia and multiple 
abscesses scattered through the liver usually produce few decisive local 
symptoms. The liver enlargement is uniform and generally indistin- 
guishable from the cloudy swelling of sepsis; fluctuation is rare; the 
portal circulation is rarely obstructed; pain and tenderness are usually 
present; jaundice is inconstant; the spleen is swollen from sepsis; the 
course is rapid. 

2. The second variety, from infection through the portal vein (31 per 
cent.), has been known since Morgagni's time and is clinically the most 
important type. Any ulcerative or suppurative affection in parts con- 
taining the portal branches may be causal, for instance, amebic dysentery 
(the most frequent cause), appendicitis (in 6 per cent, of its fatal cases), 
neglected hemorrhoids, gastric ulcer or cancer and disease of the bile 
vessels. Pyogenic organisms, the Ameba dysenterise, foreign bodies 
(as fish-bones, pins and parasites) may enter by the portal circulation. 
Pus organisms may infect tuberculous, echinococcic or actinomycotic foci, 
of which latter 40 cases are recorded. The lesion is (a) the solitary or 
tropical liver abscess (v. i.) or (6) there may be suppurative pylephlebitis, 
which is less a suppuration of the liver substance than an inflammation 
in the portal vein itself, following in a dendritic fashion through all of 
its intrahepatic ramifications; its branches are distended and present 
small accumulations of pus, which may appear as yellowish foci through 
the capsule, but show more clearly on section as portal vein suppuration ; 
the whole liver may be involved or certain areas may be exempted by 
total thrombotic occlusion of the larger branches. In some cases the 
purulent thrombophlebitis may be traced back to the original lesion in 



576 DISEASES OF THE LIVER 

the stomach or intestine; the liver is enlarged but the diagnosis is rarely 
more than a probable one. 

3. The third variety is infection by the bile vessels (10 per cent.), in 
which an ascending cholangitis (q. v.), often calculous in origin, produces 
multiple small abscesses throughout the liver substance; this is rather 
similar in appearance to the pylephlebitic form. 

4. Infection in infants through the navel is infrequent. 

5. Direct involvement of the liver by contiguity, may occur in suppuration 
of the gall-bladder or gastric ulcer. 

Solitary or Tropical Abscess. — The abscess is solitary in 75 per cent, 
of cases; in 11 per cent, there are two and in 14 per cent, more than two 
foci. Twenty to 30 per cent, of cases of amebic dysentery, by far the 
most common cause, are complicated by liver abscess. Amebic abscess 
may even occur without intestinal ulceration, though amebse are found 
in the stools; in 5 out of 27 of Futcher's cases there were no intestinal 
symptoms. Bacillary dysentery is rarely a cause, and trauma, pyemia, 
typhoid or hydatid cysts occasionally. Though seen in the Southern 
States and sometimes in the North, it occurs chiefly in the tropics, and 
among Europeans; alcoholism and a rich diet are predisposing factors; 
97 per cent, occur in males and 50 per cent, in those between twenty and 
thirty years of age. 

Pathology. — Amebse reach the liver by the portal vein and cause 
necrosis by their toxins, followed by suppuration. The smaller foci 
contain glairy, gelatinous, translucent fluid ; the larger foci contain white, 
yellow, green, reddish (like anchovy sauce) or serous, bloody or viscid, 
chocolate-colored fluid. Absence of leukocytes in the walls and contents 
is pathognomonic. Red disks and necrotic liver cells are frequent and 
the pus is usually sterile. The amebse are more abundant in the abscess 
wall than in its contents and may be found outside of the abscess, 
necrosing the liver cells. In contrast to other abscesses, the walls of the 
amebic type are soft, ragged and show little granulation or fibrous tissue. 

Symptoms. — Latency occurs in 13 per cent, of cases. 

1. Septic Symptoms. — {a) Fever is remittent or intermittent, less 
often continuous and in chronic cases there may be a normal or sub- 
normal register, (b) Rigors and sweats are frequent, even independent 
of fever (Lafleur). (c) Leukocytosis occurs in 50 per cent. only. In 43 
uncomplicated dysentery cases the leukocyte count was above the 
average count of the abscess cases in 23.4 per cent. (Futcher). (d) The 
pulse is small and frequent, (e) Progressive emaciation is usual, and 
the facies is a combination of hectic, subicterus and cachexia. (/) The 
urine is febrile and may contain albumin or albumose. 

2. Hepatic Symptoms. — (a) The liver is enlarged from the abscess and 
from sepsis. The abscess in 70 per cent, is located in the right lobe; venous 
blood from the pancreas and intestine is conveyed to the right lobe 
(whence its involvement in intestinal ulceration or cancer), while the 
blood from the stomach and spleen finds its way to the left lobe. The 
enlargement is more often upward than downward, wherein abscess differs 
from cancer and resembles echinococcus. The swelling is often localized, 
occasioning a dome-like dulness on the upper border of the liver (Frerichs), 



ABSCESS OF THE LIVER 577 

which may be corroborated by the x-rays, and may also give Grocco's 
dulness to the left of the vertebrae; in other cases there is bulging of the 
lower interspaces or of the hypochondrium. The entire organ may be 
greatly swollen, as in one abscess which contained 2\ gallons of fluid. 
When it occurs below the ribs, fluctuation in the liver and, less often, 
edema of the abdominal wall may be noted. The liver consistence may 
be increased at first, (b) Pain is usually present and is due to increased 
weight or to capsular tension and perihepatitis or pleurisy, causing a 
friction rub, or adhesions in more chronic cases. The patient usually 
lies on the back or right side (to avoid pain caused by sagging of the 
liver in the left lateral decubitus). Pain is referred to the right shoulder 
in 17 per cent., being reflected from the phrenic filaments on the liver 
convexity along the phrenic nerve to the acromial branch of the fourth 
cervical nerve; in rare cases the deltoid may waste, (c) Tenderness 
over the liver is usually circumscribed. The right rectus is frequently 
tense. 

3. Other Symptoms; Complications. — (a) Icterus occurs in 16 per 
cent, of cases; it may be slight from sepsis or compression of some 
bile ducts within the liver, or it may be complete from catarrh of the 
common duct. (6) The spleen is seldom enlarged, except from a causal 
septicopyemia, (c) A dry spasmodic reflex cough may be noted (tussis 
hepatica). (d) Rupture may be the first sign of abscess of the liver. In 
Waring' s 300 cases, 56 per cent, remained intact, 16 per cent, were 
operated on and 28 per cent, ruptured, (i) It occurs into the lungs in 
43 per cent.; lung abscess results more often from direct rupture than 
from indirect metastasis. The patient presents signs of lung abscess 
(q. v.) and expectorates chocolate-, anchovy- or cream-colored pus con- 
taining amebse, often liver and lung tissue, hematoidin crystals and 
perhaps bile. Death may be caused by profuse hemoptysis, (ii) Rup- 
ture into the pleura causes empyema (15 per cent.). Pleurisy, both 
fibrinous and serous, may also result from infection passing through 
the lymphatics of the diaphragm; a right-sided friction rub, serothorax 
or empyema always suggests the possibility of an hepatic etiology, (iii) 
Rupture into the peritoneum causes localized or diffuse peritonitis (15 
per cent.). A subacute serofibrinous peritonitis or an encapsulated 
serous effusion over the liver rarely results, (iv) Rupture into the 
bowels (colon 2 per cent, and duodenum 1 per cent.) gives pus, some- 
times in large amounts in the stools, (v) Less frequent are ruptures 
into the stomach, pericardium, pelvis of the kidney, portal or hepatic 
vein, inferior cava, bile vessels or abdominal wall, (e) Less frequent 
complications are pyloric obstruction (from abscess of the left lobe), 
pseudorheumatism or clubbed fingers (from toxemia), cerebral abscess 
and intestinal obstruction. 

Diagnosis. — Diagnosis is based on (a) an etiological factor; (b) symp- 
toms of sepsis; (c) hepatic signs, e. g., localized enlargement, pain and ten- 
derness; the x-rays may be useful when the bulging of the convexity is 
covered by the lung; (d) exploration with the aspirating needle, which 
the author has seen result in two deaths from peritonitis and one from 
an enormous hemorrhage into the peritoneum; puncture should be 
37 



578 DISEASES OF THE LIVER 

performed only when an operation can be done immediately after pus 
is found; pus is far less often withdrawn in multiple small abscesses 
than in the large solitary form. 

Differentiation. — Five types of liver abscess are often described: 
(a) The latent, (b) typhoid (page 46), (c) malarial, intermittent, (d) 
phthisic, and (e) a type declared by rupture. 

Subphrenic abscess simulates pneumothorax (q. v.) rather than liver 
abscess, because of the presence of tympany; in its etiology and treat- 
ment it resembles liver abscess (see page 611). In gall-stones, with or 
without suppuration, the fever usually occurs in paroxysms separated 
by long intervals, the history is different and marasmus is rare. Dif- 
ferentiation from pleurisy, echinococcus and cancer is considered under 
these topics and on page 587. 

Prognosis and Treatment. — Ninety-three per cent, of unoperated cases 
die from rupture (peritoneal, pleural, pulmonary), sepsis and amyloid 
disease. It is possible for an abscess to desiccate or to heal after break- 
ing into the lung or bowel, but this cannot be depended upon. The 
treatment is solely operative; Solonoff estimates the mortality of 1094 
cases at 30 per cent. 

TUMORS OF THE LIVER. 

Tumors of the liver are chiefly carcinomata. Benign tumors possess 
little clinical interest, as fibroma, lipoma, teratoma, adenoma or angioma ; 
single adenoma may develop from the liver cells or bile ducts; multiple 
adenomata occur chiefly in cirrhosis. Three cases are reported of adrenal 
"rests," and scant 20 of sarcoma; it may develop as a single primary 
tumor, multiple primary tumors or diffuse infiltration; a melanotic 
growth is almost always secondary to melanotic sarcoma of the eye or skin. 

Cancer of the liver occurred in 2.7 per cent, of Virchow's autopsies, 
and ranks fourth among internal cancers (in order of frequency, uterus, 
stomach, mamma and liver), (a) Primary cancer is 20 to 48 times as 
infrequent as secondary cancer; 66 per cent, occur in males. It originates 
from the liver cells (88 per cent.) or bile vessels (12 per cent.). The main 
forms are observed (i) as a sharply outlined massive local swelling (in 
23 per cent, of EggeFs 163 cases); (ii) as sharply demarked multiple 
nodes of moderate size (in 65 per cent.) of which one of the tumors is 
primary and the rest secondary; (iii) as diffuse infiltration, fusing with 
the parenchyma (in 12 per cent.) ; (iv) the last form develops in hepatic 
cirrhosis (or hepatic cyst). Metastases occur in 66 per cent. (6) Second- 
ary cancer results from primary cancer in the stomach (33 per cent.), 
colon (12 per cent.), esophagus, pancreas, gall-bladder, uterus, ovaries, 
mamma, etc., by metastasis or contiguity; cancer cells may enter by 
the portal vein and hepatic artery, much less frequently by retrograde 
metastasis through the hepatic vein and never by the lymph vessels, 
as their current flows from within to without the liver. 

Symptoms. — 1. Hepatic Symptoms. — (a) The liver enlarges rapidly, 
even to eight times its normal size and may weigh 30 to 40 pounds. Its 
edge is uneven; on its surface are lumps which may present a central 



TUMORS OF THE LIVER 579. 

umbilication. Great unevenness is more characteristic of secondary than 
of primary tumor, in which the liver is more uniformly swollen. The 
enlargement is chiefly downward, though sometimes upward from ascites, 
tympanites or adhesions. Nodules in the falciform ligament may be 
felt near the navel or linea alba. Sudden increase in size occasionally 
results from hemorrhage due to icterus. There is no enlargement when 
the nodules are few and small, and the liver is smaller than normal in 
10 per cent, of cases (liver cirrhosis plus malignant adenomata). (6) 
Hepatic pain is more conspicuous than in any other liver lesion, from cap- 
sular tension, perihepatitis, pleuritis or, less frequently, from rupture of 
tumor particles into the bile passages, simulating gall-stones, (c) The 
liver is often tender, (d) Exceptionally there may be pulsation trans- 
mitted from the aorta or a venous hum over the liver. 

2. Cachectic Symptoms. — These are adynamia, marasmus, anorexia, 
secondary anemia, leukocytosis (in any carcinoma, but especially in 
hepatic), stupor and illusions, probably from the katabolic toxins elabo- 
rated by the tumor, and hepatargia. Fever may result from the tumor 
alone, or terminal infection. 

3. Compression Symptoms. — (a) Jaundice occurs in over 50 per cent., 
more frequently in secondary than in primary cancer and usually from 
mechanical pressure on the larger bile ducts by the tumor or carcinoma- 
tous glands. Pressure on the ducts within the liver often produces 
moderate jaundice and some bile then appears in the stools; complete 
icterus may result from concomitant catarrhal or calculous obstruction, 
especially significant when there is no ascites. Exceptionally the tumor 
grows into and along the bile ducts, thereby totally obstructing them. 
(b) Ascites is present in 50 per cent, of cases. It is usually moderate in 
degree and results from pressure on the portal vein, peritonitis or pyle- 
thrombosis; occasionally it is due to the cirrhotic form of cancer, growing 
of the tumor into the hepatic or portal vein, rupture — perhaps with 
syncope and great hemorrhage — of a cancer nodule into the peritoneum, 
or rarely to plugging of the liver capillaries by the pigment of a melano- 
sarcoma. A collateral circulation or perihepatic friction may be noted. 
The fluid is usually serous or hemorrhagic, rarely adipose, chylous, 
opaque or melanotic, (c) Other compression symptoms include splenic 
tumor from marantic pylephlebitis (14 per cent.), hydronephrosis, vom- 
iting, dyspnea and edema. 

4. Other Symptoms. — The cervical glands are seldom swollen unless 
there is coincident gastric cancer. Carcinomatous nodes in the navel 
or skin over the liver are due to regional extension. In liver cancer 
combined with cirrhosis any cirrhotic symptom may occur. The urine 
shows increased destruction of the tissue nitrogen; acetone and diacetic 
and beta-oxybutyric acids, indican, leucin and tyrosin are not infrequent. 
The urine is decreased, high-colored and often icteric. Albuminuria is 
due to stasis and toxemia. Melanuria (sarcoma) is sometimes detected 
by adding to the urine a solution of ferric chloride; the pigment exists 
in the blood as melanin or melanogen; melanuria nearly always indicates 
a melanotic tumor of the liver and is often confounded with indicannria 
and alkaptonuria, 



580 DISEASES OF THE LIVER 

Diagnosis. — The chief features are rapid enlargement of the liver, 
irregular tumors, pain, icterus, ascites, cachexia and in 50 per cent, of 
cases the recognition of the primary tumor. (See page 587.) 

Differentiation. — Cirrhosis (see both forms); syphilis (q. v.); the 
amyloid liver is equally large and causes confusion only when complicated 
by gummata; amyloidosis of the spleen, kidneys and intestines usually 
coexists with amyloid liver. Hydatid cysts develop more slowly and 
earlier in life and cachexia appears late, if at all. The rare multilocular 
echinococcus produces enlarged liver, ascites and icterus, but the spleen 
is also enlarged; puncture may give characteristic findings. Puncture 
often excludes those doubtful cases of cancer in which fever, leukocytosis 
and semifluctuation of the necrotic neoplastic nodes simulate liver abscess. 
Congested liver; the writer saw 4 cases of nutmeg liver in which stasis 
caused more local than general hepatic enlargement. The corset liver 
can be easily differentiated if the general symptoms, such as cachexia 
and the compression symptoms of cancer, are duly considered. Cancer 
of the stomach (q. v.) is readily differentiated by its chemism and stag- 
nation; gastric cancer may cause hepatic involvement. Renal or adrenal 
tumors are covered by the inflated colon, encroach less upon the thorax, 
evert the ribs less, and often are separable from the liver by an interven- 
ing strip of tympany, which occurs in but 13 per cent, of hepatic tumors. 

Differentiation between primary and secondary tumors is somewhat 
irrelevant, as the causal growth leading to hepatic metastasis is latent 
in 50 per cent.; the following characteristics are subject to many excep- 
tions: the solitary tumor, its rapid growth, less emaciation, more rapid 
course and death in less than four months. Secondary tumors cause 
death within seven months from cachexia, ascites and intercurrent disease, 
as pneumonia — or in a shorter period, from hemorrhage, peritonitis, icterus, 
galloping carcinosis or acidosis. 

Treatment. — Treatment is palliative for the pain and ascites except 
when, in very exceptional cases, early operation (for primary growths) 
can be performed. Liicke reported the first recovery, which afterward 
proved to be a gumma; Keen collected 76 operated neoplasms with, 63 
recoveries. 

ECHINOCOCCUS CYSTS OF THE LIVER. 

The parasite is considered on page 305. Its hepatic localization con- 
stitutes 60 per cent, of echinococcus disease. 

Symptoms. — Fully half the cases of liver echinococcus are clinically 
latent. Cases with symptoms show the following liver findings: (i) A 
cyst on the lower border or anterior surface may produce a visible, palpable, 
round and smooth bulge which everts the right costal arch or much less 
often distends the left lobe; cysts in the right lobe may lead to com- 
pensatory hypertrophy of the left lobe. The tumor is as large or larger 
than an orange. It is tense, elastic and dull; on percussion it may fluc- 
tuate and give the "hydatid thrill," a vibration elicited by laying three 
fingers over the cyst and tapping with the middle one; the thrill may 
also occur in ascites and sarcoma. The cysts rarely contain gas, due to 



ECHINOCOCCUS CYSTS OF THE LIVER 581 

the Bacillus coli. In large cysts (36 to 70 pints are reported), the liver 
may tip so that the right lobe is lower and the left higher than normal, 
(ii) Cysts on the convexity crowd the diaphragm upward, cause symptoms 
resembling pleurisy (q. v.), produce a dome-like dulness, as in cancer and 
may compress the lung or heart, (iii) Liver pain and tenderness are rare 
without suppuration, which may induce perihepatitis; pain may be 
referred to the right shoulder, (iv) Exploratory puncture may precipitate 
severe nervous toxemia and cardiac collapse, as described on page 306, 
where also the finding of pus, membrane, chemical contents and hooklets 
are enumerated. 

Rupture may occur into the lungs (in 11 per cent, of liver echino- 
coccus); it may simulate phthisis or gangrene of the lungs; cysts may 
rupture into the pleura, peritoneum (witheosinophilia), kidney, stomach, 
bowel, bile passages, pericardium, portal vein and cava; heart embolism 
or external rupture may occur. 

Pressure symptoms are rare, as icterus (5 per cent.), ascites, albumin- 
uria, caput Medusce, edema of the legs, dyspnea or vomiting. In some 
cases there is a distaste for fat or meat. The eosinophiles are usually 
increased in non-suppurating cysts. Urticaria may occur after puncture 
or rupture or without either incident. 

Diagnosis. — Diagnosis depends on the history of the case, including 
contact with dogs; the smooth, round tumor; the thrill; slow develop- 
ment; the infrequency of constitutional disturbance, pain and fever, 
the signs predominating over the symptoms. 

Diffekentiation. — (a) From other liver cysts; the small cysts in 
cirrhosis and obstructive icterus are of no clinical importance. Simple 
serous cysts may, in exceptional cases, hold several (even 13) pints; 
they rarely cause symptoms, rupture or hemorrhage. Diffuse, congenital, < 
cystic disease may cause dystocia; in adults also the cysts are probably 
developmental in origin and are associated with cystic kidneys, in 15 
per cent, of cases; Moschcowitz collected 85 cases; they are usually 
multiple and subcapsular and are often associated with other congenital 
anomalies, such as hare-lip, and are due to inflammatory hyperplasia of 
aberrant bile ducts or to congenital obstruction in them. Hoffman 
reported 18 operated cases. (b) Malignant disease causes cachexia, 
more pain than echinococcus, multiple tumors, ascites and icterus, (c) 
Syphilis of the liver (q. v.). (d) From pleurisy; the z-rays may show 
the localized tumor on the liver convexity; the upper line of pleuritic 
dulness is much less often convex upward; there may be thoracic symp- 
toms, as hemoptysis, when there is rupture into the lung; the sputum 
or aspirated fluid shows the diagnostic hooklets. (e) In rare cases a 
pendulous, pedunculated, movable cyst may resemble a pancreatic cyst, 
enlarged kidney, gall-bladder or ovarian cyst. Rupture into the bile 
passages may simulate the pain of gall-stones, (f) Liver abscess; there 
may be doubt in suppurating cysts; the eosinophiles are not increased 
in liver abscess (page 587). 

Prognosis. — Cysts may calcify or indurate. The mortality of rupture 
into the peritoneum is 90 per cent., into the pleura 80, bile ducts 70, 
bronchi 57, stomach 40, intestines 15 and externally 10 per cent. 



582 DISEASES OF THE LIVER 

Treatment. — When drainage by the trochar is performed (Hippo- 
crates), 60 per cent, of cases recover. A few die suddenly from a tox- 
albumin, formed when the parasite dies; it causes urticaria, convulsions, 
cardiac failure and other symptoms similar to mussel-poisoning. Direct 
surgical intervention is attended with the least risk. 

Multilocular or Alveolar Echinococcus.— This form is due to another 
parasite (see page 307) ; 100 cases are recorded. 

Symptoms. — The right lobe of the liver alone is involved in 65 per 
cent, of cases and the left alone in 10 per cent. The liver is fibrosed, 
nodular and seldom fluctuates. This rare affection is attended by splenic 
tumor (90 per cent.), icterus (80 per cent.), dyspepsia, ascites and, less 
commonly, by fever, polyuria, collateral circulation, emaciation and 
metastases in the heart and lungs; death may occur after years from 
cholemia or gastro-intestinal hemorrhages. The diagnosis is very diffi- 
cult, especially from cancer. The only hope of recovery is in extirpation. 



FATTY LIVER. 

"Fatty liver" (hepar adiposum) includes infiltration and degeneration; 
they may be considered together. 

Etiology. — (a) Obesity and (b) decreased oxygenation from carcinosis, 
rickets, profound anemia, stasis and kindred causes may produce fatty 
liver, (c) Toxemias, as tuberculosis, the acute infections, infantile 
diarrhea, acute yellow atrophy or suppuration, (d) poisons, as phosphorus, 
arsenic or chloroform, and (e) local diseases of the liver, as cirrhosis or 
nutmeg liver, are etiological factors. 

Pathology. — The fat may amount to over 40 per cent, (normally 2 
to 5 per cent, of its weight). The liver is enlarged and may weigh 4500 
gm. Its surface is smooth, its edges rounded, consistence is decreased 
and its color yellow. On section it is anemic, smooth and yellow when 
oleic acid predominates or pale when there is more palmitin and stearin. 
Slight quantities are detected only on microscopic examination. When 
cut with a warm knife the fat is seen on the blade. Microscopically, fat 
is seen which, in fatty infiltration, is located principally in the periphery 
of the lobules and obscures the liver cells; when the fat is dissolved by 
ether, the normal liver cells are clearly seen. In fatty degeneration, fat 
forms at the expense of the liver cells, i. e., the percentage of albumin is 
decreased. The statement that fatty infiltration occurs in large and 
fatty degeneration in smaller globules is not wholly correct. Pathologists 
consider infiltration more important. 

Symptoms. — (a) The positive findings are as follows: the liver is sym- 
metrically enlarged and smooth and rarely extends below the navel. Its 
edge is rounded, soft and usually palpable, even in obese persons. (6) The 
negative findings are absence of pain, tenderness, icterus, splenic tumor, 
ascites or gastro-intestinal hemorrhage. 

The diagnosis is considered on page 587. 



AMYLOID LIVER 58 



AMYLOID LIVER. 



o 



Amyloid degeneration was first clearly described by Rokitansky. 

Etiology. — (a) Ulcerative tuberculosis of the lungs or bones causes 
over 50 per cent, of amyloidosis, and (b) inveterate syphilis, particularly 
ulcerative and osseous types, 25 per cent, (c) Chronic suppuration has 
become uncommon since the introduction of antisepsis. Krawkow 
produced amyloid degeneration experimentally by inoculations of the 
staphylococcus. (d) As exceptional causes, intestinal ulcerations, 
exhausting diarrheas, rickets, leukemia, pseudoleukemia and ulcerating 
neoplasms may be mentioned; 78 per cent, of cases occur in males. 

Pathology. — Amyloid degeneration is much less frequent in this country 
than in Europe. Its localization, in order of frequency, is in the spleen, 
kidneys, liver and intestines. The liver is uniformly enlarged and may 
weigh 5000 to 6000 gm., even in a child. It is hard, smooth and very 
pale. Its edges are blunt. On section the appearance is waxy, speckled, 
resembling raw ham, the edges slightly translucent and the lobules 
indistinct. If a thin slice is placed in diluted Lugol's solution, the amyloid 
areas assume a brown color (Virchow), the name (amyloid) referring to 
this starch-like reaction; the waxy substance, however, is a proteid and 
reaches the liver by the hepatic capillaries, whence it is first deposited 
in the middle zone of the lobule, and later infiltrates the central and 
peripheral zones. It is essentially an infiltration. 

Symptoms. — The large, tense, symmetrical, painless, smooth liver, 
with rounded edges, is characteristic. Its dimensions may attain those 
of cancer. The onset and development are usually slow, but acute 
amyloid may develop in a month. Splenic amyloid enlargement is usually 
also noted, as well as albuminuria from renal amyloidosis (q. v.). In only 
0.8 per cent, of amyloid degeneration is the liver alone involved. Gastro- 
intestinal symptoms, as nausea, vomiting and diarrhea, may result from 
amyloidosis of the alimentary capillaries. In advanced cases cachexia, 
edema and ascites may develop. Hepatargia is rare. 

Diagnosis. — Diagnosis depends on (a) the recognition of a cause; 
(b) the characteristic, smooth, symmetrical enlargement, which is less 
hard than that of cirrhosis; (c) the associated amyloid disease of the 
spleen, kidney and alimentary tract; (d) the absence of icterus (very 
rarely from amyloid portal glands) and of portal stasis (ascites is an in- 
frequent, late and renal symptom) ; and (e) the small amount of urobilin 
in the stools. Differentiation from cirrhosis (q. v.) and cancer (q. v.) 
presents no difficulties. Gummata in the liver plus amyloid disease 
may cause confusion. No diagnosis is possible in the exceptional cases 
in which the liver is slightly enlarged (because slightly diseased) or in 
which splenic tumor and albuminuria are absent (v. page 587). 

Prognosis. — The prognosis of pronounced cases is unfavorable though 
light grades may exceptionally regress. 

Treatment. — Treatment is prophylactic and symptomatic. 



584 DISEASES OF THE LIVER 



ANOMALIES OF FORM AND LOCATION OF THE LIVER. 

In situs viscerum inversus the liver lies on the left side. Fenger en- 
countered a case of icterus and gall-stones in situs inversus which was 
diagnosticated as acute yellow atrophy! 

Tilting of the liver, dislocation downward by pleuritis, pneumothorax 
or tumors, or upward luxation require but passing mention. 

"Wandering Liver." — Hepar migrans s. mobile occurs in women (88 
per cent.), usually in multipara?. Its causes are those of enteroptosis, 
with which it usually occurs, viz., flaccid abdominal walls, congenitally lax 
suspensory ligaments, lacing or very rarely from traction by a tumor. 
Clark and Dolley collected 118 cases; 1 had a mesohepar attached to the 
diaphragm and absence of the coronary and right lateral ligaments. 

Symptoms. — The onset is usually gradual; in 5 per cent, it is acute. 
Subjectively, oppression over the liver, gastro-intestinal or nervous 
symptoms may be present. Objectively, there is sometimes cardioptosis, 
usually gastroptosis and in 20 per cent, nephroptosis. The hepatic notch 
can be distinctly felt, often also its convex surface and sometimes the 
tense, stretched ligaments. It can be replaced. In a recent case there 
was tympany between the left costal arch and the prolapsed spleen and 
tympany between the right arch and the liver, even though the patient 
was five months pregnant. In very rare instances there may be pain 
similar to gall-stones and ascites or splenic tumor from torsion of the 
portal vein. 

Treatment. — The treatment is (a) mechanical, replacing and supporting 
the liver with binders; (b) symptomatic, for the neurasthenia; (c) dietetic, 
to increase the body weight and (d) operative; hepatopexy cures about 75 
per cent. 

Corset Liver. — The corset liver is found in 25 per cent, of female 
cadavers, but much less frequently here than abroad. Corsets cause 
pressure atrophy of the liver substance, followed by induration, deformity 
and peritoneal thickening, most conspicuously and usually in the right 
lobe. The liver may be merely constricted, dislocated upward or the part 
below the constricting zone may hang loosely as upon a hinge, causing 
confusion with floating kidney or other tumors. The gall-bladder is 
dilated in 60 per cent., but icterus is infrequent. Corset liver is regarded 
as a factor in gall-stone formation. Subjective manifestations are often 
absent. Sometimes paroxysmal syncope and vomiting may occur, due 
to congestion of the snared-off portion. Respiratory excursion prevails 
in most cases. Confusion arises when the intervening gut causes a 
narrow zone of tympany between the hard, hinged segment and the liver 
proper, but even then careful palpation frequently demonstrates its 
continuity with the liver. Congenital tongue-like lobes may be con- 
fused clinically with corset liver; they are often the seat of cirrhosis, 
malignancy, suppuration or syphilis. Treatment is seldom important. 



AFFECTIONS OF THE BLOODVESSELS OF THE LIVER 585 



AFFECTIONS OF THE BLOODVESSELS OF THE LIVER. 

I. Active Hyperemia of the Liver. — A degree of arterial hyperemia 
is physiological during digestion. An accentuation of this condition is 
common in heavy eaters and drinkers and acute infections, in which it 
may be combined with venous hyperemia. Heat is probably not the 
cause of " tropical hyperemia." The alleged vicarious hyperemia from 
suppressed menstruation, the menopause or diseases of the internal 
female genitalia is based on theory. The symptoms resemble those of 
passive hyperemia (v. i.). A simple or milk diet, calomel and saline 
purgation are indicated. 

II. Passive Hyperemia of the Liver. — Etiology. — Passive congestion of 
the liver results from stasis, the stress of which is felt in the efferent 
intrahepatic (sublobular) veins. It results (a) from cardiac insufficiency, 
valvular, particularly mitral diseases, myocardial or pericardial lesions; 
(b) from pulmonary stasis, emphysema, chronic bronchitis, asthma, 
induration or obliterative pleurisy; (c) from stasis caused by spinal 
deformity, aneurysm, mediastinal tumor, perihepatitis or pressure on the 
cava inferior. 

Pathology. — The essence of passive congestion is overfilling of the 
sublobular or the hepatic venous circulation, malnutrition of the liver 
cells (fatty degeneration) and in some advanced cases, increased con- 
nective tissue. The liver is usually symmetrically enlarged, firmer and 
darker red than normal, though hepatic hyperemia lessens after death. 
The capsule is often thickened or edematous. On section the so-called 
nutmeg appearance is noted, but seldom over the entire liver. The 
central veins with their radiating offsets are dark and cyanotic, while the 
periphery of the lobule is yellowish-white from cloudy or fatty change 
(malnutrition or impaired oxygenation). Long-standing congestion 
results in atrophy and pigmentation of the cells in the periphery of the 
lobule (Virchow's red atrophy) ; there is usually increased connective tissue 
with fine granulations, the atrophic cyanotic liver or cardiac cirrhosis of the 
French; fibrosis is for the most part relative or apparent, for the liver 
parenchyma atrophies; true cirrhosis may coexist with cardiac disease. 

Symptoms and Diagnosis. — (a) The causal heart (or lung) lesion has 
its appropriate symptoms, (b) The liver is evenly enlarged, on palpation 
and sometimes on inspection; if ascites is present thrusting palpation 
with the finger-tips usually outlines the organ; the liver may reach below 
the navel or evert the ribs. Its edges are firmer, somewhat rounded, 
sensitive (from capsular tension) and descend with inspiration; the incis- 
ure is clearly felt. If there is relative tricuspid insufficiency, a systolic 
expansile pulsation is detected by palpating with both hands, which are 
separated from each other with each systole, and is differentiated from the 
non-expansile pulsation transmitted from the aorta, (c) The hepatic 
intumescence varies greatly, as the heart responds to rest and digitalis, or 
compensation fails, (d) The skin shows cyanosis and slight icterus; to the 
experienced eye it has a characteristic appearance, probably due to a 
static catarrh of the finer intrahepatic bile radicles, (e) For other symp- 



586 DISEASES OF THE LIVER 

toms and treatment see Valvular Disease; the spleen is seldom enlarged 
save from cardiac infarcts or complicating liver cirrhosis. Ascites is 
usually late in onset and moderate in degree; a cardiac ascites sometimes 
occurs without general edema. Before death there may be signs of renal 
and hepatic insufficiency. In some cases with somnolence, delirium and 
a terminal toxemia, Oertel describes a cytolytic necrosis of the liver with 
stasis, fatty infiltration of the middle zone and hemorrhagic extravasations. 

Differentiation is seldom complicated, for the fundamental heart 
lesion, the evenly enlarged, tender liver, which varies in size from time 
to time, and the slight icterus with cyanosis are usually unmistakable. 
Certain features may sometimes mislead, as the occasional unequal dis- 
tribution of the liver changes, which may suggest tumor, or the tender- 
ness which may resemble suppuration. (See page 587.) 

III. Pyiethrombosis — Pylephlebitis. — Thrombosis or phlebitis of the 
portal vein is practically always secondary to compression or obstruction, 
as liver cirrhosis, with which 33 per cent, of pylephlebitis cases occur; 
to cancer, ulceration, abscess or inflammation of contiguous structures, 
gall-stones, cholangitis and proliferative peritonitis; and to diseases of 
the intima, as phlebosclerosis and syphilitic endophlebitis. Pylephlebitis 
occurs chiefly in males over forty years of age. 

Symptoms. — These may be entirely absent because of collateral com- 
pensation through the hepatic artery or Sappey's accessory portal vein. 
The onset is usually sudden, with symptoms of acute portal stasis. The 
spleen is enlarged in 75 per cent., unless fibrous changes in its pulp or 
capsule prevent its swelling. Ascites develops in 66 per cent, and rapidly 
recurs after tapping. G astro-intestinal symptoms are usual, as hemor- 
rhage (44 per cent.), intense, sudden epigastric pain, vomiting, diarrhea 
or sometimes acute intestinal obstruction. The portal vein is sometimes 
varicose below and is generally obliterated at and above the point of 
obstruction (pylephlebitis adhesiva) ; this leads to shrinking of the liver, 
particularly if the hepatic artery is sclerotic, in which rare event the 
entire liver may be hemorrhagically infarcted. Liver lobulation results 
from antecedent syphilis. Hepatargia and alimentary glycosuria may 
develop. Edema of the abdominal wall, development of a collateral 
circulation and icterus are uncommon. 

Diagnosis. — Diagnosis is difficult, unless the onset is typically sudden; 
otherwise the findings are those of atrophic cirrhosis; a caput Medusa 
indicates occlusion of the portal radicles. The ascites may suggest carci- 
noma or peritonitis or the hemorrhage may simulate gastric ulcer or 
hepatic cirrhosis. 

Course and Treatment. — Death may occur in a few days or six to 
twenty years. Treatment is ineffectual, save in early syphilis. Citric 
acid (5 j) may be given to lessen thrombosis. 

Pylephlebitis suppurativa is a pyemia of the portal vein; metastasis 
or extension occurs in the main portal trunk and its branches from infec- 
tion of its radicles of origin; inflammations in the gastro-intestinal tract 
are its cause in 75 and appendicitis in 40 per cent, ("appendicular liver") 
and gall-stones, infected piles and pancreatic or umbilical suppuration 
cause most of the other cases (v. page 575). 



DIAGNOSIS OF AFFECTIONS OF THE LIVER 



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588 DISEASES OF THE GALL-BLADDER AND BILE VESSELS 

The symptoms are those of the original disease, sepsis and portal stasis. 
In very rare cases the thickened vein may be palpated. The spleen is 
enlarged, chiefly from sepsis, the liver is tender and somewhat enlarged 
and icterus occurs in over 50 per cent. The diagnosis is always difficult, 
but is based on symptoms suggesting liver abscess (though without the 
findings) and sepsis. Treatment is futile. 

IV. Affections of the Hepatic Artery and Vein. — Infarction of the 
hepatic artery with complete necrosis of the liver is very rare. Aneurysm 
(v. page 409). 

Thrombosis of the hepatic veins, of which only 12 cases are reported, 
may follow perihepatitis or, less often, compression by a neoplasm or 
fibrous obliteration of the inferior cava. Ascites and splenic tumor 
sometimes result. Suppurative thrombosis is always secondary to liver 
suppuration. Retrograde embolism (Heller) is mentioned under Liver 
Abscess. 



DISEASES OF THE GALL-BLADDEE AND BILE 

VESSELS. 

ICTERUS. 

Jaundice is a symptom of various affections of the liver and bile 
vessels; it is characterized by staining of the skin, mucosae and urine by 
retained bile pigments. 

Etiology. — Most cases of icterus are due to obstruction within or about 
the liver and biliary system; little obstruction is necessary because the 
bile is secreted under low pressure, (a) Hepatic diseases. It is (i) fre- 
quent in acute yellow atrophy, biliary cirrhosis, multilocular echinococcus, 
carcinoma, passive congestion and syphilis; (ii) infrequent in atrophic 
cirrhosis, unilocular echinococcus and abscess; (hi) absent in fatty and 
amyloid liver and in simple pylephlebitis. (See page 587.) Possibly 
functional liver disturbance may produce icterus (parapedesis of bile or 
" diffusion-icterus")? analogous to transient albuminuria (in its relation 
to B right's disease). (6) Diseases of the biliary tract, as (i) catarrhal, 
croupous or purulent inflammation; (ii) calculous obstruction; (iii) con- 
genital and (iv) cicatricial occlusion; (v) malignant growths; (vi) parasitic 
obstruction by ascaris, distoma or hydatid vesicles, (c) Disease in 
contiguous structures, as (i) duodenal ulcer, cicatrix, catarrh or cancer; 
(ii) tumors of the colon or lymph glands ; (iiji) tumors or inflammation of 
the pancreas, stomach, kidney, omentum, mesentery and peritoneum, 
and (iv) rarely from aneurysm, (d) Hematogenous or urobilin icterus. 
It was formerly maintained that toxic and toxemic conditions, breaking 
down the blood cells (hemolysis) cause hemolytic icterus. It is now 
thought that most of these cases are due to blocking of the capillaries 
by fibrin, thickening of the bile or cholangitis of the smallest bile radicles, 
though the obstruction is not complete; Eppinger maintains that the 
smaller bile radicles dilate and sometimes rupture, letting the bile into 



ICTERUS 589 

the lymph vessels which absorb it. The jaundice in these cases is slight, 
bile pigment (bilirubin) is not found in the urine and the stools are bile- 
stained. This type occurs in various infections, pernicious anemia, and 
poisoning by phosphorus, chloroform, etc. 

Icterus neonatorum, (a) The physiological type occurs in 66 per cent, 
of children; it appears on the second day, lasts two weeks and is never 
fatal; hemolysis, increased blood-pressure within the liver, etc., are 
suggested as causes. Perhaps every jaundice falls under (b) the patho- 
logical type, caused by sepsis, syphilis, Winckel's disease, or more excep- 
tionally by congenital obstruction, gall-stones, acute yellow atrophy or 
catarrhal icterus. Glaister reported a family in which 6 cases of jaundice 
developed after birth and Rolleston an instance in which the mother, and 
also the babes, had icterus in four pregnancies (v. page 590). 

Symptoms. — Bilirubin, found normally in bile, enters the blood in biliary 
obstruction, by the bloodvessels and produces the following symptoms: 

1. Skin and Mucosa. — In three days the sclerse, skin and mucosae 
become yellow and in chronic cases dark brown. The skin itches because 
of its dryness or the action of the bile on the nerves. 

2. Urine. — The urine contains bilirubin before icterus is seen in the 
skin. Adding nitroso-nitric acid to the urine in a porcelain dish or on 
filter paper gives the Gmelin play of colors, of green, yellow, violet and 
red. If the urine is agitated the yellow color appears in its foam. Con- 
fusion is possible with melanuria, hematuria, urobilinuria or staining of 
the urine with rhubarb, picric acid, santonin, senna, etc. Urobilinuria 
is thought to indicate disease of the hepatic cells; urobilin is formed in 
the intestine by the reduction of bilirubin, whence it is absorbed and 
excreted by the urine; it never stains the skin and icterus results from 
bilirubin alone. There are three classes of cases; (a) in complete biliary 
obstruction with icterus only bilirubin is found in the urine, for none 
of it reaches the intestine to be converted into urobilin; (b) in partial 
obstruction bilirubin is found in the blood and urine and also some 
urobilin; (c) in slight obstruction there is no bilirubin but much urobilin 
in the urine. Albuminuria may occur or cylindruria alone and the 
hyaline casts and desquamated epithelium are then bile-stained. Increase 
in the sulphates and indicanuria are due to greater intestinal putrefaction. 

3. The Digestive Tract. — The coated tongue, disagreeable breath, 
bitter taste in the mouth and nausea are toxemic. There may be an 
especial aversion to fats and sometimes to proteids. The abdomen is dis- 
tended, possibly from absence of the antiseptic action of the bile. Starch 
and albumin digestion are impaired and fat in the stools {steatorrhea) 
reaches 50 or 80 per cent, (normally 7 to 10). The function of the pan- 
creas in this respect is far more important than that of the bile. The 
stools are clay-colored, constipated and stinking; they may shimmer when 
the fatty soap crystals are abundant; they are also dry (the bile normally 
amounts to nearly a quart a day). If the obstruction is incomplete — as 
in many intrahepatic diseases — the stools are merely somewhat lighter 
than normal. The feces may appear brown from a nitrogenous diet or 
dark if voided with the urine which lends a yellow color to their surface. 

4. Cholemia. — Cholemia (hepatargia or hepatic insufficiency) may 



590 DISEASES OF THE GALL-BLADDER AND BILE VESSELS 

finally develop, probably from injury to the liver cells which fail to 
destroy the intestinal toxins. Its symptoms resemble acute yellow 
atrophy, i. e., nervous excitation followed by stupor, irregular breathing 
or cutaneous and other hemorrhages. The hemorrhages are thought to 
result from pancreatic involvement (diminished lime salts or fat necrosis) . 
Most subjects of icterus are depressed, irritable, sleepless and somewhat 
emaciated. 

5. Other Symptoms. — (a) The heart rate is slow, particularly in catarrhal 
forms or recent cases and in the absence of pain, fever and intoxication; 
it may fall to 21; it is probably caused by vagus stimulation, for atropine 
raises the rate. The arterial pressure is low and the capillaries wide. A 
functional heart murmur is usually caused by myocardial weakness; Potain 
holds that the lung capillaries contract reflexly, thereby causing dilata- 
tion of the right heart. The respiration rate is decreased, even to seven a 
minute; the temperature is usually normal, (b) The blood shows the 
bile stain and in severe cases delayed coagulation, anemia, leukocytosis 
and sometimes a Widal reaction (typhoid cholecystitis?), (c) The liver 
cells may suffer mechanically and chemically from bile stasis and may 
be smaller, altered in form, pigmented, necrotic and bile-stained. The 
gross and minute anatomy varies with the cause. The bile vessels are 
often dilated, sometimes thickened and occasionally ruptured. The 
condition of the gall-bladder will be discussed under Gall-stones and 
Pancreatic Cancer. Simple biliary stasis never causes induration of the 
liver, (d) Splenic tumor is no part of bile stasis except from infection 
or portal stasis, (e) The tissues, secretions and excretions are bile-stained; 
the muscles and nervous tissues, except in the severe type of icterus 
neonatorum, are seldom icteric. (f) Xanthopsia, yellow coloring of objects 
seen, is due to the action of the bile pigment on the nervous tissues. The 
explanation of nyctalopia and hemeralopia is uncertain, (g) Of xanthel- 
asma multiplex 23 cases were collected, and Futcher in 1905 reported 3 
cases; 80 per cent, occur in chronic icterus, due to gall-stones, stricture 
of the bile ducts, cirrhosis, hydatids and cancer. They are often sym- 
metrical, often begin on the eyelids or the folds and creases of the skin, in 1 
case were found in the bile ducts, rarely disappear and are probably toxemic. 

Diagnosis. — Icterus is not noticed in artificial light and daylight is 
absolutely essential for its certain detection. It is seldom confused with 
anemia, cachexia, Addison's disease or vagabondism. Pingueculae are 
only mistaken on superficial examination. 

In ictero-anemia (Widal' s syndrome) there are icterus, splenic enlarge- 
ment, urobilinuria and blood changes. The icterus is non-obstructive; 
the splenic tumor results from hemolysis and urobilinuria is marked. 
The anemia, fatigue, low blood-pressure and hemorrhages are explained 
by the fragility of the red globules (not observed in ordinary icterus); 
the red cells number 1,000,000 to 3,000,000, the index is over one and 
the leukocytes are increased (to over 40,000) . The course is chronic and 
attacks like gall-stones are common. 

In chronic family jaundice (Minkowsky) also, hemolysis and globular 
fragility are causal. There is anemia (1,000,000 to 4,000,000 reds), with 
free hemoglobin in the plasma; in the bone-marrow there is intense 



C HOLE LI THIASIS 59 1 

reaction, with normoblasts and myelocytes. Icterus is congenital, perhaps 
through four generations, or appears early in life; it is neither intense nor 
obstructive and, lasting through life, the patients are icteric rather than 
ill (Chauffard). The spleen is enlarged, the urine contains no bile but 
urobilin, the stools are dark and attacks of gall-stone colic are frequent. 
Over 100 cases are reported. Iron and arrays are helpful and in some 
instances splenectomy appeared justifiable. 

Prognosis and Treatment. — The prognosis and treatment cannot be 
considered, as icterus is but a symptom (v. i. Catarrhal, Jaundice). 
Icterus may subside after six or even fifty-two years. 

CHOLELITHIASIS. 

Etiology. — 1. Immediate Cause. — The causes are (i) catarrhal inflam- 
mation of the gall-bladder or bile vessels and (ii) stagnation of bile. 
Bacteria play an important role, especially the typhoid (found in 33 
per cent.) and colon bacilli; they have been found in calculi, and cholelith- 
iasis has been experimentally produced by their inoculation ; the Bacillus 
typhosus may live seven years in the gall-bladder, (iii) Hypercholester- 
emia, in typhoid, pregnancy, nephritis, diabetes and obesity, is considered 
a frequent factor by Aschoff. 

2. Predisposing Factors. — (a) Age; 75 per cent, of cases occur in persons 
over forty years of age and only 1 per cent, under twenty years, (b) Sex; 75 
per cent, occur in women, in whom pregnancy, menopause, lax abdominal 
walls and lacing are promoting factors; it is said that 40 per cent, of 
women who have gall-stones also have the corset liver. Gall-stones are 
found in 25 per cent, of autopsies on women over sixty years; 90 per 
cent, of women affected have borne children (Naunyn). They are found 
in 8 per cent, of autopsies. 

Properties of Gall-stones. — (a) Site; calculi are formed in the gall- 
bladder, very rarely in the intrahepatic ducts. (b) Size; they range up- 
ward from the size of sand or gravel; a calculus 12 inches in length is 
recorded; the heaviest reported was 135 gm. (c) Form; they are usually 
round and rarely spinous; when multiple they are polygonal and facetted. 
Intrahepatic calculi may be cylindrical or branching like coral, (d) 
Their number averages a dozen; according to Riedel 44 per cent, are 
single; Otto reports 7802 stones in 1 case. In Chopart's case the liver 
could scarcely be cut because of the numberless stones in the intrahepatic 
ducts, (e) Consistence; gall-stones can usually be indented by the finger. 
(/) The time required for their growth is about six months, (g) Chemistry; 
the most common form consists of cholesterin and bile pigment with lime 
as a cementing substance; these calculi are small, numerous, usually yellow, 
laminated and contain about 75 per cent, of cholesterin. Pure choles- 
terin stones are not common; they are translucent, become opaque when 
dry, are light in weight and color and are combustible; they present a 
crystalline fracture like that of camphor, they dissolve in ether and 
alcohol, from which the crystals are precipitated and produce a red 
tinge on addition of chloroform and sulphuric acid; cholesterin comes 
from the blood, bile or gall-bladder mucosa. Pigmentary stones are 



592 DISEASES OF THE GALL-BLADDER AND BILE VESSELS 

uncommon; bilirubin imparts a brownish and biliverdin a greenish tint 
to them. Calcium carbonate stones are rare, are grayish in color and 
heavy. Stones in the liver are constituted of calcium and bilirubin. 
Traces of magnesium, bile acids, fatty acids, iron and copper have been 
found. The nucleus is mucin, bacteria, epithelium, blood clot, cholesterin, 
calcium, bile pigment or rarely a foreign body. 

Symptoms. — Kehr and Riedel assert that 95 per cent, of persons with 
gall-stones have no symptoms, especially elderly subjects with atrophic 
gall-bladders, and stones very rarely may be felt in the gall-bladder, or 
be found in the feces in these cases. The writer believes that latency is 
less common than above figured and that gastric symptoms are exceedingly 
common (75 per cent.). 

Biliaky Colic. — (a) Colic is usually sudden in onset and frequently occurs 
at night. Many women state that the pain is more severe than labor pains. 
It begins in the epigastrium and may radiate to the back, navel, hypo- 
gastrium, left side and even to the arms, legs, testes or chest. Irregular 
or large stones cause the greatest agony, controlled only by large or 
repeated hypodermics of morphine. The pain usually endures for a few 
hours and may soon recur. The cause of biliary colic is mechanical — 
the attempt of the stone to migrate produces the spasm of the cystic and 
common ducts during its passage — or inflammatory, cholecystitis starting 
the stones moving by the exudation it induces; pain is less or shorter 
if the ducts are patulous. Quiescent gall-stones may be started onward 
by palpation of the gall-bladder, trauma, exercise, reduction of flesh, 
menstruation or delivery. (6) Reflex nausea and vomiting are frequent; 
they may indicate cholecystitis. Vomiting relieves the pain, whence the 
frequently erroneous diagnosis of gastralgia. A cramp of the stomach 
has been seen with the x-rays. Torsion of the cystic duct may cause vom- 
iting but not colic, (c) Chills and fever occur in 66 per cent, and indicate 
bacterial inflammation, (d) The gall-bladder is tender, there being hyper- 
esthesia over the ninth costal cartilage or over a point two-thirds of 
the distance between it and the navel, and around the chest to the spine. 
In 33 per cent, the gall-bladder is palpable. The right rectus muscle is 
rigid (defense musculaire). (e) Icterus, present in but 15 per cent., may 
be calculous, infectious or compressive. (/) Other symptoms of the par- 
oxysm are rapid pulse, sweating, prostration, concentrated urine, con- 
stipation, abdominal retraction and, after the seizure, marked prostration.. 
Attacks of migraine are not infrequent. There may be reflex coughing 
or reflex contraction of the pulmonary capillaries, which overtaxes and 
dilates the right heart. The patient may collapse and the writer observed 
death in an attack. Glycosuria, albuminuria, leukocytosis and splenic 
swelling are inflammatory in origin. The stone may fall back into the 
gall-bladder or pass into the bowel if it measures under 1 cm. ; confusion 
with lumps of olive oil, given to relieve the colic, is unnecessary ; a round 
calculus suggests that it is the only one. Stones passing into the bowel 
may be dissolved, unless coated with cholesterin. The great importance 
of gall-stones lies in their complications: 

Complications. — They may be grouped as mechanical or inflammatory, 
but are best combined topographically. 



£OQ 



CHOLELITHIASIS 59 

1. Gall-bladder. — Mechanical complications include pressure on the 
duodenum or pylorus and rupture of the gall-bladder, which, however, 
are generally inflammatory; pressure on the common duct; hyper- 
chlorhydria and hypersecretion and cancer of the gall-bladder (q. v.). 
Inflammatory complications are more serious; all forms and sequences 
of cholecystitis (q. v.) may develop, as hydrops, empyema, gangrene, 
ulceration, deformity, hemorrhage, atrophy or calcification; also pyle- 
phlebitis, adhesions producing pyloric obstruction with hyperchlorhydria, 
dyspepsia and sometimes hemorrhage into the stomach; adhesions caus- 
ing duodenal obstruction; and peritonitis, either local (near the gall- 
bladder or subphrenic abscess) or diffuse. A friction-rub may be heard 
over the gall-bladder a day or two after the colic. The distended gall- 
bladder rarely exceeds the size of the fist, is pyriform, can be moved 
laterally and moves with the liver, from which it may seem separated by 
a groove; it may be confused with appendicitis, the kidney, ovarian cyst 
or ascites and has been found in a femoral hernia. 

2. Cystic Duct. — Mechanical impaction causes icterus by catarrh of 
the common duct (in 12 per cent.) or by directly compressing it. The 
duct may become twisted, stenosed or obliterated. 

3. Common Bile Duct. — Its mechanical occlusion is usually preceded 
by colic; impaction occurs oftenest at its lower end (50 to 67 per cent.), 
and is caused most frequently by 1 stone; 88 have been found. Per- 
manent occlusion by stone in the common duct or in the cystic duct 
pressing upon it causes marked icterus, usually without sepsis. The 
occlusion may be partial or intermittent, by a ball-valve action of the 
stone, described by Osier and Fenger, which allows some bile to enter 
the gut and some bacteria to enter the duct, thus adding bacterial to 
mechanical injury. Usually the icterus is sudden in onset and slow in 
subsidence. In partial or intermittent obstruction there is often the 
intermittent hepatic fever, first described by Charcot and comparable to 
urethral fever. During the paroxysms the fever rises to 103° or 105°, 
often with chills, sweats, leukocytosis, vomiting and increased tender- 
ness, pain and icterus. The spleen may swell, and also the liver from 
saccular dilatation of the channels and cholangitis. Osier correctly 
insisted that these symptoms occur without suppurative cholangitis, 
though with infection. The gall-bladder is not enlarged, but is usually 
shrunken, following Courwisier's law; Courvoisier found the gall-bladder 
enlarged in 92 per cent, of non-calculous obstruction of the common duct 
and shrunken in 80 per cent, of calculous obstruction; this is caused by 
infection (Hanot). In some cases suppurative cholangitis may complicate 
stones of the common duct, with remittent fever (rather than intermittent 
fever), enlarged liver, subcapsular abscess, septic symptoms and more 
rapidly fatal course. Cicatricial stenosis of the common duct is rare; 
pylephlebitis may develop. Malaria is excluded by examination of the 
blood; malignancy will be considered under tumors of the pancreas, 
though in common duct obstruction the nutrition is little impaired. 
Practically, stress may be placed on (a) the periodic fever, (b) the icterus, 
sudden in onset and subsiding slowly, and (c) tenderness (without pain 
over the liver). 

38 



594 DISEASES OF THE GALL-BLADDER AND BILE VESSELS 

BREWER'S DIAGNOSIS OF DISEASES 



Pathological 
condition. 


Pain. 


Fever. 


Vomiting. 


Jaundice. 


Tumor of gall- 
bladder. 


I. Calculous Disease. 












(a) Stone in healthy 


No. 


No. 


No. 


No. 


May be present 


gall-bladder, ducts 










from large 


free. 










number or 
size of stones. 


(b) Stone in healthy 


May be absent; gen- 


No. 


May be pres- 


No. 


Maybe present 


gall-bladder, cystic 


erally present dur- 




ent when 




from disten- 


duct temporarily ob- 


ing obstruction ; par- 




colic occurs. 




tion. 


structed. 


oxysmal. 










(c) Stone impacted in 


No. 


No. 


No. 


No. 


Present; may 


cystic duct. 










attain large 


(d) Stone in hepatic 


Frequently present; 


Occasionally 


May be pres- 


Frequent. 


size. 
No. 


duct. 


irregular type. 


present. 


ent during 
pain. 






(e) Stone in common 


Present; acute, par- 


Generally 


Present. 


Present. 


No. 


duct ; acute obstruc- 


oxysmal, radiating 


present. 








tion. 


to back. 










(/) Stone in common 


Periodic attacks of 


Present with 


Present. 


Present ; in- 


Rarely present. 


duct; movable; 


acute radiating pain 


chills and 




termittent. 




chronic. 




sweats. 








(g) Stone in common 


May be absent; fre- 


May be pres- 


Often present. 


Present; pro- 


Rarely present. 


duct; impacted ; 


quently present 


ent; vari- 




gressive ; 




chronic. 


early; may be in- 
termittent ; vari- 
able. 


able. 




may vary in 
intensity. 




II. Inflammatory 












Disease 












(a) Cholecystitis sub- 


Present; paroxysmal 


Present dur- 


May be pres- 


No. 


Present dur- 


acute. 


during periods of 


ing attacks 


ent. 




ing attacks 




cystic duct closure 


of colic. 






of cystic duct 




from stone or swol- 








obstruction. 




len mucous mem- 












brane. 










(6) Cholecystitis acute. 


Acute paroxysmal 


Present with 


Present often; 


No. 


Present ; ten- 




radiating pain; ex- 


chills and 


severe. 




derness ; oft- 




tending to back and 


sweats. 






en muscular 




shoulder ; may be 








rigidity. 




very severe. 










(c) Cholecystitis chron- 


Severe radiating pain 


Present; 


Present at 


No. 


Present; with 


ic (empyema of gall- 


at first; may disap- 


severe at 


first. 




tenderness; 


bladder) . 


pear later; tendency 


first, may 






may attain 




to recur. 


diminish 
later. 






large size. 


(d) Cholecystitis in pre- 


Present; often severe; 


Present; 


Present. 


No. 


No (occasion- 


viously diseased and 


paroxysmal. 


often with 






ally present 


contracted gall- 




chills and 






due to peri- 


bladder. 




sweats. 






cystic exu- 
date) . 


(e) Cholangitis of hepa- 


May be absent; gen- 


Present ; 


Present. 


Present; vari- 


No. 


tic and common 


erally present when 


chills ; 




able. 




ducts. 


obstruction exists, 
or severe infection; 
tenderness and pain 
over liver in intra- 
hepatic cholangitis. 


sweats ; 
severe 
prostra- 
tion ; gen- 
eral sepsis. 








III. New Growths. 












(a) Carcinoma of gall- 


No; may occur late 


No. 


No. 


Present late 


Hard, irregu- 


bladder. 


in disease. 






(portal 
glands) . 


lar, movable 
tumor at first, 
later diffuse 
infiltration. 


(6) Tumor of cystic 


No; may occur late. 


No. 


No. 


No. 


Present when 


duct. 










obstruction 
exists. 


(c) Tumor of hepatic 


No; may occur late. 


No. 


No. 


Present; pro- 


May be present 


or common duct. 








gressive. 


from disten- 
tion with bile. 


(d) Tumor of neighbor- 


No; may occur late. 


No. 


No. 


Present; pro- 


Present; gen- 


ing viscera producing 








gressive ; 


erally from 


chronic obstruction 








may become 


distention 


of common duct. 


' 






extreme. 


with bile. 



CHOLELITHIASIS 

OF THE GALL-BLADDER AND DUCTS. 



595 



Urine. 



Stools. 



Liver. 



Spleen. 



Ascites. 



Remarks. 



Negative. 



Negative. 



Negative. 



Contains bile 
pigment 
at times. 

Contains bile, 
pigment. 

Contains bile 
pigment. 



Contains bile 
pigment. 



Negative. 



May contain 
albumin 
and casts. 



Negative. 



Negative. 



May contain 
bile pig- 
ment, albu- 
min and 
casts. 



Negative (at 
first). 



Negative. 

Contains bile 
pigment. 

Contains bile 
pigment. 



Normal. 



Normal. 



Normal. 



May be clay- 
colored if 
obstruc- 
tion occurs. 

Clay-colored, 



Clay-colored. 



Clay-colored, 



Normal. 



Normal. 



Normal. 



Normal. 



May be clay- 
colored. 



May be clay- 
colored 
late. 



Normal. 

Clay-colored. 

Clay-colored. 



Not enlarged. 



Not enlarged. 



Not enlarged. 



Frequently 
enlarged. 



Not enlarged. 



May be en- 
larged dur- 
ing attack. 

Enlarged. 



Not enlarged. 



Not enlarged. 



Not enlarged. 



Not enlarged. 



Enlarged. 



E n 1 ar 
late 
ease. 



in 



dis- 



Not enlarged. 



May be en- 
larged. 

Enlarged. 



Not enlarged. 



Not enlarged. 



Not enlarged. 



Not enlarged. 



Not enlarged. 



May be enlarged 
from pressure 
of stone on vein. 

May be enlarged. 



Not enlarged. 



May be enlarged 

(sepsis) . 



Not enlarged. 



May be enlarged 
(sepsis) . 



Enlarged (sepsis) 



No. 

No. 

No. 
No. 

No. 

No. 

No. 



May be enlarged 
late (pressure 
on vein). 



Not enlarged. 
Not enlarged. 



May be enlarged 
late. 



No. 



No. 



No. 



No. 



No. 



Present 
late. 



No. (?) 



May be 
present 
late. 

Present 
late. 



Generally discovered by accident; 
often unrecognized. 



All symptoms promptly relieved 
as soon as obstruction removed. 



Hydrops of gall-bladder often 
unrecognized. 

Diagnosis extremely difficult; 
symptoms generally due to co- 
existing cholangitis. 

Symptoms rapidly disappear when 
stone passes papilla. 

"Fievre intermittente hepatique" 
of Charcot resembles malaria; 
all symptoms disappear during 
interval. 

Condition may remain for many 
years; may only be jaundice 
with digestive disturbances and 
loss of weight; history of pre- 
vious attacks (?). Ascites may 
be present from pressure of 
large stone or possibly from 
hydremia. 



Tenderness over gall-bladder; ten- 
dency to recurrence; generally 
associated with stones in gall- 
bladder. 



May follow typhoid or other sep- 
tic diseases; onset often sudden; 
rapid development of severe 
symptoms resembling appendi- 
citis; may be necrosis of walls 
of gall-bladder with perforation; 
local or general peritonitis. 

Frequently follows acute chole- 
cystitis; occasionally becomes 
quiescent, presenting practically 
no symptoms. 

Generally tenderness over gall- 
bladder area, but no tumor; 
local peritonitis; diagnosis often 
extremely difficult. 

Often follows severe infections of 
gall-bladder; generally associated 
with stones in common or hepa- 
tic duct; severe sepsis; generally 
fatal in virulent infections (strep- 
tococcus). 



Digestive disturbances, progres- 
sive loss of weight and asthenia ; 
cachexia; rapidly fatal. 



Very rare; both benign and ma- 
lignant growths have been re- 
ported; diagnosis difficult. 

Very rare; diagnosis difficult. 



Malignant tumors most common; 
chronic interstitial pancreatitis 
from previous infection of biliary 
passages may remain after cause 
has disappeared; enlarged portal 
glands; Hodgkin's disease. 



596 DISEASES OF THE GALL-BLADDER AND BILE VESSELS 

4. Ampulla of Vater. — Calculous retention in the ampulla may 
obstruct the flow of the pancreatic juice, though the accessory duct 
may carry it into the intestine; retention may allow bile to enter the 
pancreatic duct, and result in (a) acute pancreatitis; (b) chronic indu- 
ration of the head of the pancreas resembling malignancy; (c) pancreatic 
fibrosis with pancreatic calculi due to stasis and infection; or (d) rarely 
glycosuria. 

5. Intestinal Obstruction. — The obstruction may not occur for 
some time, the stones sometimes receiving new layers of magnesia or 
phosphates; it is in the ileum in 66, duodenum in 21, ileocecal valve in 10 
and sigmoid in 3 per cent. ; 50 per cent, of cases die. (See page 551.) 

6. Fistula. — Courvoisier assembled 499 cases. The external form 
constitutes about 50 per cent, of cases; they are most often located near 
the navel and about 40 per cent, of them heal. In the duodenal form (28 
per cent.) the fistula is between the duodenum and gall-bladder and less 
often between the common duct and gall-bladder. In 13 per cent, there 
is a fistulous opening into the colon. Courvoisier and Graham collected 
34 cases of bronchial fistula. In rare cases stones enter the stomach 
(5 cases recorded, Snively, 1903), portal vein (as in the autopsy upon 
Ignatius de Loyola), hepatic artery, kidney, urinary bladder (200 gall- 
stones evacuated in the urine in the case of Barraud-Palletan), pericar- 
dium, retroperitoneal tissue, vagina or even the pregnant uterus. 

Diagnosis. — The diagnosis is easily made when colic, vomiting, tender- 
ness of the gall-bladder and icterus are present. The arrays are positive 
in 50 per cent. (Case). 

1. The Colic. — This is most apt to be confused with (a) gastralgia 
or hepatic neuralgia; due regard for other symptoms of gall-stones and 
reserve in the diagnosis of gastralgia save many mistakes, (b) Gastric 
or duodenal ulcer, hyperchlorhydria and hypersecretion (q. v.) are easily 
distinguished, (c) Lead colic has the characteristic gingival lead line, 
obstinate constipation and often neuritic manifestations, (d) Tabetic 
crisis is attended by the Argyll-Robertson pupil, absent knee-jerk and 
ataxia, (e) Renal colic is distinguished by pain reflected down the ureter, 
hematuria and pyuria; and Dietl's crisis in floating kidney, by bimanual 
examination of the abdomen. (/) Mucous colic is differentiated by the 
characteristic stools, (g) Appendicitis is characterized by its cardinal 
symptoms (q. v.); Ochsner finds 10 per cent, of his appendicitis cases 
complicated by gall-stones and 33 per cent, of his gall-stone cases by 
appendicitis, (h) Acute pancreatitis (q. v.) which may complicate gall- 
stones, causes greater collapse and more frequent intestinal obstruction. 
(£) Febrile syphilis may simulate gall-stones as may also the abdominal 
crises observed in angioneurotic edema. 

2. Other Biliary Affections (see pages 594 and 595). 
Prognosis. — The prognosis is difficult to formulate. Stones may pass 

without recurrence of colic and the passage of smooth calculi may justify 
some hope that they are the only ones. The first attack is usually the 
worst. Fever, infection, cancer and obstruction must be covered in fore- 
casts to patients refusing operation. Riedel held that 10 per cent, recover 
spontaneously, while 90 per cent, require surgical intervention. 



CHOLECYSTITIS 597 

Treatment. — 1. Prevention. — Exercise, deep breathing and plenty of 
water aid the flow of bile. Lacing is a factor to be regarded. Digestive 
derangements should be corrected. Alcohol is contra-indicated. The 
predisposing gall-bladder inflammation seldom comes under the physi- 
cian's care, but in suspicious cases, sodium salicylate, gr. x-xv t. i. d., 
given alternate weeks, acts as a cholagogue and antiseptic. Hexamethyl- 
enamine, 5j per diem, is excreted by the bile. Potassium iodide, and 
sodium phosphate, 5 ss— j are beneficial. 

2. Colic. — Hypodermics of morphine must be given, gr. J being com- 
bined with nitroglycerin gr. t ^~q and (for the first injection) atropine 
gr. Tiro 5 repeated doses of morphine and nitroglycerin are often necessary. 
Inhalation of chloroform is indicated in severe cases until the morphine 
acts, but none of these drugs should be left in the possession of any 
patient. A full hot bath and hot fomentations over the liver are valuable 
accessories. Drinking warm water facilitates vomiting, which relieves 
the pain. 

3. Medical Treatment. — This in no w 7 ay influences the solution 
of gall-stones. Durande's solvent (oil of turpentine 1 part to ether 4 
parts) is useless and, like chloroform, is only antispasmodic. Olive 
oil only facilitates their final passage. Salicylates, calomel, salines 
(v. s.) and various "cures," as at Carlsbad, Vichy, Kissingen, Las Vegas 
or Bedford Springs, are useful in quieting concomitant or causative 
inflammation. Local massage is obviously injurious. 

4. Surgical Treatment. — The author believes that gall-stones 
should be operated on when recognized, thus saving time, suffering 
and danger. Riedel's argument for early operation — the removal of 
the calculi while they remain in the gall-bladder — holds good, as it is 
the only salvation against perforation, cholemia and carcinoma ; it is 
refused, however, in general practice. Hydrops, empyema of the gall- 
bladder and pericholecystitic abscesses, cholangitis, incapacitation, 
jaundice, impaction, and frequent resort to. morphine are strong indi- 
cations. Corpulent men do not bear the operation well. Women who 
have borne children lend themselves well to surgical procedure. If 
possible one should refrain from operating in cases of diabetes, arterio- 
sclerosis, chronic nephritis and diseases of the lungs and heart. 

In Mayo's 4000 operated cases the mortality w r as 1.8 per cent, in 
uncomplicated cases, while those complicated by suppuration or cancer 
brought the average mortality to 2.75 per cent.; the death-rate in opera- 
tions on the common duct was 8 per- cent. These figures appear to the 
writer as the best possible argument for early operation. Cholecys- 
totomy is often inferior to cholecystectomy. 

CHOLECYSTITIS. 

Etiology. — Inflammation of the gall-bladder may occur before, after, 
with or without inflammation of the bile passages, (a) Predisposing 
factors are gall-stones (especially large ones w T hich cannot pass, which 
cause 65 to 90 per cent, of cholecystitis and cholangitis), bile stasis, 
foreign bodies or previous attacks, (b) The exciting cause is bacterial, 



598 DISEASES OF THE GALL-BLADDER AND BILE VESSELS 

the colon, typhoid, pyogenic, pneumococcus, and other microorganisms. 
They may ascend the bile channels or enter with the blood current. 
Inflammation from typhoid infection (Louis and Andral) may occur 
without actual typhoid or may develop twenty years later. 

Symptoms. — The symptoms vary with the intensity of infection, 
which is almost synonymous with the type (simple, membranous, sup- 
purative, phlegmonous, ulcerative or gangrenous). In light forms 
the symptoms may not be recognized; this corresponds to postmortem 
adhesions in cases with no history of cholecystitis. In other, perhaps 
more severe cases, symptoms are obscured by the causative typhoid or 
by gall-stones. In the average case there are: (a) pain over the part, 
which may be severe or paroxysmal and may radiate toward the appendix 
or back, (b) Tenderness as in gall-stones; it is often first general and 
then local and the right rectus is tense; it is clearly elicited by a thrust 
over the part during inspiration, (c) Fever, increased pulse-rate, vomiting 
or nausea; fever is absent in mild infections; in typhoid, cholecystitis 
may be confused with typhoid relapse. There may be colic, (d) There 
may be a palpable gall-bladder. Its contents may be purulent (empyema 
cystidis fellese) or serous (hydrops cystidis fellese). Hydrops may enlarge 
the gall-bladder to the size of the fist or in extreme cases so that it weighs 
50 to 60 pounds and fills the entire abdomen, simulating ascites; the 
fluid is alkaline or neutral, serous or mucoid. If very tense the gall- 
bladder may not fluctuate or if very lax may not be palpable (see Float- 
ing Kidney). There may be pus in the gall-bladder without enlarge- 
ment. In chronic cases it may shrink, (e) Severe sepsis may intervene in 
diffuse suppurative cholangitis or pylephlebitis, evidenced by septic fever, 
chills, leukocytosis, bacteriemia, swollen liver and spleen, nephritis and 
ulcerative endocarditis. Icterus occurs in 33 per cent. (See pages 
594 and 595.) 

Prognosis. — Many cases with cholangitis die in spite of operation. 
Mild cases may subside, but recurrence and formation of gall-stones 
are frequent. Under expectant therapy the outlook is serious in severe 
cases, for perforation, peritonitis, adhesions (in 75 per cent.) or pyloric 
obstruction may result. 

Treatment. — Rest, milk diet, local heat and morphine may suffice 
for light cases, but in the more severe infections drainage is indicated. 

CHOLANGITIS. CATARRHAL ICTERUS. CONGENITAL OCCLUSION. 

Suppurative Cholangitis. — It usually coexists with suppurative chole- 
cystitis and infection is usually hematogenous, but may be ascending — 
cholangitic sepsis (v. pages 594 and 595.) 

Acute Catarrhal Jaundice. — Cholangitis catarrhalis, icterus simplex, 
results from gastroduodenal catarrh which causes swelling with ob- 
struction of the papilla; in the few autopsied cases a small plug of mucus 
occludes the opening of the common duct; Eppinger found swelling of 
the lymphoid follicles where the duct lies in the wall of the bowel. Its 
usual causes are practically those of acute gastritis or enteritis. Favoring 
factors include passive congestion, acute infections, toxic causes, nephritis 



TUMORS OF THE GALL-BLADDER AND BILE VESSELS 599 

and other diseases of the liver or bile tracts. Epidemic forms seem to be 
a separate type of infection (v. Weil's Disease). 

Symptoms. — G astro-intestinal catarrh occurs first in half the cases 
and after a few days icterus appears, with its usual symptoms, sudden 
decolorization of the stools and bright yellow staining of the skin and 
urine; in the other half, there is primary infectious, catarrh of the bile 
ducts. The liver is not enlarged at first, but may become slightly 
swollen later; there is no pain or emaciation, the spleen and gall-bladder 
are seldom enlarged and the diagnosis depends on the mode of onset 
in young, healthy subjects, sequence of symptoms and exclusion of 
other causes of obstruction; in advanced life catarrhal jaundice is less 
common than gall-stones and cancer. (See page 594.) 

Prognosis. — Cases may clear in a week or last five months; a course 
of over the average — four to eight weeks — renders the diagnosis uncer- 
tain. Cases with fever may run a prolonged course. Death rarely occurs 
from hemorrhage, exhaustion or sudden heart failure. 

Treatment. — (a) Causative factors, as gastritis or stasis, are appro- 
priately treated; dyspeptic symptoms yield most readily to gastric 
lavage and fractional doses of calomel at night followed by a mild saline 
in the morning; active catharsis augments or initiates catarrh. 

1$ — Acidi hydrochlorici diluti 5j 

Tincturae nucis vomicae 3iv 

Tincturae gentianae co q. s. ad. oiv 

M. et S. — One teaspoonful after meals in half a glass of water. 

The green "bilious stools" from calomel are not due to bile but to 
mercuric sulphide, (b) In the diet fats are particularly to be avoided, 
as neither the stomach nor intestine can digest them ; tea, coffee, alcohol 
and coarse foods should be interdicted; skimmed milk, well-cooked 
carbohydrates, toast, eggs and mealy soups may be given; meat is 
often poorly tolerated, seemingly because of exclusion of the pancreatic 
secretion, (c) As long as acute dyspepsia exists, rest in bed is indicated, 
in order to maintain nutrition on the lowest possible diet, (d) The 
bowels are regulated by copious injections of water, to incite peristalsis 
and dislodge the obstructing mucus plug, (e) The itching is allayed 
by 1 per cent, carbolic solution, the use of which requires care, as the 
urine sometimes becomes cloudy; acetanilide, gr. v, q. i. d.; potassium 
bromide, 5ss, well diluted, by rectum once or twice daily; an occasional 
hypodermic of pilocarpin hydrochloride gr. J; and by warm baths. 

Chronic Catarrhal Cholangitis. — (v. Gall-stones, Pancreatic Cancer and 
Icterus.) 

Congenital Occlusion of the Bile Ducts. — Seventy-six cases are 
recorded (Howard and Wolbach), due perhaps to cholangitis or con- 
genital atresia. Icterus develops within a month after birth and death 
results in weeks or months from cholemia or hemorrhages. 

TUMORS OF THE GALL-BLADDER AND BILE VESSELS. 

I. Cancer of the Gall-bladder. — Tumors other than cancer are rare, 
as sarcoma, papilloma, fibroma, lipoma or adenoma. 



600 DISEASES OF THE GALL-BLADDER AND BILE VESSELS 

Etiology. — The most striking etiological factor is gall-stones, present 
in 70 to 91 per cent. (Courvoisier) ; the estimate that 9 per cent, of cases 
of gall-stones result in cancer of the gall-bladder seems very high; 80 
per cent, occur in women over fifty years of age. 

Pathology. — The tumor may be scirrhus or medullary, but usually 
adenocarcinoma; spheroidal and squamous types are rare. 

Symptoms. — (a) Gall-stones which irritate the mucosa and cause 
most cases, usually produce no symptoms, though previous colic may 
be noted in the history. (6) A tumor of the gall-bladder is palpable in 
over 66 per cent., first as a smooth oval and later as a larger and more 
nodular swelling; it is usually due to the growth, for the gall-bladder 
itself is generally shrunken. The fundus is the usual point of origin, 
being most irritated by calculi, much more rarely the neck of the gall- 
bladder or least frequently the cystic duct. The tumor appears below 
the edge of the liver with which it moves. There may be local discomfort 
and, in rare cases, severe pain like that of gall-stones, (c) Cachexia 
appears with all its attendant symptoms. 

Complications. — Secondary growths in the liver occur in 58 per cent, 
by lymphogenous routes or by invasion from contiguity and sometimes 
cause hepatic enlargement; from the liver extension by the hepatic 
veins may occasion systemic metastases. Icterus occurs in 69 per cent. ; 
cholemia is a common termination. Growths in the peritoneum, lungs 
or pleura, abdominal lymph glands and into the colon occur in about 
10 per cent. each. Warthin records adrenal metastases with vitiligo 
and pigmentation like that of Addison's disease. Pressure on the pylorus 
may cause its stenosis, vomiting or dyspepsia. Ascites occurs in 25 per 
cent, and is due to compression of the portal vein or to malignant peri- 
tonitis. Suppurative cholangitis may develop, with death from sepsis. 
The differential diagnosis is considered under gall-stones. The clinical 
course averages six months. Treatment is palliative, unless the affection 
is diagnosticated early or is accidentally found in operating for other 
conditions. 

II. Tumors of the Extra-hepatic Bile Ducts. — Rolleston collected 80 
cases, and Zezas 34 cancers at the junction of the three great bile ducts. 
These tumors are small, seldom infiltrate and are of the columnar type. 
The common duct is most often affected, the hepatic duct less and the 
cystic duct least frequently. The salient symptom is intense icterus, which 
develops early, increases steadily, occurs in nearly all cases, causes 
icteric necrosis of the liver cells in the central zone and precipitates 
early cholemia before metastases or cholangitic sepsis have time to 
develop. The gall-bladder is almost always dilated anatomically in 
tumors of the common duct and is felt clinically in over 50 per cent. 
Pain is not common, though gall-stones may be simulated. Ascites, 
dyspepsia and gastro-intestinal hemorrhages from cholemia may develop. 
Differentiation from duodenal or pancreatic tumors (q. v.) is usually 
impossible. Treatment consists of draining the gall-bladder or extirpa- 
ting the tumor. 



ACUTE PANCREATITIS— FAT NECROSIS 601 



DISEASES OF THE PANCREAS. 

ACUTE PANCREATITIS; FAT NECROSIS. 

Etiology. — Infection ascending from the intestines is the leading cause. 
(a) Calculus obstructing the common duct, by allowing bile to regurgitate 
into Wirsung's duct, may cause acute pancreatitis (Opie), especially 
when the gall-bladder, the natural reservoir for obstructed bile, ■ is 
shrunken; gall-stones cause 42 per cent, of cases of acute fat necrosis. 
Bile salts may initiate inflammation and fat necrosis, without infection. 
The accessory duct of Santorini may carry off the pancreatic juice when 
there is obstruction of Wirsung's duct, but it is too small for much 
compensation in 66 per cent, of cases; (b) metastatic infection is an 
infrequent cause; the author observed one case in which an acute ulcer 
of the leg was the atrium; (c) suppuration or ulceration in contiguous 
tissues may be causative. 

Peedisposing Factors. — (a) Age and sex; 90 per cent, occur in 
males beyond middle life, (b) Obesity; (c) alcoholism; (d) trauma; (e) 
gastro-intestinal catarrh; and (/) parturition in 6.6 per cent, of Peiser's 
128 cases. 

Symptoms. — The clinical picture was clearly described and defined by 
Fitz (1889), though cases were reported earlier by Oppolzer. The onset 
is sudden in adult, stout males who have enjoyed previous good health 
or who have a history of alcoholism or of gall-stones. 

1. Epigastric pain is the initial symptom; it is very sudden and agon- 
izing, constant or paroxysmal and may be confused (or coincident) 
with gall-stone colic, though it is even more intense; it is diffusely epi- 
gastric or rarely over the head of the pancreas. The author has seen 
radiation into both axillae. The intensity of the pain is referable to 
pressure on the celiac plexus (neuralgia or neuritis celiaca). 

2. Epigastric tenderness is usual, often over the head or sometimes 
more over the tail of the pancreas, whence the inflammation may extend 
to the left pleura with tenderness and friction. The recti are tense and 
the epigastrium is swollen. 

3. Vomiting is early, severe and sometimes brings up blood. 

4. Collapse follows; it often threatens immediate dissolution and too 
often prevents surgical interference. It is due to pressure on, or actual 
inflammation of, the closely contiguous celiac plexus and semilunar 
ganglia. In one of the author's cases there were relapsing shock with 
cyanosis, dyspnea and a pulse of 140, which was so weak that no surgeon 
would operate during the two weeks before recovery. Collapse usually 
causes death in 2 to 4 days in unoperated cases. 

5. Fever is not constant; there may be no elevation or an irregular 
rise to 103° or 104°. Chills are most common in late suppuration. 

6. The pancreas can rarely be felt because of its deep position and 
the tense and tympanitic epigastrium. 

7. The bowels are constipated, simulating obstruction, though flatus is 
passed. Operation or autopsy at this stage shows an acute pancreatitis 



602 DISEASES OF THE PANCREAS 

with swelling, a variegated yellowish-red or black color, exudation of fibrin, 
pus cells, blood (hemorrhagic pancreatitis) and areas of acute fat necrosis 
(Balser, 1882). Fat necrosis is caused by the fat-splitting steapsin 
(Langerhans), which produces glycerin and insoluble fatty acids from 
the pancreas and contiguous adipose tissues, i. e., omentum, mesentery 
and peritoneum; the glycerin is absorbed, the fatty acids are pre- 
cipitated with lime as opaque white areas of necrosis and some of the 
ferment occasionally escapes into the blood, producing toxemic symptoms 
or necrosing fatty tissue elsewhere, as in the pericardium or skin. 

8. If the patient lives a localized peritonitis develops in the upper 
abdomen; pus may fill the lesser peritoneal cavity; the pain may be- 
come general from diffuse fat necrosis or dyspnea may develop from 
diaphragmatic pleurisy. 

9. Septicopyemic symptoms may appear, as rigors, hectic fever, pleurisy, 
icterus, diarrhea and loss of weight and strength; the author saw splenic 
tumor, nephritis and universal lymph adenitis. 

10. Acute glycosuria was present in one of the author's cases. 

In the third week rupture into the colon may occur, attended by 
lancinating pain and intestinal hemorrhage. 

Suppurative types, of which Korte collected 46 cases, may begin 
gradually, without acute gangrene, fat necrosis or hemorrhage; the 
symptoms are less acute and severe. The suppuration is localized or 
there is a diffuse purulent infiltration; it may cause pylephlebitis, liver 
abscess, subphrenic abscess, burrowing of pus into the peritoneum, 
loin (which Korte considers rather characteristic), peripheral tissues or 
alimentary tract. Protracted suppuration is said to cause glycosuria, 
skin pigmentation and anasarca. Korte collected 40 cases of acute 
gangrenous pancreatitis. 

Diagnosis. — The cardinal features are the sudden onset, violent epi- 
gastric pain, distention and tenderness, vomiting and collapse. The 
absence of indican, leucin and ty rosin in the urine is suggestive. Robson 
finds calcium oxalate crystals in 30 per cent, of all varieties of pan- 
creatic disease. The pancreatic reaction of Cammidge is unreliable. 

Differentiation. — (a) Acute poisoning is eliminated by the history 
and gastric contents, (b) Intestinal obstruction is less severe in onset; 
collapse is attended by distention, intestinal rigidity or peristalsis above 
the obstruction; indicanuria is usual; epigastric distention alone is 
unusual; in one pancreatic case, the author saw obstruction lasting nine 
days. Operation may be necessary for diagnosis, (c) Gall-stone colic 
is rarely as severe as pancreatic pain; collapse or epigastric distention is 
infrequent, (d) Perforating ulcer, mesenteric embolism and appendicitis 
must be considered. 

Prognosis. — The malady generally evinces a severe progressive ten- 
dency. A fatal attack may follow milder seizures. At autopsy fibrous 
tissue and crystals or granules of hematoidin may be evidence of previous 
inflammation. Death may occur within a few hours to three days from 
collapse, in two or three months from sepsis or in six months from diabetes 
(Fitz). The pancreas may slough into the intestine, as in Traf oyer's 
and Chiari's cases, with recovery. 



PANCREATIC APOPLEXY 603 

Treatment. — Rectal feeding and stimulation, morphine hypodermically 
and heat are indicated during the initial shock. Though early opera- 
tion is dangerous because of shock and hemorrhage, it is indicated 
lest local extension or general toxemia develop; the surgical mortality 
is 60, and the medical, 90 per cent. 

CHRONIC PANCREATITIS. 

Etiology and Pathology. — (a) Gall-stones in the common duct may 
induce chronic catarrh of Wirsung's duct, leading to chronic pancreatitis 
(Robson) . (6) Cancer, gastroduodenal catarrh and ulceration (alcoholism, 
syphilis and pancreatic calculi) may produce the same results. In these 
instances ascending infection appears to be the potent factor, causing 
interlobular fibrosis around the pancreatic lobules (Opie) ; diabetes is a 
late and uncommon sequence, (c) In liver cirrhosis and hemochromatosis 
(see pages 572 and 574) an interacinar fibrosis occurs, developing in 
the lobules, diffusely invading the islands of Langerhans and causing 
glycosuria; it does not result from obstruction of the common duct. 

Symptoms. — Riedel, who first described the affection, holds that it 
is found more frequently with increasing thoroughness of operations for 
gall-stones. Symptoms may be lacking. They vary with the cause. 
In catarrh due to gall-stones there is a history of colic, jaundice and some- 
times intermittent fever. Tenderness in the epigastrium, a fulness above 
the umbilicus and loss of flesh are noted, and if pancreatic symptoms 
predominate the pain passes from the epigastrium to the left side, to the 
scapular or renal region. If gall-stones are not the cause, the pain may 
be moderate or absent. The gall-bladder may enlarge from obstruction 
of the common duct, when the liver becomes enlarged. Marked enlarge- 
ment of the spleen is frequent, bile is found in the urine in 60 per cent., 
calcium oxalate crystals in 40 per cent, and glycosuria in 5.5 per cent. 
(Robson). Opie found glycosuria but once in 22 cases. A tumor-like 
induration of the head of the pancreas simulates cancer because of the 
emaciation and deep icterus; differentiation may be impossible, even 
during laparotomy; it is more common in subacute than in chronic 
cases. As in tumor, excessively copious, pale stools, laden with fat and 
undigested muscle fibers, are noted. Polyuria is reported. 

Prognosis. — Without surgical intervention death is likely to occur 
from emaciation, cholemia, diabetes or hemorrhagic diathesis. 

Treatment. — Drainage of the gall-bladder or anastomosis is indicated. 
Robson operated on 62 cases and Quenu and Duval on 62 cases with 13 
per cent, mortality. Hemorrhage is a dreaded complication. 

PANCREATIC APOPLEXY. 

Pancreatic hemorrhage has been described by Spiess (1866), Klebs 
(1870) and Zenker (1876); Anders (1899) collected 40 cases. The 
anemias, syphilis, alcoholism, acute infections and local lesions of the 
pancreas seem to be predisposing causes; 66 per cent, occur in men. 
Doubtless many reported cases are acute hemorrhagic pancreatitis. 



604 DISEASES OF THE PANCREAS 

Sudden onset, collapse, epigastric pain, ileus, and normal or subnormal 
temperature mark the affection; death sometimes occurs within a few 
hours. If the patient survives the initial stage suppuration may develop 
in the pancreas and tissues into which the hemorrhage burrows; hemor- 
rhagic cysts may form. The treatment is surgical. 

LITHIASIS. 

About 100 cases of sialolithiasis pancreatica are recorded. The etiology 
is probably infection of Wirsung's duct; stagnation of secretion is a pre- 
disposing factor, whence the occasional association with gall-stones, 
pancreatic inflammation and tumor. 

Symptoms and Diagnosis.— Confusion with gall-stones is often in- 
evitable, for colic without icterus is indicative of either condition and 
their coexistence is not uncommon. The pain may radiate to the left 
side and shoulder. In some cases stones were found in the feces during 
life, in others at autopsy. Salivation is reported. In Lichtheim's case 
there were colic, diarrhea and glycosuria (found in 45 per cent, of cases) . 
The stones are single or multiple (even 300), whitish-gray, round, oval, 
irregularly outlined or branching, hard or friable and vary from almost 
impalpable gravel to the size of a hazel-nut. They consist largely of 
calcium carbonate and phosphate. Shattuck described an oxalate 
calculus. The x-rays may detect them. Their sequelae are obstruction 
and inflammation of Wirsung's duct and acute suppurative pancreatitis. 
The treatment in fortunately diagnosticated cases is surgical. 

PANCREATIC CYSTS. 

To Nicholas Senn (1885) belongs the credit of establishing the clinical 
picture. Bessel-Hagen (1900) collected 149 cases. 

Etiology and Pathology. — (a) Many reported cases are extra-pancreatic, 
especially the traumatic cysts, which constitute three-quarters of cysts. 
(b) Duct obstruction (ranula pancreatica, Virchow) by calculi, strictures, 
parasites, tumors or inflammation in the smaller ducts is an etiological 
factor, (c) Cystadenoma is the cause of most true cysts (Lazarus), (d) 
Cysts rarely result from an old hemorrhage. In all forms the cyst causes 
parenchymatous atrophy, (e) Sex: Traumatic and inflammatory forms 
are most frequent in men and the cystadenomatous type in women. 
(/) Age: Over 50 per cent, are found in the third decade of life, though 
there is a congenital form, sometimes with cystic liver and kidneys 
(Richardson). 

Symptoms and Diagnosis. — 1. As to the cyst, (a) a deep retroperitoneal 
swelling is found, (6) which is more or less central, and above the navel 
in 87 per cent., where other cysts are most uncommon; it lies behind 
or between the inflated stomach and colon, sometimes below the colon 
but rarely above the stomach; very large cysts which contain 10 to 20 
quarts may fill the abdomen. Proliferative cysts developing in the tail 
of the pancreas, point toward the spleen or left kidney, (c) Its form is 
round or oval and smooth; (d) its consistence varies; (e) it is immobile on 



TUMORS OF THE PANCREAS 605 

palpation and on inspiration. (/) The fluid is alkaline, 1.010-25 sp. gr., 
mucoid, blood-stained in 82 per cent. (Korte), and in 45 per cent, contains 
one or more pancreatic ferments (diastatic, saponifying or tryptic) of 
which the latter alone is characteristic, for the other ferments occur 
in various exudates. The fluid sometimes contains fat and cholesterin; 
aspiration is dangerous, because the tension of the cyst is great and fat 
necrosis or peritonitis may result from leaking after exploratory puncture. 

2. So-called pancreatic symptoms are rare, as emaciation, salivation, 
glycosuria or stools laden with undigested fat or muscle fibers. 

3. Symptoms of peritonitis or intestinal obstruction may occur in 
traumatic or inflammatory types and after rupture. The author saw 
a case in which the picture after each rupture was that of subacute 
tuberculous peritonitis. Rupture into the bowel is followed by diarrhea 
and disappearance of the tumor. 

4. Pain like that of cholelithiasis may be present, but it more often 
radiates to the left side, shoulder and neck. Pressure symptoms include 
dyspnea, vomiting, icterus, emaciation and polyuria. 

Differentiation from other cysts is largely a topographical question. 
Ovarian cysts have their pelvic origin and connection, but hydronephrosis 
is movable and originates in the flank to which pancreatic cysts seldom 
penetrate. Fluid in the lesser peritoneal sac or mesenteric, omental 
and retroperitoneal cysts are difficult to distinguish. Cysts of the liver 
present respiratory excursion. 

Treatment. — Aspiration is never permissible. Enucleation of the sac 
is more dangerous than simple drainage. Bessel-Hagen's operative 
mortality was 6.7 per cent. Diabetes has followed operation. 

TUMORS OF THE PANCREAS. 

Cancer constitutes 67 per cent, of all pancreatic diseases but con- 
fusion with benign induration has been frequent until of late years. 
It occurs in 0.6 to 1 per cent, of autopsies. In 132 cases of pancreatic 
tumors 127 were cancer, 2 sarcoma, 2 cysts and 1 gumma (Segre). 
Sarcoma is usually secondary from contiguous lymphosarcoma in the 
retroperitoneal glands; 21 cases are reported. 

Cancer is usually scirrhus, less often medullary, colloid or adenomatous. 
It most often begins in the head of the organ. In some cases it may be 
secondary to pyloric cancer. 

Symptoms. — (1) Tumor is the commonest and surest symptom, occur- 
ring in 25 to 50 per cent.; it lies deep, beside the spine at the level of the 
navel and between the pylorus and colon. It is tender* and immobile; 
small tumors are commonest ; in some instances it may show propagated 
pulsation from the aorta or a bruit from its compression. Palpation should 
be made with the stomach and bowels empty. (2) Icterus occurs in 72 per 
cent., increases gradually and is more often continuous than remittent. 
Occasionally, just before death, the growing anemia seems to lessen the 
jaundice. Bard and Pic state the liver is usually rather small. (3) 
The gall-bladder is usually enlarged (perhaps shrunken when the hepatic 
or cystic duct is obstructed.) (4) Pain and early vomiting are usual. 



606 DISEASES OF THE PANCREAS 

The pain is epigastric, severe and sometimes neuralgic (neuritis celiaca) 
or radiating, as in pancreatitis or lithiasis. (5) Cachexia is marked and 
rapid; great prostration, emaciation and a syncopal tendency occur as 
in other pancreatic lesions. The temperature is subnormal. (6) The 
stools may contain much fat (Kuntzmann, 1827, and Bright, 1833); 
in steatorrhea the fatty acids and neutral fats are more abundant than 
the fatty soaps (Muller); its significance grows if diarrhea and icterus 
are not present. The stools also contain many undigested muscle fibers 
(lientery) and sometimes blood is present. (7) The urine. Mirallie 
encountered glycosuria in 26 per cent.; in Robson's 15 cases it was 
absent. It is said to be an early symptom and to disappear with the 
increasing icterus. Albuminuria is more frequent. The indican is 
decreased. Peptone, maltose and fat have been found. Polyuria and 
bronzing of the, skin are rare findings. Complications include compression 
of the aorta or cava; retention cysts of the pancreas; and extension 
by contiguity to the portal vein, pylorus, bowel, peritoneum, ureter or 
lungs. 

Differentiation. — 1. Chronic pancreatitis with icterus and tumor may 
not be differentiated even by laparotomy (Riedel), though ascites 
indicates neoplasm and recovery means inflammation. 

2. Duodenal cancer above the papilla causes rather the picture of 
pyloric stenosis; in cancer below the papilla pancreatic juice may be 
recovered from the stomach. 

3. Liver disease, with the frequent icterus, ascites and splenic enlarge- 
ment, causes little difficulty in differentiation. 

4. Calculus in the Common Duct. vs. Compeession of Common Duct by 

Pancreatic Tumor. 

1. History of colic usual. Absent. 

2. Tenderness of gall-bladder usual. Absent. 

3. Icterus, often remittent. Permanent. 

4. Liver less large than in — pancreatic tumor. 

5. Intermittent fever, and rigors. Subnormal temperature. 

6. Gall-bladder (see gall-stones) shrunken Dilated in 92 per cent. (Courvoisier's. law). 

in 80 per cent. 

7. Slower course. Very rapid emaciation. 

According to Bard and Pic the icterus, enlarged gall-bladder, rapid 
emaciation, cachexia, subnormal temperature and normal or smaller 
liver of pancreatic cancer can only be confused with some few cases 
of gall-stones, cancer of immediately adjacent parts, primary cancer 
of the liver or bile-passages and primary duodenal or gastric cancer 
with early diffuse generalization in the liver. Kehr states that chronic 
obstruction of the common duct is cancerous in 70 per cent., pancreatic 
in 20 per cent, and calculous in 10 per cent. 

Treatment is largely symptomatic; morphine should be given for 
pain, the gall-bladder should be drained (cholecystotomy) or it should be 
sutured to the intestine (cholecystduodenostomy). Very few permanent 
recoveries follow extirpation. 



ACUTE DIFFUSE PERITONITIS 007 



DISEASES OF THE PERITONEUM. 



ACUTE DIFFUSE PERITONITIS. 

Peritonitis was once far more important as an independent affection 
than at present; we now regard it as chiefly symptomatic of some other 
disease, e. g., appendicitis, salpingitis, puerperal sepsis, etc. 

Etiology. — The actual cause is mycotic. Some writers classify peritonitis 
as bacterial (suppurative forms), chemical (serous and serohemorrhagic 
forms) and mechanical (adhesive forms). The Streptococcus pyogenes 
(puerperal and traumatic forms) and Bacillus coli (forms due to intestinal 
lesions) are the two most frequent organisms; the staphylococcus, pneu- 
mococcus and tubercle bacillus are frequent and less often the Bacillus 
pyocyaneus, proteus, anthracis, typhosus, aerogenes encapsulatus, the 
ray fungus, gonococcus, Ameba coli, etc. Generally speaking, mono- 
infections are less common than mixed injections. 

Factors lessening physiological resistance include nephritis (in 10 per 
cent.), alcoholism, cardiac disease, etc.; in other words peritonitis may 
be a terminal infection, fatal to reduced subjects. 

Atrium. — Compared with pleurisy and pericarditis, peritonitis is 
seldom primary. Though it may follow inflammation of every abdominal 
viscus, it is most commonly a secondary manifestation of intestinal 
disease (e. g., appendicitis) or of pelvic disease in women, (a) Infection 
through the alimentary tract; appendicitis, bowel ulceration (typhoid, 
carcinomatous, tuberculous), bowel obstruction, perforation, traumatism 
and infarction may cause it. Gastric are less frequent than intestinal 
lesions and ulcer and cancer rank first. (6) The female genitalia; it may 
result from gonorrhea (Nogerrath), extra-uterine pregnancy, puerperal 
infections and septic abortion; peritoneal infection from diseases of the 
male genitalia is rare, (c) Liver and bile vessels; local or general peritonitis 
may result; peritonitis is more common as a result of hepatic abscess 
and syphilis than of echinococcus, cancer, pylephlebitis or cholecystitis. 
(d) Pancreas; acute pancreatitis, (e) Kidney and bladder; pyonephrosis, 
calculi or ulcerations of the bladder. (/) Rarer causes are splenic affec- 
tions, retroperitoneal adenopathies, spinal or costal caries, lesions of the 
thoracic duct or the abdominal parietes or extension through the dia- 
phragm, (g) Metastatic peritonitis is not common, though observed 
in septicopyemia and acute infections, (h) In children fetal peritonitis 
has been observed by transplacental infection; in the newborn the 
umbilical vein may convey infection, though peritonitis occurs in but 
8 per cent, of fatal cord infections. It occurs more commonly through 
the lymph vessels of the cord. 

Age and Sex. — Most cases occur between the ages of fifteen and 
forty and women are more often affected than men. 

Symptoms. — 1. Local or Abdominal. — (a) Pain, the usual initial 
symptom, is almost invariable, is continuous, begins near the navel and 
remains greatest there; a causal gastric ulcer may produce pain in the 
back, salpingitis is attended with early pelvic pain and appendicitis 



608 DISEASES OF THE PERITONEUM 

has its own initial localization, but the pain of diffuse peritonitis is felt 
at or below the navel. (6) Tenderness accompanies pain and is deep 
rather than superficial; they are very rarely absent and are inflammatory; 
at the operation or autopsy the visceral and parietal investments are 
reddened, lustreless, covered with a thin film of fibrinous exudate which 
binds the intestinal coils together; not infrequently the peritoneum is 
dotted with minute petechia?, (c) The attitude is characteristic: the head 
is lifted and the knees are drawn up to relieve tension or to keep the 
bedclothes from contact with the abdomen, (d) Vomiting is reflex; it 
occurs early and greatly aggravates the pain; the vomitus contains food 
and later bile; it may be green (vomitus herbaceus), rarely dark brown or 
fecal. It is accompanied by redness and dryness of the tongue, great 
thirst and singultus which is a sensory phrenic symptom; before the fatal 
issue vomiting and singultus cease, (e) The abdomen is at first tense, 
retracted and scaphoid, but later becomes tympanitic from paresis of the 
inflamed intestinal coils (Stokes) and decomposition of their contorts; 
the diaphragm stands high and its movement is restricted; in sRne, 
especially muscular subjects, the abdomen may be retracted throughout 
the course. Percussion may elicit dulness, usually due to serous, sero- 
purulent or perhaps serohemorrhagic exudation, which may be effused 
in small pockets between fresh adhesions or may fill the entire cavity, 
amounting to even 30 or 40 quarts and sometimes fluctuating to the hand ; 
as a ride a tympanitic note prevails; in some cases dulness suggests the 
presence of fluid which, however, is not found on exploration; because 
of adhesions, the fluid changes little on change of posture. On ausculta- 
tion a friction-rub is sometimes heard (Beatty and Bright), chiefly over 
the liver. (/) Constipation results from inflammatory infiltration of the 
intestine (Stokes); in the puerperal streptococcic and in pneumococcic 
peritonitides, diarrhea is common. 

2. General Symptoms. — (a) Shock is a conspicuous symptom. Col- 
lapse may occur early and directly from perforation or later from toxemia. 
The pidse is frequent, hard, wiry and about 120; later it becomes thready 
and runs to 140 or 170. The fades Hippocratica is pronounced, with 
its anxious expression, wrinkled, clammy, cyanotic, lead-colored skin, 
pointed nose, hollowed temples and sunken eyes. The voice whispers 
(vox cholericd) to avoid movement of the diaphragm and the breathing 
is costal, shallow, difficult and rapid, (b) Fever is usually present. It 
may rise abruptly with a chill at the onset but follows no set type; it 
may be continuous or remittent and is usually found by rectum, even 
during collapse. The fever and pulse curves may run parallel in peritonitis 
with a slow course, (c) The lungs and heart are crowded upward by the 
abdominal distention. The apex-beat is high and further to the left as 
the heart lies more horizontally, (d) The urine is scant from lessened 
absorption and from cardiac weakness; albuminuria is frequent; indican- 
uria is constant from increased putrefaction in the paretic bowel; dysuria 
is usual; tenesmus is less common than retention. 

Course. — The issue is fatal within two days in the rapidly fatal toxemic 
form in which there is only roughening of the peritoneum without exuda- 
tion; the slower cases rarely last more than five days. Consciousness 



ACUTE DIFFUSE PERITONITIS 609 

is usually preserved to the end, though stupor or delirium occasionally 
intervenes; the pulse becomes thready, the breathing shallow and sighing, 
the superficial temperature is low and the patient succumbs to toxemic 
cardiac failure. In exceptional cases death occurs within a few hours 
or relative recovery results with encapsulation of pus. Treves found 
inhalation pneumonia in 17 per cent, of his cases and Tilger found serous 
pleurisy in 25 per cent.; of the latter, 63.3 per cent, were right-sided, 
3.3 per cent, left-sided and 33.3 per cent, bilateral. 

Types. — (a) Peritonitis serosa usually follows the fibrinous form; 
the fluid is yellow or light green, its specific gravity is 1.015 or more, 
it contains 2 or 3 per cent, of albumin and flocculi of fibrin, epithelial 
cells, red cells and leukocytes, (b) P. pundenta may occur in pockets 
or as a massive pyoperitoneum, amounting to 30 or 40 quarts, (c) 
P. putrida occurs in septicopyemia and puerperal fever, but especially 
in perforating carcinoma; fetid peritonitis may occur without perfora- 
tion, (d) P. perforatum is characterized by two groups of symptoms, 
(i) those of peritonitis and (ii) those of gas in the peritoneal sac (pneumo- 
peritoneum, pneumatosis peritonei); there is often the initial subjective 
sense of perforation, sudden pain, collapse and retracted abdomen; in 
four to twelve hours diffuse peritonitis sets in; free gas may obliterate 
the dulness of the liver and spleen, though this also results from great 
tympanites without perforation; the liver dulness may be found only 
in the posterior axilla, but when the patient is turned on his left side the 
free gas entirely obscures it; the abdominal contents may be putrid or 
fecal; when due to perforating gastric ulcer there is seldom any odor. 
The diaphragm is pushed to its highest possible level; a succusion splash 
may be elicited and the intestines may be compressed against the spine. 
Gas may develop through the action of the Bacillus pyogenes fetidus 
and B. aerogenes encapsulatus, but pneumoperitonitis without perfora- 
tion is rare, (e) P. puerperalis, usually streptococcic, is described on 
page 22; it is characterized by moderate pain, enormous tympanites, 
diarrhea and the usual septic manifestations. (/) P. pneumococcica; 
Barling (1912) collected 234 cases; 73 per cent, occur in young girls. 
There are three types : (i) the very acute form, in which the lower abdomen 
is especially involved, often simulating appendicitis, with abrupt onset, 
severe pain, high fever, vomiting and early, continuous, fetid diarrhea; 
one-half of the cases die. .(ii) With the above symptoms or perhaps 
pneumococcic involvement of the joints, ear, meninges, etc., there are 
signs of pneumonia and peritonitis; most patients die. (iii) The last type 
is more subacute, uniting symptoms of sepsis with those of pneumonia 
and peritonitis; nearly all of this form die. The mortality of all types 
is 80 per cent. The process is diffuse and fibrinopurulent; operation is 
indicated later. It often points at the navel, through which a creamy, 
greenish pus may rupture. Sometimes it ends by crisis; an encysted 
pus sac often remains. The pneumococcus may be found in the blood. 
(g) The streptococcic, colon and staphylococcic peritonitides are described 
under Appendicitis. 

Diagnosis. — Peritonitis is usually diagnosticated with ease from the 
cause (appendicular, salpingitic, gastric ulcer, septic abortion), by the 
39 



610 DISEASES OF THE PERITONEUM 

febrile onset, pain, tenderness, vomiting, distention, effusion and collapse. 
Aspiration is dangerous. In certain cases only the fact of peritonitis 
can be established, perhaps even at operation. 

Differentiation is necessary from (a) intestinal obstruction (q. v.); 
(b) biliary or renal colic; (c) acute pancreatitis (q. v.); (d) ruptured tubal 
pregnancy, in which the menstrual history, pelvic localization, acute 
anemia and shock are present; (e) ruptured abdominal aneurysm; or 
infarction of the superior mesenteric artery in which a cause for embolism, 
acute obstruction and bloody vomiting or diarrhea with later peritonitis 
are often distinctive; (J) acute enterocolitis, which is attended by less 
pain and tenderness and by more diarrheal colic, tenesmus and collapse; 
(g) hysteria (q. v.), which may simulate peritonitis, as it may resemble 
every other disease; if its presence is once suspected the other stigmata 
are usually definitive, (h) The referred abdominal pain of thoracic 
disease (pleurisy and pneumonia) is very seldom accompanied by tender- 
ness, and is distinguished by examination of the chest, especially of its 
posterior parts, (i) Mild infections with much exudation may simulate 
ascites (q. v.). 

Treatment. — Surgical treatment alone is efficacious. In older statistics 
the percentage of recoveries was small (Krogius, 680 cases, 28 per cent.). 
At present, 90 per cent, recover under drainage, semi-erect posture and 
continuous enemata of normal salt solution at low pressure. 

Palliative treatment is of little value, (a) Opium controls pain; the 
doses recommended by Alonzo Clark (over 1000 grains in one week!) are 
now only of historical interest. Morphine, given hypodermically, pro- 
duces the best results, (b) The patient should have absolute rest, (c) Tait's 
saline purgation to increase osmosis is productive of more harm than good. 
(d) Vomiting is treated as in acute gastritis; the stomach should be 
washed out; all medication, food and water by mouth should be withheld 
and given only by rectum, (e) Tympanites should be treated by the 
turpentine stupe and by enemata containing emulsum asafetidse 3hj, 
spts. chloroformi 5j and ol. terebinthinse 3ss. 

CHRONIC DIFFUSE PERITONITIS. 

Aside from tuberculous peritonitis, chronic diffuse peritonitis is uncom- 
mon, (a) The serous or serohemorrhagic form will be considered under 
ascites; (b) the diffuse adhesive form results from acute and tuberculous 
peritonitis; the peritoneal sac is obliterated and at operation or necropsy 
the knife cuts directly into the intestine. . (c) Chronic proliferative 
peritonitis may occur in peritoneal cancer or tuberculosis, chronic alco- 
holism, cirrhosis of the liver or cardiac, disease. It may develop with or 
without adhesions, as a diffuse sclerosis of the peritoneum and as a sub- 
peritoneal proliferation. Its extreme form was described by Virchow 
(1885) as peritonitis deformans. The peritoneum is white, lustreless and 
diffusely thickened, though in some places more than in others. The 
omentum is retracted upward, so that it lies as a hard, transverse roll 
above the navel; the mesentery is indurated (mesenteritis retrahens), 
as described under Tuberculous Peritonitis and as it retracts it may 



LOCALIZED PERITONITIS 611 

gather the intestinal coils into a ball the size of a child's head, lying cen- 
trally or to the right of the median line. Here and there may be found 
multilocular serous encapsulations or palpable tumor-like thickenings. 
The spleen, liver, stomach, cecum or colon may be particularly, indurated. 
In some cases it is but part of a multiple serositis (polyserositis, polyor- 
rhomenitis), invading also the pleura and pericardium. Miliary fibromata 
resembling miliary carcinosis or miliary tuberculosis, may sometimes form 
around parasitic ova or cholesterin crystals. 



LOCALIZED PERITONITIS. 

I. Suppurative Forms. — 1. Subphrenic Abscess and Pyopneumothorax 
Subphrenicus. — First diagnosticated by Barlow (1845) and especially 
described by Leyden (1879), Piquand collected 890 cases (1909), upon 
which the following figures are based: 

Etiology. — (a) Gastric ulcer and cancer accounted for 251 cases, (b) 
Appendicitis caused 191 cases; (c) trauma; (d) intestinal ulceration (duo- 
denum 36 cases and the rest of the intestine 20 cases); (e) cholangitis 
and cholecystitis (66 cases); liver disease (echinococcus, abscess) 70 cases; 
(/) splenic disease (40 cases); (g) renal disease (28 cases); (h) thoracic 
disease (32 cases); (i) pancreatic disease (27 cases), tuberculosis (23 cases), 
female genitalia (17 cases), trauma (20 cases) and unknown causes 
(69 cases). 

Symptoms. — Pus is ensacculated beneath the diaphragm (pyothorax 
subphrenicus), associated in over 25 per cent, with gas formation (pyo- 
pneumothorax subphrenicus). The subphrenic abscess is right-sided in 
59 per cent., left-sided in 38 and bilateral in 3 per cent., is limited by 
the suspensory ligament of the liver and may be intra- or extraperitoneal ; 
in the latter instance the abscess is most often appendicular or peri- 
nephric and lies well back in the abdomen. Simple pus formation is often 
difficult to localize ; the symptoms are those of sepsis, with pain, tenderness 
or dulness on the liver convexity, which suggest liver abscess. The 
retroperitoneal forms give most dulness posteriorly, and intraperitoneal 
forms chiefly anteriorly; edema of the chest wall may occur without 
suppuration; the z-rays may produce a subphrenic shadow. 

In pyopneumothorax subphrenicus there are signs "of a cavity beneath 
the diaphragm, filled with gas and pus, pushing the diaphragm upward 
and simulating pyopneumothorax" (Leyden). (a) Tympany and absence 
of vesicular murmur and of vocal fremitus are found from the third rib 
downward, above which is the compressed lung and below which is (b) 
the dulness of the liver whose exposed surface and edge, dislocated down- 
ward, are easily percussed and palpated. Sometimes the tympany 
entirely covers the liver dulness. As in pneumothorax (c) succussion 
and, on change of posture, the clearly shifting line of dulness may be 
elicited, (d) Puncture evacuates gas and putrid pus; sometimes on a 
higher puncture serum is found in the pleura, for pleurisy develops in 
66 per cent, of the cases. The needle ascends during inspiration and 
descends during expiration, which is the converse of the findings in pleural 



612 DISEASES OF THE PERITONEUM 

exudation (Furbringer) . If a manometer is attached to the exploring 
needle, a rise in the indicating column during inspiration and a fall during 
expiration denote a subphrenic lesion (Pfuhl). (e) The x-rays may 
show a shadow between the diaphragm and the liver and no respiratory 
excursion, (f) Perforation into the lungs occurs in 16 per cent, (more 
often in extra- than in intraperitoneal forms), into the pleura in 19 per 
cent, and into the pericardium in 1 per cent. At the beginning and until 
perforation there is generally an entire absence of thoracic symptoms, 
as cough or sputum; this is of value in differentiation from true pyo- 
pneumothorax, (g) The history of the subphrenic pyopneumothorax is 
usually that of some abdominal lesion (v. Etiology). 

Treatment is surgical. Without operation the mortality is over 90 
per cent.; with operation 30 per cent. 

2. Suppuration in the Lesser Peritoneum. — This may result from gastric 
or duodenal ulceration, acute pancreatitis, etc. Closure of the foramen 
of Winslow confines the pus; a tumor appears in the epigastric, umbilical 
or left hypochondriac region, with relations like those of pancreatic 
cyst; variability in size occurs when the stomach is filled with gas and 
fluid. When gas and pus coexist the diaphragm and liver are pushed 
upward. Treatment is surgical. 

3. Other Forms. — The appendicular abscess has been described. The 
pelvic abscess occurs especially from tubal, but also from uterine and 
ovarian inflammation; it follows abortion, puerperal fever, gonorrhea, 
tuberculous and pneumococcic peritonitis in young girls. Other types 
are suppuration around the gall-bladder, colon and sigmoid and in other 
rare localizations. 

II. Adhesive or Indurative Forms. — Local thickening or adhesions 
may occur over any viscus, especially over the spleen, next the liver and 
less commonly the intestines, which may become strangulated. 

Perisplenitis is most common over chronic malarial, leukemic and 
pseudoleukemic enlargements of the spleen. 

Perihepatitis may cover small areas of the liver like soldier's spots 
in the pericardium or may engross its entire surface, as described by Budd 
(1852) and Curschmann (1884), who called it the "icing liver" (Zucker- 
gussleber). It is frequently associated with deforming proliferative 
peritonitis. Nichols describes it as a hyaline degeneration, hyaloserositis. 
There are three groups of cases: (a) multiple serositis (polyorrhomenitis, 
Concato's disease); this borders closely on Pick's " pseudocirrhosis peri- 
carditica." (b) Arteriosclerosis and interstitial nephritis occurred in 86 
per cent, in Hale White's series, (c) Rarer factors are syphilis, tuber- 
culosis, malignancy and alcoholism (page 616). 

III. Chronic Hemorrhagic Peritonitis. — This rare disease was de- 
scribed first by Virchow, Avho likened it to pachymeningitis hemor- 
rhagica. It occurs chiefly in the pelvis and is most often circumscribed. 
Pachyperitonitis is characterized by hemorrhagic inflammation; from 
the laminae of the resulting fresh connective tissue, deposited layer by 
layer, repeated fresh hemorrhages arise, 



ASCITES 613 



CARCINOMA OF THE PERITONEUM. 

Primary endotheliomata are very rare. 

Cancer is most frequently secondary to cancer of the stomach, ovaries, 
intestines, pancreas and liver. Histologically it is that of the primary 
growth. Its gross forms are (a) miliary carcinosis, resembling miliary 
tubercles; (b) vegetative; (c) ulcerative; (d) cystic and (e) infiltrative. The 
primary tumor may be latent clinically, so that the peritoneal compli- 
cation is apparently primary. The secondary growths spread by contact, 
the lymphatics and implantation of free particles. They may be felt 
in the omentum, mesentery and Douglas's cul-de-sac. The diagnosis is 
reached by the symptoms and signs of the initial growth or by those of 
an ascites, which is serous, hemorrhagic, pseudochylous or adipose; 
its progress is rapid and attended by cachexia. Groups of cancer cells 
may be found in the aspirated fluid and secondary cancer may develop 
at the point of puncture (page 616). In Hodenpyl's remarkable case, 
which recovered, the ascitic fluid exerted a curative action when injected 
into animals with cancer. 

ASCITES. 

Hydroperitoneum is a symptom of various diseases. 

Etiology. — (a) Stasis explains most of the cases; the chief varieties are 
cardiac lesions (40 per cent.), pulmonary, mediastinal or pleural disease 
and portal stasis (10 per cent.), due to disease of the liver or portal vein. 
Stasis causes increased pressure in the portal system, followed by mal- 
nutrition of the vessels and pouring out of serum, (b) Hydremia or 
cachexia causes malnutrition and increased permeability of the vessel 
walls; it occurs in amyloidosis, chronic nephritis (10 per cent.); marantic 
conditions, profound anemias and occasionally in acute infections, (c) 
Inflammation, as simple, tuberculous (10 per cent.), suppurative or can- 
cerous peritonitis (20 per cent.), (d) Abdominal tumors, leukemic spleen, 
etc. More than one factor may operate; tuberculous peritonitis may 
complicate liver cirrhosis or ascites may be due to the hydremia of 
nephritis, accentuated by weakness of the heart (v. i. Etiological 
Diagnosis). 

Symptoms. — 1. Inspection. — A symmetrical enlargement of the abdo- 
men in the average case presents rather more lateral than anterior 
bulging. The abdomen resembles that of a batrachian (ventre de batracien) . 
The skin is pale, tense, striated, edematous; the pouting navel and dias- 
tasis of the recti muscles are noted. A caput Medusa? may be noted in 
cirrhosis cases. Dilated veins over the ribs and upper abdomen indicate 
compression of the cava inferior. Sometimes the heart imparts systolic 
waves to the fluid. 

2. Palpation. — Fluctuation (ballottement) , due to the transmission 
of a fluid wave from side to side, is usually present but may be absent 
because of tense abdominal walls or great accumulation of fluid. Pseud o- 



614 DISEASES OF THE PERITONEUM 

fluctuation may be caused by accumulation of fluid other than ascitic, 
as intestinal contents, or by lax, obese abdominal walls; in the latter 
condition a third hand placed in the median line of the abdomen, will 
break the deceptive wave, due to parietal vibration. In women the water- 
pillow fluctuation of Landau may be elicited by vaginal examination and 
the uterus seems remarkably movable. Thrusting palpation may disclose 
the outline of the liver, spleen or possibly some neoplasm even through 
the abundant fluid (placing the fingers vertically on the abdomen and 
suddenly thrusting them inward, thus anticipating any muscular rigidity 
and pushing aside the ascitic fluid) . 

3. Percussion. — A pint to a quart of fluid must be present for clinical 
detection. With small effusions the patient should be examined in the 
genupectoral position. Elevation of the buttocks directs the scanty fluid 
to the flanks where it is more easily demonstrable. Classically, the fluid 
in dependent parts gives dulness and the supernatant intestines are located 
by tympany in the highest parts of the abdomen. These areas vary with 
change of position. This rule is void when the mesentery is retracted 
and does not allow the gut to float; adhesions between the intestinal 
loops prevent shifting of the fluid; when the gut is adherent there is per- 
manent tympany in that location. Light percussion is employed, because 
heavy tapping elicits tympany from the more deeply situated intestine. 
The author withdrew two gallons of ascitic fluid from a patient in whom 
no dulness could be elicited in any position. 

Diagnosis. — Fecal accumulations cause dulness in either flank, simu- 
lating fluid, but its immobility and the use of enemata preclude error. 
Kiissner published a case in which fluid in the intestines was mistaken 
for ascites. Leube confused ascites with an enormously dilated stomach 
and John Hunter thrust a trocar into a dilated bladder. Hydronephrosis, 
hydatid cyst, pregnancy and tympanites are frequently sources of error. 
Rostan (1837) noted that tympany might be absent in ascites when 
the intestines contained little or no gas, a point sometimes forgotten 
in differentiation between ascites and ovarian cyst; the latter may thrust 
itself in between the coils of gut and simulate ascites; ovarian cyst usually 
produces a central flatness with tympany in the flanks, and neither the 
dulness nor tympany shifts with change of posture. Adami collected 
42 cases of fibrolipoma and myxolipoma in which ascites was closely 
simulated. 

Etiological Diagnosis. — 1. Stasis. — In cardiac disease the dyspnea 
develops early; dyspnea caused by ascites pressing upward on the dia- 
phragm is a late symptom. Swelling of the feet usually antedates the 
ascites, though pericarditis and valvular disease may produce ascites 
without anasarca. The liver is peculiarly an etiological factor in ascites 
(see page 587). Portal ascites commences in the peritoneum; the legs 
swell secondarily from pressure on the cava inferior or from cardiac 
weakness due to great ascites (see page 616). 

2. Hydremia. (Cachexia, Increased Vascular Permeability.) — In 
renal disease the eyelids often become edematous before other symptoms 
develop and the nephritic ascites is seldom great unless the liver and 
heart are involved. Cachectic ascites is not uncommon in leukemia 



ASCITES 615 

and kindred affections and in acute infectious diseases in children; the 
author has seen three instances of ascites in typhoid convalescence. 

3. Peritonitis. — The specific gravity and the percentage of albumin 
in the fluid are important factors in differentiating between exudate 
and transudate. Three divisions are distinguished : (a) A specific gravity 
of 1.010 or lower indicates a cachectic transudate, e. g., in nephritis, with 
less than 1 per cent, albumin. A very low specific gravity and percentage 
of albumin occur in amyloidosis. (6) A hypostatic transudate has a specific 
gravity which ranges between 1.010 and 1.014 and has between 1 and 3 
per cent, of albumin, (c) An exudate has a specific gravity of more than 
1.015 (or 1.018) and the albumin reaches 4 to 6 per cent. The lower 
strata are heavier and the specific gravity should be measured several 
times during the paracentesis. Less than 1 per cent, of albumin excludes 
disease of the peritoneum or portal vein. Reuss's formula computes 
the albumin percentage from the specific gravity — the percentage of 
albumin = f (specific gravity minus 1000) minus 2.8. Ascites due to 
a carcinoma in the liver substance has a low specific gravity and albumin 
is present to 1 or 2 per cent.; if carcinomatous peritonitis develops, the 
specific gravity and percentage of albumin increase. An ascites due to 
nephritis has a low specific gravity but the figures rise when stasis due 
to weak heart or intercurrent inflammation develops. In simple transu- 
dation (ascites and hydrothorax), the characters of an exudate may 
develop, due to the long-continued irritation of the serosa. 

Ascitic fluid contains the constituents of the blood — albumin, globulin, 
urea, uric acid, sugar, etc. (a) Ascitic fluid due to stasis is clear yellow 
or yellowish-green, opalescent and alkaline and microscopically contains 
some lymph cells, erythrocytes and peritoneal endothelium. (6) Exudates 
show a microscopic picture varying w T ith the cause; fibrin threads, pus, 
blood, adipose, chylous or chyliform fluid, intestinal contents, cancer 
cells, tubercle bacilli, diplococci or pyogenic organisms, may be found. 
In exudates are found the polymorphonuclear leukocytes and some 
erythrocytes; lymphocytes and red cells are detected in tuberculous 
exudates (see page 460) ; the fluid must be examined at once. Rieder 
and Dock describe cells in carcinomatous peritonitis in which asym- 
metrical karyokinetic figures appeared. Quincke states that red disks, 
lymph cells and peritoneal endothelium are found in every ascites. 

Primavera found that a drop of glacial acetic acid will leave a white 
cloud as it falls to the bottom of a vessel containing an exudate, while 
its addition to transudates gives no reaction. 

"Essential" ascites is usually tuberculous peritonitis. 

4. Tumors. — Tumors, as uterine fibromata may produce hydro- 
peritoneum. Very small uterine myofibromata may excite considerable 
peritoneal effusion. There is a direct relation between the malignancy of 
the tumor and the amount of the fluid found. Ascites is infrequent in 
uterine tumors but when observed is most common in adenomyoma 
(Freund). It is more often seen in papillomatous cysts, whose walls 
rupture by fatty degeneration and pour out their contents into the 
abdominal cavity; serum is secreted by the peritoneal surface because 
of the irritation, even though the ruptured cyst be very small (Quenu). 



616 



DISEASES OF THE PERITONEUM 



The fluid in cysts contains more solids (50 to 60 pro mille) than does 
the ascites of renal disease (25 pro mille, Menu). Ascites is most often 
observed in solid ovarian tumors. 





' ' Zuckergussleber ; ' ' 


Atrophic cirrhosis 


Chronic tuberculous 


Carcinoma of 




chronic perihepatitis. 


of liver. 


peritonitis. 


peritoneum. 


Age. 


Occurs about mid- 


Oftenest about 


Between ages of 20 


Late in life. 




dle life or later. 


middle life. 


and 40. 




Sex. 


Both sexes equally 


More frequent in 


In females. 


More frequent in 




liable. 


males. 




females. 


Previous 


Often a history of 


History of alco- 


Often a chronic 


In some cases a his- 


History. 


acute pericarditis 


holism, syphilis 


cough, diarrhea, or 


tory of cancer of 




or perihepatitis. 


or digestive dis- 


genital tuberculo- 


stomach, ovaries, 






turbances. 


sis. Often with 
pleurisy (polysero- 
sitis) . 


etc. 


Alcoholism. 


No influence. 


Frequent. 


None. 


None. 


Syphil[s. 


No influence. 


Occasionally. 


None. 


None. 


Heredity. 


No influence. 


Unimportant. 


May be familial. 


Unimportant. 


Incidence. 


Acute becoming 
chronic or insid- 
ious from first. 


Insidious. 


Onset may be acute 
or insidious. 


Insidious. 


Chronicity. 


Cases last for 2-20 


May last for years 


Prolonged. 


Rapid course. 


Fever. 


years. 
Generally absent ex- 


May be afebrile; 


Usually slight; often 


Rarely absent; due 




cept during exacer- 


when present is 


absent. 


to complication or 




bation or some 


slight. 




cachexia. 




complication. 








Patn. 


Indefinite and tri- 
fling. 


Slight. 


Often marked. 


Variable; often 
marked. 


Digestive 


Slight or none. 


Constant; dyspep- 


Fairly common. 


Often marked ; ali- 


Disturbance. 




sia, nausea, 
vomiting, gastric 
hemorrhage, 
melena. 




mentary origin or 
pressure. 


Ascites. 


Constant and ex- 


Constant. Low 


Never extreme, may 


Moderate grade; may 




treme ; nutrition 


specific gravity. 


be absent, may 


be hemorrhagic or 




long maintained : 


Low albumin. . 


be hemorrhagic. 


pseudochylous. 




may be tapped 




Often sacculated. 






over 800 times; 




Tubercle bacilli ; 






may resemble peri- 




lymphocytic for- 






tonitis; albumin 3 




mula. Higher spe- 






per cent.; fibrin. 




cific gravity. 




Anasarca. 


Constant but slight. 


Slight. 


None. 


Frequent. 


Jaundice. 


Absent. 


Occurs in 15 per 
cent, of cases. 


Rare. 


Common when liver 
is enlarged. 


Liver. 


Not cirrhotic; at first 


Cirrhotic; at first 


Seldom enlarged. 


May be enlarged, 




enlarged, then 


enlarged, then 


Matting of omen- 


with nodules. 




small; smooth. 


small and warty. 
Hepatargia. 


tum may simulate 
hepatic enlarge- 










ment. May be 








nodes lower; 










doughy feel. 




Spleen. 


Gradual enlarge- 
ment. 


Gradual enlarge- 
ment ; often 
marked. 


No enlargement. 


None. 


Omentum. 


Thickened and con- 


Normal. 


Often matted up. 


Often matted up. 




tracted. 




Mesenteritis re- 
trahens. 


Mesenteritis. 



Treatment. — The treatment of ascites varies with its cause, for which 
reference should be made to valvular heart disease, atrophic cirrhosis, 
tuberculous peritonitis and nephritis. 

Paracentesis in peritoneal carcinoma and chylous ascites (v. i.) hastens 
the fatal issue. Hale White asserts that cases of cirrhosis survive but 
few punctures, while cases of perihepatitis may be punctured more than 
200 times. Lecanu reports a case of ascites in which 886 tappings were 
performed in fifteen years. In puncture, surgical antisepsis is most 
necessary, for reduced subjects are easily infected. The bladder should 
be emptied by catheterization. The trocar should be introduced in 
the linea alba to avoid injury to the bloodvessels. It should be pushed 



ASCITES 617 

carefully and is felt to penetrate the parietal peritoneum by the sense 
of something giving way. A dull-pointed probe should be sterilized, 
with which to push back the omentum if it should prolapse against the 
canula. The fluid should be evacuated slowly to obviate collapse which 
may result from dilatation of the abdominal veins, if they are suddenly 
relieved of the pressure of the effusion. A cat-o '-nine-tails bandage may 
be applied as the tapping progresses, to compress the abdominal contents. 

Chylous and Adipose Ascites. — The peritoneal cavity, more fre- 
quently than any other serous sac, is the seat of those unusual exudates 
known as chylous, chyliform, lactiform or adipose ascites. The first 
authentic case is Poncy's (1699). The literature gives about 200 cases. 
Seven have come under the author's observation. 

Chylous ascites properly designates an effusion of chyle. Adipose ascites 
contains a large percentage of fat, with no chylous admixture. Some 
authors use the terms "adipose," and "chyliform" interchangeably. 
Chyliform ascites is a chyle-like fluid in which lymph or chyle is mixed 
with exudate or transudate. 

1. Chylous Ascites. — Straus's case is the clearest example, in which 
typical chyle was extravasated through two fistulas. Ingested butter or 
olive oil is recognized in the fluid withdrawn by paracentesis. Chylous 
ascites contains sugar, which is said to be diagnostic when diabetes is ex- 
cluded. Sugar when primarily present may disappear later. Its presence 
is very suggestive; it has been detected not more than two dozen times. 
Many clinicians discount the importance of the presence of sugar as a 
diagnostic test; Bock found sugar (0.04 to 0.07 per cent.) in all cases 
of hydrops, and Eichhorst in 10 out of 17 cases of pleural exudate. A 
small amount of fat (0.9 per cent.) indicates chyle. Chylous ascites 
is rich in solids, mineral salts and albumin. Albumin and fat occur in 
small punctiform granules, susceptible of chemical differentiation. The 
escape of chyle may occur through a visible rupture or by transudation 
through the altered walls of the chyle vessels; among the most frequent 
causes of lymph or chyle obstruction are compression of the thoracic 
duct or lymph system by glands, neoplasms, peritonitis, occlusion of 
left subclavian vein, lifting or coughing, filarial disease or occlusion of 
the thoracic duct. Rupture may occur in any part of the lymphatic 
system, in the thoracic duct, receptaculum, lacteal vessels, lymph glands 
and chylous cysts. 

2. Adipose or Chyliform Ascites. — Adipose ascites is characterized 
by the absence of sugar and a higher percentage of fat. The opacity 
may be due to emulsionized albumin. Fat is found in most cases; its 
highest figure was in one of the author's cases, 6.5 per cent. The granules 
of albumin and fat are much coarser in adipose than in chylous ascites. 
Hydropic and fatty carcinoma cells may, if numerous, cause a cream}' 
layer. Red blood disks may occur, also fibrin, casein, mucin, sodium 
alkali albuminate, peptone, lecithin, cholesterin, fibrinogen, etc. Among 
the numerous etiological conditions are tuberculosis of the peritoneum 
and glands; carcinoma of the glands, peritoneum and lymph vessels; 
chronic peritonitis; liver cirrhosis, heart disease and sarcoma of the 
omentum or mesentery. 



618 DISEASES OF THE PERITONEUM 

Diagnosis. — A diagnosis has been made prior to puncture only in 
Morton's early case. The local signs and symptoms do not differ from 
those of serous ascites. Some cases diagnosed as the vulgar ascites, 
healing without treatment, are probably chylous hydrops. It is not 
easy to differentiate between chylous and adipose effusions, even at 
necropsy. 

Prognosis. — About 90 per cent, of both types die. Continuous chylous 
fistulse are always fatal. The immediate prognosis is seemingly more 
favorable in the adipose form. 

Treatment. — Surgical interference is chiefly indicated in tuberculous 
peritonitis. Paracentesis should be avoided as much as possible for it 
is weakening and precipitates the fatal issue. 



SECTION V. 

DISEASES OF THE KIDNEYS. 



ACUTE NEPHRITIS. 

Etiology. — (a) Resulting from infections, the scarlatinal nephritis (q. v.) 
is the most frequent type and develops after desquamation. Acute 
nephritis occurs in diphtheria, at the height of the disease; it is found 
in a large percentage of cases of acute enterocolitis in children; it may 
result from malaria, variola, sepsis, ulcerative endocarditis, pneumonia, 
tuberculosis and syphilis, or occasionally in typhoid, typhus, measles, ton- 
sillitis or epidemic meningitis; it is rare in German measles, varicella or 
purpura. Infections operate (i) more often by their toxins than (ii) by the 
causal microbe, though the typhoid bacillus, pneumococcus, streptococcus 
and others are found in the kidneys and urine ; (iii) in some instances hemo- 
lysins apparently cause nephritis (nephritis hemoglobinurica) . (b) Toxic 
substances, taken internally or applied to the skin, may induce acute 
nephritis, as turpentine, salicylic compounds, phenol, potassium chlorate, 
cantharides, etc. (c) Exposure to cold and dampness (with alcoholism) 
lessens the tissue resistance or acts as a hemolysin, (d) Skin diseases, 
burns, eczema and psoriasis, may impair the skin functions or produce 
hemolysins, (e) Pregnancy (v. i.), chronic B right's disease, cardiac 
affections and the dyscrasise predispose to acute nephritis. (/) Acute 
nephritis may occur independently of any known cause, and sometimes 
epidemically. 

Pathology. — Gross changes may not be apparent in mild cases, though 
in some the kidneys are swollen from marked interstitial exudation and 
are dark and heavy. In other cases the kidney is yellowish-white and 
perhaps mottled from small hemorrhages. The edematous capsule 
strips readily and the cut section drips blood. On section the cortex 
is swollen and granular, and its striations are blurred and pale in con- 
trast with the dusky medulla; the glomeruli are frequently visible as 
red or later as yellow dots. Without the microscope, lesser degrees of 
acute nephritis may be confused with fatty or parenchymatous degenera- 
tion. Microscopic changes are usually diffuse, (a) Glomerular changes. 
Glomerulonephritis, best exemplified by the scarlatinal form (q. v.), 
is caused by toxins reaching the tufts through the blood current. The 
glomerular capillaries show infiltration with leukocytes, an albuminous 
or cellular exudate escapes into the capsule and the epithelium of 
Bowman's capsule degenerates, desquamates and later proliferates. 



620 DISEASES OF THE KIDNEYS 

(b) Tubular changes. Cloudy swelling, hyaline and fatty degeneration 
occurring especially in the cortex may be difficult to differentiate from 
febrile and other degenerations, but interstitial exudation occurs in 
every case of nephritis. In severe or diphtheritic cases some cells necrose 
entirely and desquamate. The swelling around the convoluted tubules 
is one cause of the kidney enlargement, (c) Vascular and interstitial 
changes are essential to the pathological diagnosis and are more focal 
than diffuse. Serum exudes into the connective tissue, tufts and tubules 
and coagulates in them; leukocytes escape into the parenchyma and 
interstitium and in some cases red cells also (hemorrhagic nephritis). 
Councilman thinks that Unna's plasma cells are conveyed to the kidney 
from the spleen and bone-marrow. 

Symptoms. — The onset may be sudden, especially following exposure. 
Again it develops gradually in the course or convalescence of a causal 
scarlatina, diphtheria, etc. Many cases may be unrecognized without 
frequent analyses of the urine or until uremia develops. 

1. Urinary Findings. — (a) The urine is decreased to ten or twelve 
ounces or in severe cases is suppressed; this is due to glomerulitis, stop- 
page of the tubules by coagulated albumin and desquamated epithelium 
or swelling of the capillaries; the decrease usually runs parallel with the 
intensity of inflammation and hydrops. During convalescence the 
urine becomes abundant and clear, (b) Its color ranges from that of 
febrile urine to a dark, smoky tinge ; it is seldom red or actually bloody ; 
in the hemoglobinuric form it is chocolate-colored, (c) The specific 
gravity averages 1.025 to 1.030 and (d) the reaction is acid, (e) Albu- 
minuria amounts to ^ to 1 per cent, and 5 to 8 gm. daily. There is serum 
albumin, considerable globulin and if there are many cells, as in tubular 
nephritis, nucleo-albumin. The author has seen 6 fatal cases of acute 
diffuse nephritis, confirmed by autopsy, in which there was no albumin- 
uria. (/) Urea is decreased even to | its normal quantity, as are also 
the chlorides and phosphates; the uric acid remains normal and the 
xanthin (alloxur) bases may be increased. (g) The sediment in 
mild acute tubular nephritis consists of many epithelial cells, some 
red and ivhite corpuscles and hyaline casts with crystals of oxalate 
of lime and uric acid and sometimes hemoglobin granules, which 
also may be found as free granules. In diffuse glomerular nephritis 
there are almost always red cells, leukocytes, epithelium, fatty, hyaline 
and granular casts and granules of fat. Senator maintains that the 
leukocytes from the kidney are mononuclear. Waxy and epithelial casts 
are found only in the severest types. Blood and casts may appear before 
and may also outlast the albuminuria. For the significance of cylindruria 
see page 625. 

2. Anasarca. — This is often the first symptom to attract attention. 
(a) It occurs about the eyes early in the morning and later in the day in 
other parts, as the limbs and external genitalia. As the process advances 
it may become general, (b) It changes its location readily and with 
anemia gives a rather characteristic fades, (c) Anasarca occurs most 
commonly in cases due to scarlatina and exposure, less commonly in 
pregnancy, malaria, alcoholism and skin diseases and seldom in sepsis, 



ACUTE NEPHRITIS 



621 



pneumonia, typhoid or diphtheria, (d) It is caused by inflammation of 
the skin vessels, which is identical and associated with the inflammation 
in the glomerular vessels, (e) Identical changes may occur in the serous 
sacs (pleura, pericardium or, far less often, peritoneum, meninges and 
joints), mucous membranes (glottis or intestinal tract) or viscera (pul- 



4M 



'.*:<■ ::::■::■■:•;■ 

INI 



!'.&/& fit 




m 
w 

Ml 



, ■ 



, : ' 






~>,0?' 



If 

(■■-.:■ .v.";. 



y 

■ J* 




is.VHt" 






Fig. 46. — Casts. 1-4, amyloid; 5, cast, epithelial in its upper, and granular in its lower, part. 

monary or cerebral edema) . (/) It parallels the intensity of the nephritis 
and the decrease of urine. 

3. Anemia. — The red cells and hemoglobin are reduced, often early 
and with the dropsy is suggestive of acute nephritis. 

4. Cardiovascular Symptoms. — Hypertrophy of the left ventricle is 
uncommon, though observed within ten days of the onset. The pulse 







,. >■*£ ...V 

• ^ . V 

U;- ,*? : >0i 



Fig. 47. — Urinary casts. 1, hyaline, with fat droplets and cells; 2, hyaline, with leukocytes; 

3, cast with fat droplets. 



is usually slow and tense; the sphygmogram shows increase of the tidal 
and decrease of the dicrotic wave and the sphygmomanometer shows the 
blood tension increased even to 180 or 200 mm.; these phenomena are 
probably due to vascular' contraction induced by metabolic products 
retained in the blood or by glomerulitis. The second aortic tone may 



622 DISEASES OF THE KIDNEYS 

become accentuated and, if heart fatigue develops, the gallop-rhythm 
is heard. 

5. Tempekature. — Fever is exceptional. There may be pain and 
tenderness in the back, frequent and painful urination, emaciation and 
epistaxis. Constipation is the rule. The skin is generally dry. 

Diagnosis. — The urinary findings are characteristic; albuminuria (q. v.) 
may result from other causes, as fever, amyloidosis or stasis; casts, 
leukocytes, epithelia and even red cells also occur in chronic nephritis, 
but the history and evolution determine the diagnosis (v. page 640); 
cases without urinary findings are extremely rare. The greatest danger 
lies in confusing acute nephritis with an acute exacerbation of a chronic 
process; fully half of the author's acute cases belonged to this category. 
In renal hematuria the urine contains no casts (save perhaps red cell 
casts), few leukocytes and practically no epithelia; there is no anasarca; 
the urine is clear at one time and is laden with blood at another. Ana- 
sarca (y. s.) occurs in certain types only and also in various cachectic 
states. 

Diagnosis of Type. — (a) The kidney of pregnancy usually develops 
in the last half of gestation and infrequently before the third month. 
Its pathogenesis is disputed, though toxemia due to the double task 
imposed upon the maternal kidneys seems the most probable cause. 
It has been suggested that anaphylaxis or decreased antitoxic activity of 
the thyroid gland is a causal factor or that the placenta elaborates toxins 
(syncytiolysins) . The urine is decreased, pale and of low specific gravity; 
it contains much albumin and not much sediment, though red and white 
cells, lymphocytes, fatty epithelia and sometimes casts are found. The 
attendant anasarca, like that* of stasis, develops from below upward. 
When retinitis develops its prognosis is more favorable than in other 
nephritides. The convulsive seizures (eclampsia) are often uremic, 
though Ingersley collected 106 cases in which there was neither clinical 
albuminuria nor renal alteration at necropsy; Fehling remarks on the 
slight anatomical changes in the kidney and on the fact that but 5 
per cent, of pregnant patients having an old nephritis develop eclampsia. 
The embolism of placental cells in the brain or lungs (Schmorl) is probably 
rather a result than a cause of eclampsia. Zweifel maintains that the 
oxidation of the albumins is decreased, the nitrogen output decreased, 
the ammonia increased and that acidosis occurs. The maternal mortality 
is 30 per cent, and that of the child over 50 per cent. Very few cases 
develop chronic nephritis. (6) The cholera nephritis is parenchymatous 
and chiefly tubular and by some is considered renal ischemia rather than 
nephritis, (c) In hemoglobinuric nephritis hemolysins disorganize the 
blood and irritate the kidneys by the hemoglobin set free. It is found 
in burns, acute infections (typhoid, pernicious malaria, scarlatina, 
yellow fever, Winckel's disease of the newborn), exposure, hemoglobin- 
emia and drug poisoning, notably that of chlorate of potash, (d) Acute 
recurrent hemorrhagic nephritis is uncommon. 

Prognosis. — In general there are more recoveries than deaths. The 
following factors are important: (a) Recovery is usual in atypical or 
light forms not involving the glomeruli, (b) The causal affection; the 



ACUTE NEPHRITIS 623 

scarlatinal type has a mortality of 33 per cent.; the virulence of the 
epidemic is an important factor, as are also heart complications, (c) 
Complications, as (i) intercurrent inflammations, such as pneumonia, 
pleuritis, pericarditis or erysipelas; (ii) edema of the pharynx, larynx, 
lungs or serous sacs; and (iii) uremia, which will be fully covered under 
chronic interstitial nephritis; uremia is more often an adult than an 
infantile and a late rather than an early complication; headache, delirium, 
dyspnea, convulsions, coma and vomiting are among its salient signs. 

The average duration is less than two weeks, though one or two years 
may elapse before recovery, and gradual transition into chronic nephritis 
sometimes results. 

Treatment. — Most of the points mentioned will be considered more 
fully in the treatment of chronic nephritis, (a) Prophylaxis is of limited 
value. Drugs which irritate the kidneys should be withheld in acute 
infections or pregnancy. In fevers water should be given freely by 
mouth or by enema; hydrotherapy is prophylactic, save in scarlatina 
when cold baths are contra-indicated. Induction of labor is indicated 
in severe cases, (b) Diet. Milk is diuretic, non-irritant and contains 
little or no extractives or salt. It should be given as in typhoid (q. v.). 
Thoroughly cooked carbohydrates, as gruels, are well combined with 
it. Alcohol, broths, meats and beef -tea are contra-indicated, (c) 
Absolute rest in bed is imperative to protect the skin and spare 
the kidneys from the products of the tissue waste; the patient should 
lie between flannel blankets and should be dressed in flannel nightgowns. 
(d) No drug modifies the nephritis; tannin and ergotin (of each 5 
grains three times daily) seem to restrict renal hemorrhage. Salt should 
be withheld (see p. 635). (e) The best diuretics are water and milk, which 
flush out detritus from the kidneys; excessive quantities are often given; 
potassium citrate is given in doses of half a dram with sweetened, weak 
lemonade. Sweet spirits of nitre 3ss-j, q. i. d., is diuretic and also 
dilates the bloodvessels. All stronger diuretics are to be avoided. (/) 
Skin. Warm baths are diuretic and stimulate some vicarious elimina- 
tion through the skin. Careful covering and rest in bed relax the skin, 
materially aid its functions and relieve renal hyperemia, (g) Saline 
catharsis lowers arterial tension and aids compensatory elimination. 
As salts often derange the stomach, an ounce should be given by rectum 
with two ounces of glycerin and one of water. One-half to one dram of 
compound jalap powder or j-q grain of elaterin is indicated when uremia 
impends, '(h) Treatment of uremia. For suppression of urine a full 
warm bath lasting fifteen to twenty minutes should be given; a hot pack 
should be applied, followed by wrapping in blankets and covering heavily 
with a rubber sheet; or the alcohol sweat or hot-air sweat may be given. 
Cups applied to the back may divert blood away from the kidneys, 
because the vessels of the loin anastomose with those of the kidney. 
Pilocarpin, catharsis, incision of the legs, venesection, saline infusions, 
stimulation, etc., are considered fully under Chronic Nephritis, (i) In 
convalescence, iron and other mild tonics should be given, irritating foods 
and beverages interdicted, exercise carefully restricted and cold and 
exposure avoided by sending the patient, if possible, to a warm climate. 



624 DISEASES OF THE KIDNEYS 



CHRONIC NEPHRITIS. 

Aetius, Avicenna, Cotugno (1770) and other writers mentioned the 
association of hydrops and albuminuria, but to Richard Bright (1827) 
is due the credit of correlating renal disease, albuminuria and dropsy; 
he also noted the etiological importance of alcohol and cold, as well as 
the cardiac hypertrophy, uremia, brain hemorrhage, coma, convulsions, 
blindness and the tendency to serositis. 

The following classification of nephritis covers typical cases, though 
combined or mixed types are equally frequent. As a cause of death 
chronic nephritis ranks sixth, after pneumonia, tuberculosis, heart 
disease, endocarditis and unknown causes. 

I. Chronic Parenchymatous Nephritis. — Definition. — Chronic Bright's 
disease, with special involvement of the parenchyma, much albuminuria 
and abundant formed elements in the urinary sediment. The affection 
constitutes 3 per cent, of all diseases. 

Etiology. — It may result from (a) infections, as tuberculosis (which 
causes 25 per cent.), malaria and syphilis; (6) from exposure to cold 
and dampness; (c) from toxic factors, as alcohol, lead, less frequently 
mercury or arsenic; (d) from cardiac disease, which accounts for 14 per 
cent, of nephritis; (e) exhausting discharges, suppuration and ulcera- 
tion; (/) acute nephritis is a somewhat predisposing factor, (g) Most 
cases occur between twenty and fifty years of age; it is rare in children. 
Males are affected more often than females. 

Pathology. — There are three types besides the mixed forms. 

1. The "Large White Kidney," or "Inelamed Fatty Kidney." — 
This is never decreased in size and may weigh 10 to 12 ounces and 
measure two or three times the normal size. 

Gross Characters. — The capsule is non-adherent; the surface is smooth, 
yellowish-gray, with prominent stellate veins and sometimes dots of hem- 
orrhage. On section the cortex is broader, the striations are poorly 
marked and when cut streaks of fat may show; the glomeruli and con- 
voluted tubules are yellow and contrast with the gray bands of newly 
formed connective tissue. The medulla shows fewer changes and is red, 
in sharp contrast with the light cortex. 

Microscopic Characters. — The most essential changes are hyaline and 
fatty degeneration and atrophy, chiefly in the convoluted tubules, in 
which lie desquamated epithelia and coagulated albumin. The glom- 
eruli are always diseased, but to a varying degree; they are enlarged, 
their vessels show hyaline and fatty degeneration and nuclear multipli- 
cation; albumin is found in their capsules and the epithelium is swollen, 
fatty or even necrotic. The connective tissue is always increased, which 
histologically separates chronic nephritis from acute nephritis and mere 
degeneration. 

2. The "Large Red" or "Variegated Kidney." — Gross Characters. 
— It is also large, but is firmer than the kidney just described or that 
of acute inflammation, for it has more connective tissue, which may 
cause some tearing and loss of the cortex when the capsule is stripped off. 
The surface may be perfectly smooth. The cortex is swollen, indistinctly 



CHRONIC NEPHRITIS 625 

striated, dotted yellow from fatty glomerular change or red from minute 
ecchymoses and sometimes streaked yellow and red from similar tubular 
changes. 

Minute Characters. — These are essentially those of the large white 
kidney, except that fatty degeneration is less marked and connective 
tissue alteration and hemorrhages are more conspicuous. 

3. The Secondary Contracted Kidney. — This form may develop 
after a year or two from the above forms. 

Gross Characters. — It may be as large as the "large white" or "large 
red kidney" and the name refers rather to its connective tissue than to 
any visible renal shrinkage. The capsule is adherent in places and, when 
stripped, tears off small areas of the renal substance. The surface is 
rough and shows in some places reddish, depressed areas (fibrous contrac- 
tion or granulations and parenchymatous atrophy) and in others yellow 
areas (which are more normal, though fatty). Section shows decrease 
in the cortex corresponding to the reddish foci. It differs from the 
genuine contracted kidney (primary interstitial nephritis) in the follow- 
ing respects: it is secondary, much more rapid in development, contains 
fewer cysts, is more yellow and its red granulations and yellow promi- 
nences are larger. 

Minute Characters. — Epithelial changes resemble those of the two forms 
described. The membrana propria of the tubules thickens, adheres and 
obliterates many tubules. The glomeruli collapse, thicken and shrink 
to small, dark gray granular bodies, which sometimes calcify. The 
retracted areas, capsular adhesions and cortex shrinkage correspond 
to connective-tissue contraction. 

Symptoms. — The onset is in most cases gradual and insidious, the 
earliest symptoms being loss of strength, pallor, emaciation, simple 
decline of health, indigestion, anorexia, headache, shortness of breath 
on exertion or chronic bronchitis. 

1. Urinary Findings. — Except in the secondary contracted kidney 
(a) the urine is decreased to 1000-200 c.c; (b) the color is dark yellowish- 
red, opaque or rarely smoky; the urates are held in suspension by the 
albumin; sometimes its surface is shimmering from fatty cells and casts; 
(c) the specific gravity is 1.020 to 1.040 and (d) the reaction is acid; 
(e) albumin is more abundant in the day time than at night and amounts 
to 1 to 3 per cent, and 15 to 30 gm. daily; it coats the bubbles formed 
by agitation of the specimen and preserves them for a long time. (/) 
The absolute amount of solids is generally decreased; for example, the 
urea (which normally constitutes 90 per cent, of the nitrogen output and 
amounts to about 35 gms. daily), kreatin and sodium chloride are 
decreased and the freezing-point of the urine is lowered (v. i.). (g) The 
sediment is abundant and hyaline, granular, fatty and epithelial casts 
abound (first noted by Simon and Nasse); coarsely granular and waxy 
casts appear late in the disease; the granular type is due chiefly to fat 
particles, which may darken the casts. They have been long regarded 
as significant of nephritis. Key, Nothnagel, Rosenstein and others 
afterward observed their occurrence in the urine of normal individuals 
and of late there has been a tendency to underestimate their impor- 
40 



626 DISEASES OF THE KIDNEYS 

tance. According to Senator, casts originate in the kidney chiefly from 
epithelial cells and always indicate some renal disease. They may be 
dissolved in the bladder by the pepsin contained in the urine. Leuko- 
cytes and fatty epithelia and, in some forms of nephritis, red cells occur 
in considerable amounts. In Ackermann's case no casts were found in 
the urine, but were found in masses in the renal pelvis at necropsy. 

In the secondary contracted kidney the urine amounts to 1500 to 2000 
c.c, is clearer, is somewhat lower in specific gravity and contains some- 
what less albumin and casts. 

2. Edema. — Edema is very frequent. Its absence argues for little 
glomerular involvement. It commences about the eyes, changes its loca- 
tion readily and is at first evanescent, but soon becomes general, obstinate 
and ominous. It is more pronounced in the "large white kidney" than in 
other types and increases as the urine decreases. The puffy and promi- 
nent eyes, pale, swollen cheeks, dull expression and distended abdomen 
and shapeless wrists and ankles often suggest the diagnosis. The serous 

' and mucous membranes are similarly involved, though to a lesser degree, 
and also as possible terminal events, pulmonary or cerebral edema may 
develop. Edema is caused (a) by hypalbuminosis and hydremia of the 
blood (Bright's theory), especially in hemorrhagic types, (b) by abnor- 
mal permeability of the vessel walls, a theory advanced by Cohnheim 
and Lichtheim, or (c) glomerular changes, causing chloride and water 
retention. 

3. Anemia. — Anemia distinguishes chronic parenchymatous nephritis 
from the genuine interstitial type. There is usually retention of urea, 
uric acid and chlorides; sometimes the blood is cloudy. 

4. Cardiovascular Findings. — The pulse is more often small, soft, 
rapid and associated with a weak apex, indicating dilatation, than 
tense and associated with a loud second aortic tone and strong apex, 
indicating hypertrophy. Secondary contraction and mixed nephritis 
are likely to develop findings similar to those of the genuine interstitial 
nephritis; Senator finds eccentric hypertrophy in parenchymatous and 
simple or concentric hypertrophy in interstitial nephritis. Myocardial 
degeneration is common. 

Complications and Causes of Death. — (a) Marasmus results from the 
anemia, indigestion, diarrhea, edema of the alimentary mucosa or its 
irritation by decomposed urea. (6) Intercurrent infections may result, 
as inflammation of the pleurae or pericardium, cellulitis and especially 
pneumonia; many pneumonia deaths really result from nephritis; in 
one instance the writer saw acute necrosis and sloughing of the scrotum. 
Other complications are (c) edema of the lungs, larynx, serous sacs and 
extremities, impeding respiration and obstructing the peripheral arterial 
flow; (d) hemorrhages (8 per cent.) in the brain or other organs; (e) 
retinitis (18 per cent.); (/) uremia, with its numerous nervous, circula- 
tory and digestive symptoms (v. page 630) ; (g) acute exacerbations, par- 
ticularly in the chronic hemorrhagic type; and (h) cardiac insufficiency. 

Diagnosis. — The diagnqsis rests upon three cardinal symptoms: (a) 
the urinary, which are characteristic when twenty-four-hour specimens 
are carefully and repeatedly examined in every patient; (6) the anasarca, 



CHRONIC NEPHRITIS 627 

which is sometimes absent in secondary contracted kidney and in Wag- 
ner's hemorrhagic type; and (c) the anemia. (See pages 640 and 641.) 

Prognosis. — Though some cases suggesting an arrest of the process are 
found at autopsy, the clinical course is usually progressive and fatal. 
Dropsy usually causes death in a few months to a year, though the 
author saw 5 typical cases recover after two and a half years; they 
did not result from acute infections like the recoveries reported by 
Senator and Rosenstein. The outlook is better in children than in adults. 
The large, white kidney causes death in one-half to one year, the large, 
variegated kidney and the secondary, contracted kidney in one and a 
half to three years. The treatment is considered on page 633. 

II. Chronic Interstitial Nephritis. — Definition. — A primary, interstitial, 
contracting sclerosis of the kidney, characterized clinically by abundant 
urine of low specific gravity, with small amounts of albumin and few 
cellular elements; and by marked cardiac hypertrophy, arteriosclerosis, 
hypertension, retinitis and uremia. 

This genuine contracted kidney must not be confused with secondary 
contracted kidney, arteriosclerotic contraction, embolic contraction or 
the contraction resulting from ascending infection. 

Frequency. — In ten years Eichhorst treated 31,562 cases, of which 1.4 
per cent, had contracted kidneys (six and a half times as frequent as the 
parenchymatous form). 

Etiology. — The etiology is that of arteriosclerosis, with which contracted 
kidney has a threefold relation: arteriosclerosis may cause the arterio- 
sclerotic kidney; contracted kidney may cause arteriosclerosis; or 
both may result from a common cause. The often unknown toxin reaches 
the kidney through the blood stream. 

The disease may result from (a) chronic alcoholism combined with 
exposure or overeating; (b) chronic lead poisoning; (c) gout, caused 
by the alloxur bodies; (d) syphilis; (e) diabetes, caused by sugar or 
acidosis; the diabetes lessens or ceases when induration develops; (/) 
age; it begins between the years of thirty and fifty and is clinically mani- 
fest after fifty years of age. Sawyer collected 24 cases in children, (g) 
Sex. The disease is three times as frequent in men as in women. In the 
infantile form most cases occur in girls, (h) Infrequent causes are 
acute nephritis, the kidney of pregnancy, hereditary tendency, as in 
Dickinson's series through four generations, and endocarditis. 

Pathology. — It is undecided whether the process is inflammatory or 
atrophic; probably induration follows cellular degeneration. 

Gross Pathology. — (a) The kidneys are contracted even to one-third 
their original size and may weigh but 21 gm.; contraction is rarely sym- 
metrical in both. (6) Their consistence is increased, (c) The capsule 
is thick, tendinous and adherent and strips off particles of cortex when 
removed, (d) The surface is uneven; the small reddish or sometimes 
paler prominences, measuring 0.5 to 5 mm. represent the more normal 
tissue; the paler retracted areas are fibrous, (e) Small cysts are fre- 
quently found, usually with clear contents; their size ranges from that 
of a pin-point to a cherry; they result from glomerular and tubular con- 
striction by connective tissue (retention cysts). (/) On section the cortex 



628 DISEASES OF THE KIDNEYS 

is shrunken, even to 1 mm., irregular and gray from fibrillar connective 
tissue. The medulla is less changed, though also shrunken; pale fibrous 
lines alternate with red, dilated vessels; uric acid or calcium salts are 
deposited. 

Minute Pathology. — The changes are largely cortical, focal, asym- 
metrical and interstitial, (a) The glomeruli early exhibit round cells, 
nuclear increase, desquamated cells and albumin; later they atrophy 
from degeneration of the afferent artery; in the extreme stage the 
glomeruli become hyaline and fibrous; some tufts may visibly hyper- 
trophy, Sabourin's compensatory adenomata, (b) The epithelium is 
always changed, though much less than in parenchymatous forms; in 
the sunken areas many tubules disappear and degenerated cells are 
seen in the prominent surface granulations; in the medulla the collecting 
tubules are larger, even cystic, and are filled with colloid material, (c) 
The connective tissue is increased everywhere, but more in the cortex 
than in the medulla; round-cell infiltration occurs early and induration 
late; the vessels are sclerotic in all their coats, but especially in the 
intima, which some consider is the earliest and causative alteration. 

Symptoms. — Long latency for years, insidious onset and protracted 
compensation by heart hypertrophy are characteristic of this type. Many 
cases are first discovered during an acute infection, as pneumonia, on 
examination for life insurance or at the coroner's autopsy after accidents. 
It may appear for years, to be a physiological or cyclic albuminuria. 
Polyuria, cardiac symptoms, retinitis, indigestion or depreciation of 
health may be the first symptom. The edema, pronounced urinary find- 
ings in a single specimen and anemia of chronic parenchymatous nephritis 
are seldom conspicuous and almost never early symptoms in this type. 
The condition may be first declared by heart incompetence, uremic 
coma or convulsions. 

1. Urinary Findings. — Urinary findings are generally the earliest 
signs. Twenty-four-hour specimens should be examined repeatedly in 
doubtful cases, with a fresh specimen for microscopic examination. As 
a general statement, the urine is increased, pale and voided frequently; 
it is low in specific gravity and contains small amounts of albumin 
and solids; and the scanty sediment contains few casts. In detail: (a) 
The amount is gradually increased (polyuria) as the kidneys lose their 
power to condense the urine; this is a frequent cause for consulting the 
physician. Nagel found polyuria in only 47 per cent. The urine is also 
passed frequently (pollakiuria) , especially at night, alw T ays suspicious 
when the prostate is normal. In well-developed cases it totals 2000 to 3000 
c.c, rarely 8000 to 12,000. (b) It is pale and weakly acid, (c) The specific 
gravity averages 1.010 (1.005 to 1.012). (d) Albumin is present in most 
cases, but is not abundant; the merest traces are found up to a daily 
total of 2 to 5, rarely 10 gm. It is often absent in single specimens, 
especially in the morning, whence a twenty-four-hour specimen should 
always be examined. Delicate tests are often necessary (v. Albumin- 
uria). It may appear only after eating, exercise or fatigue, whence its 
greater frequency toward night; it may increase after dyspepsia or 
bronchitis. Senator's statement that its alleged absence is due to an 



CHRONIC NEPHRITIS 629 

arteriosclerotic kidney and not to interstitial nephritis is not invariably 
correct. Albuminuria may be absent for weeks or months. A 'permanent 
foam due to the albumin is frequent, (e) Solids are decreased, i. e., the 
urea, uric acid, ammonium, chlorides and phosphates. The determination 
of the freezing-point, cryoscopy, employed by Koranyi to estimate the 
amount of soluble molecules in the blood and urine, is not of prac- 
tical value in medical cases. (/) Tests of renal function show decreased 
activity (v. i. Therapy.) (g) The sediment is scant, absent or obtained 
only by the centrifuge. Hyaline, granular and epithelial casts are found 
in small numbers when the light is moderated by the diaphragm, some- 
times only after repeated search; the granular casts are often wide, 
originating in the dilated tubules of the medulla. A few epithelia, leuko- 
cytes and crystals of uric acid and oxalate of lime are found. Red cells 
are infrequent. 

The urinary findings are modified by intercurrent uremia, fever and 
heart failure, all of which concentrate the urine. 

2. Cardiovascular Symptoms. — Cardiovascular symptoms were noted 
by Bright, but their significance was first established by Traube. They 
appear in 75 per cent, of cases. Briefly stated, they are the signs 
of cardiac hypertrophy and arterial hypertension — a heaving apex, a 
metallic, second aortic tone, hard vessels and raised blood-pressure. 
Cardiac hypertrophy is more quickly detected clinically than patho- 
logically, especially in the young, because the urine is increased before 
the signs of hypertrophy prevail and concentric hypertrophy is present 
long before dilatation appears. Emphysema may obscure the precordial 
evidences of hypertrophy, such as the heaving apex-beat and double 
impulse at the apex, and one must therefore depend on the evidences 
presented by the tense pulse, the hardness of the arteries, the sphygmo- 
graphic tracings with a square apex, the loud, ringing, second aortic tone 
or other manifestations of increased arterial tension, as epistaxis, vertigo, 
headache, tinnitus, palpitation or cardiac asthma. The systolic blood- 
pressure in interstitial nephritis may exceed 200 mm., and is one of the 
most constant and early symptoms. (See pages 395 and 396.) The cause 
of the hypertrophy or hypertension is not definitely known — mechanical 
obstruction to the blood flow by renal contraction (glomerular changes) 
and vasomotor constriction excited by retained waste substances are prob- 
able causes. Though hypertrophy occurs in interstitial rather than in 
parenchymatous nephritis, the two types often mingle, with the urinary 
findings of the "large white kidney" and the cardiovascular findings of 
a renal contraction. In the last stage of contracted kidney the hyper- 
trophied heart weakens, the hypertension falls, the apex becomes weaker, 
a systolic murmur appears from myocardial insufficiency and Potain's 
gallop-rhythm, a sign of heart fatigue, is heard. 

3. Retinitis. — Retinitis albuminurica may be the first declaration of 
the disease and thus come under the observation of the ophthalmologist. 
It occurs more frequently than in other renal lesions, 25 per cent. Its 
forms are stellate, white areas of fatty and fibrous tissue, a white zone 
surrounding the disk, degeneration of the disk or retina, "flame-like" 
hemorrhages and choked disk whose large veins are compressed where 



630 DISEASES OF THE KIDNEYS 

the arteries cross them. Identical findings occur in other conditions. 
(See Plate VI, Fig. 8.) 

4. Uremia. — Uremia is the most dreaded and frequent complication; 
its nature and immediate cause are unknown; it can only be stated that 
it is an auto-intoxication, due to disturbance of renal function, probably 
with retention within the blood of nitrogenous substances. Further 
explanations are theoretical, such as acidosis; failure of the "internal 
secretion" of the kidney; the toxic action of abnormal products of 
metabolism or breaking up of the proteids by nephrolysins; it is not 
due to retention of urea alone or to mechanical conditions alone, as 
edema or anemia of the brain. It occurs most often in chronic inter- 
stitial, next in acute, then in chronic parenchymatous nephritis and is far 
less common in other diseases of the urinary tract, as pyelonephritis, etc. 

Uremic symptoms may be acute, perhaps developing precipitately; 
more frequently it is chronic; prodromal headache is followed by chronic 
gastric irritability, vomiting and epigastric oppression; dyspnea and 
high arterial tension, alternate with restlessness, anxiety, insomnia or 
disturbed vision; and finally psychic disturbance, poly visceral scleroses, 
myocardial incompetency, gallop-rhythm, Cheyne-Stokes's breathing or 
angina pectoris terminates — rapidly or with miserable remissions — in 
uremic convulsions, uremic coma or apoplexy. These manifestations 
will be considered as nervous, digestive, respiratory and cardiac: 

Nervous Symptoms. — (a) Acute convulsions (eclampsia) are due to 
irritation of the cortex by toxins, and closely resemble the epileptic 
attack. There are usually prodromes, as pain or pressure in the head, 
neuralgia, insomnia, vertigo, visual disturbance, tinnitus, nausea, vomit- 
ing or dyspnea; there is usually no "epileptic cry." Then clonic or 
tonic convulsions appear, usually generalized and involving especially 
the flexor or extensor muscles of the arms and legs; the abdomen is 
retracted; there are dyspnea, cyanosis and involuntary evacuations; the 
reflexes, especially the patellars, are increased, and even ankle-clonus 
and Babinski's sign may develop, sometimes unilaterally and thus simu- 
lating apoplexy; the pupils are wide and reactionless; the pulse is full 
and slow before the attack but becomes rapid during the convulsions. 
The skin is covered with sweat and the temperature is usually elevated. 
The convulsions cease after fifteen to thirty minutes and coma intervenes, 
during which the convulsions may recur. Death is the usual outcome, 
but recovery is possible, as in one of the author's cases, in which the 
anterior third of the tongue was bitten off. (b) Other motor manifesta- 
tions. Landois's general statement is as follows : Paralysis affects espe- 
cially the sensorium, to a lesser degree the special senses and rarely 
motility; irritation seldom affects the sensorium (e. g., delirium), it acts 
principally upon the motor paths (convulsions) and seldom upon the 
special senses. Uremic convulsions may resemble focal symptoms, such 
as convulsions of only half the body or rarely as convergent strabismus, 
facial spasm, Jacksonian epilepsy, nystagmus, localized trembling and 
twitchings, muscular cramps, grinding of the teeth, tetanic convulsions, 
trismus, convulsions on one side and contractures on the other, rigidity 
of the neck or opisthotonos. In 7 cases seen by the author the symptoms 



CHRONIC NEPHRITIS 631 

were those of an acute focal brain lesion; in 2, treated by lumbar 
puncture, relief was immediate. 

Paralyses in uremia are infrequent, are chiefly transitory hemiplegias 
and are due to cerebral edema, capillary hemorrhage, softening, apoplexy 
or cortical overstimulation by toxins. Hemiplegia may occur with 
aphasia, amnesia, deafness, crossed oculomotor paralysis, glossoplegia 
or conjugate deviation of the eyes. The author reported 5 cases in 
which uremia very closely resembled meningitis. Other cases have been 
suggestive of brain tumor, (c) Acute coma often occurs without ante- 
cedent eclampsia, being preceded by headache, stupor or apathy; coma 
may last for days or even months, (d) Psychic symptoms. The most 
common is a characteristic restlessness and anxiety. Obstinate headache, 
of a dull, throbbing nature is common; it often begins in the early 
morning; it may be occipital or hemicranic. Insomnia is common, 
though during the day the patient is often sleepy. Delirium and mania 
are more frequent in chronic nephritis in adults than in juvenile cases; 
melancholia and delusional insanity occur; these mental states may 
assume medicolegal importance as to the testamentary capacity of the 
patient, (e) Special senses. Sudden, complete and bilateral blindness 
is cortical in origin; this amaurosis may be an initial symptom; there 
are usually no retinal findings and the condition lasts but a few hours, 
though in exceptional cases edema or choking of the disk is found. The 
pupils are wide and reactionless in acute eclampsia, but are small and 
mobile in chronic uremia. There may be sudden or gradual uremic deaf- 
ness and tinnitus aurium. Barker remarked exophthalmos in half his 
patients, especially those with a suburemic state, retinitis and hyper- 
tension; most of these cases also exhibited the signs of v. Graefe, Mobius 
and Stellwag. 

Digestive Symptoms.— These rank second to the nervous symptoms 
in frequency. The breath is often offensive and sometimes has an odor 
of urine, which Senator considers of prognostic value, for it often precedes 
eclampsia. The tongue is foul, the mouth inflamed and the saliva 
increased (uremic stomatitis). Nausea and vomiting are partly central 
and partly local from decomposed urea, eliminated vicariously into the 
stomach; the same may be said of hiccough and diarrhea; the HC1 is 
decreased. All these symptoms may be very acute. Diarrhea may be 
serous or dysenteric from the B. dysenterise. Mathieu and Roux in 
a study of 23 cases of "uremic ulcers/' described by Treitz (1859), 
found them chiefly in cases of advanced nephritis in subjects under 
twenty years old; they rarely occur in the stomach; diarrhea is common, 
but bowel hemorrhage and constipation are rare. They are seemingly 
produced by necrosis due to toxemia. The prognosis is almost always 
unfavorable. 

Respiratory and Cardiac Symptoms. — Dyspnea is very common. It 
is sometimes toxic and central, occurring in close parallelism with cerebral 
manifestations. In other cases asthma uremicum is cardiac. Prodromal 
slotting of the heart to 60 to 40 beats is frequent in incipient uremia. 
The dyspnea may be continuous or paroxysmal and is often nocturnal; 
Cheyne-Stokes's breathing is an unfavorable sign, though recovery is 



632 DISEASES OF THE KIDNEYS 

possible. Obstinate hoarseness and a rare form of laryngeal spasm are 
recorded. 

5. Other Complications and Symptoms. — (a) Various hemorrhages 
occur; in the brain in 12 per cent, of cases; also in the dura, nose, bronchi, 
stomach, bowels, uterus, conjunctiva or retina. Purpura occurs espe- 
cially in recurrent hemorrhagic nephritis. The author observed 11 cases 
of profuse gastro-intestinal hemorrhages in uremic subjects. (6) Inflam- 
mations: Chronic bronchitis always suggests kidney disease. Pericar- 
ditis, pleuritis and pneumonia especially, may develop as terminal 
infections. Many deaths from pneumonia are due to a previously 
unnoticed nephritis. Laryngitis and acute inflammatory edema glottidis 
may occur, (e) Edema is a late symptom and results not from the neph- 
ritis, unless it is of the mixed type, but from cardiac failure. Ascites is 
nearly always cirrhotic or cardiac, (d) The skin is usually dry, harsh 
and sometimes covered with urea crystals — "urea frost" or uridrosis. 
Itching, erythema, urticaria, eczema and numbness or "dead fingers," 
cramps in the calves, unusual susceptibility to cold (cryesthesia), neuritis 
or rheumatoid pains are probably toxemic. 

Diagnosis. — There are three cardinal findings, cardiovascular, urinary 
and retinal; as Senator says, "He who examines the urine and heart in 
every case rarely fails to diagnosticate nephritis." 

Cardiac Symptoms. — The very interdependence of cardiac and renal 
changes may prove confusing; thus primary cardiac disease may cause 
renal congestion^ embolism or even acute or chronic nephritis; again 
alcohol, syphilis, etc., may be a common cause of arteriosclerosis, myo- 
carditis, high blood-pressure and nephritis; and finally, the heart lesion 
may be secondary to renal disease. Gallop-rhythm is more common 
in the cor renale than in primary cardiac affections. 

Urinary Findings. — In diabetes mellitus there is polyuria, in which the 
high specific gravity and glycosuria are distinctive; in diabetes insipidus 
the absence of albumin, casts and cardiac changes are characteristic; 
and pyelitis is characterized by albumin and pyuria but not by casts 
or cardiac changes. In the arteriosclerotic kidney arterial and cardiac 
antedate the urinary changes (the converse is true in interstitial neph- 
ritis), the specific gravity is higher, albumin less in amount and in 
frequency of occurrence and the course is much more rapid (see page 
640). 

* Uremia. — Miliary tuberculosis, meningitis, cerebral abscess and sepsis 
may be diagnosticated uremia, because nephritis is also present and 
there is danger of mistaking uremic symptoms, as hemicrania, nervous 
symptoms, dysentery, etc., for independent disease. Many authors 
have remarked on the lack of correspondence between the clinical and 
pathological findings in nephritis. Uremia is assumed to be the cause 
of nervous symptoms only when other causes may be excluded, because 
in the course of renal disease organic lesions, as cerebral hemorrhage, may 
simulate uremia. Though the urine is usually decreased, Liebermeister 
instances a case in which, immediately before a uremic seizure, both urine 
and urea were increased twofold. Biermer reports an anuria which lasted 
two hundred and twenty-two hours before uremia developed. 



CHRONIC NEPHRITIS 633 

Apoplexy is probably present when pressure symptoms, as vomiting 
or slow tense pulse, complete hemiplegia or conjugate deviation exist; 
it is rarely completely simulated by uremia. Meningitis, insolation and 
alcohol or opium coma are rarelv simulated. The author has seen a few 
cases in which uremia simulated typhoid or sepsis by the constant high 
temperature. 

Prognosis. — It is often detected only when the patient suffers from 
cardiac insufficiencv, beginning uremia, apoplexy or intercurrent inflam- 
mation; for this reason this incurable malady is seldom treated in its 
early stages. The clinical course usually runs five to ten years after 
albuminuria is found; a course of twenty to thirty years is reported. 
Much depends on the docility and financial ability of the patient. Marked 
arteriosclerosis hastens the fatal issue. Retinitis is an ominous symptom 
and increases the gravitv of the outlook fourfold; in Belt's 419 cases 72 
per cent, died in one and 90 per cent, in two years. Webstei, Wert, 
Hare and the author report cases which lived from four to ten years 
after retinitis was found. Uremia, pneumonia, apoplexy and other 
complications are unfavorable. 

Treatment of Chronic Nephritis, Parenchymatous and Inter- 
stitial. — Both forms are considered together, because they often 
blend. 

1. Prophylaxis. — Prevention and treatment of the cause have a 
very limited practical application. Irritating foods, excessive eating, 
all forms of intemperance, overwork, neglect of infections and dyspepsia 
come under this head, but are usually treated too late. 

2. Rest, Exercise. — The kidneys may be relieved by rest in the 
horizontal posture, as recognized by Bright. Rest should be absolute 
as long as the heart is weak, the urine scanty or hydrops conspicuous. 
In moderate renal involvement or in intervals of improvement moderate 
exercise is advisable. Rest in bed lessens the amount of waste products 
to be eliminated by the kidneys and so protects the skin and dilates its 
vessels that the cutaneous functions become more active. The author 
treated 2 severe cases of parenchymatous nephritis by rest in bed for 
a year and permanent recovery resulted. Fatigue, dampness and cold 
must be avoided, by rest in bed during severe symptoms or acute exacer- 
bations and by relative rest and warm clothing in cases of moderate 
severity. In men leading a strenuous life, moderate nephritis is often 
improved when nervous tension is relieved; in any event exercise should 
supplant work and not be taken after hard, nervous strain. 

3. Springs, Climate. — At water resorts the importance of diet and 
hygiene is impressed on the patient; the suggestive element is also im- 
portant. Diffuse nephritis (with both parenchymatous and interstitial 
changes) is most benefited. Only patients without edema or serious heart 
involvement should be sent to such places as Poland Springs, Bedford 
Springs, Saratoga, Vichy or Neuheim. A stay in California, Mississippi 
or Texas during the winter, at least, will materially benefit. 

4. Diet. — The diet must be non-irritative, must not especially tax 
the kidneys in its elimination, must not burden the circulation and must 
maintain nutrition. Disease of the glomeruli alone may be compensated 



634 DISEASES OF THE KIDNEYS 

by vicarious excretion of water through the lungs, skin and intestines, 
but disease of the tubules whose function is elimination of the end- 
products of protein metabolism, cannot well be compensated by other 
structures, whence the indication for limitation of albuminous foods and 
substitution by fats and carbohydrates. It is less important what pro- 
tein the kidney can eliminate than to determine what amount of protein 
must be ingested to spare the body protein, e. g., the myocardium from 
fatty change; 50 gm. is sufficient for a short time and 85 gm. over a longer 
period. The small amount of albumin lost through the kidneys can be 
offset by a glass of milk daily; in this respect nephritis differs from dia- 
betes in which the system is irritated by unappropriated sugar and loses 
a vast number of units of heat and energy. It is a mistake to gauge 
the severity of a nephritis by the degree of albuminuria or to estimate 
improvement by the influence of diet upon the albuminuria alone. Fats 
as butter, olive oil and cream, are very important in replacing albumin. 
As in diabetes the restriction of diet most of all concerns the maintenance 
of nutrition, especially when the patient suffers from parenchymatous 
nephritis, the form in which restriction of diet is theoretically most 
needed, but in which anemia and malnutrition distinguish it from the 
interstitial type. The patient is considered more than the disease or the 
type of the disease. 

The milk diet is free of extractives and poor in salt, and influences 
the albuminuria more favorably than other proteins. It has its restric- 
tions; it is bulky, 3.5 quarts being required to maintain nutrition at 
rest (2200 calories), and it therefore may cause dyspepsia, containing 
an excess of about 60 per cent, of protein; it lacks iron, but this can be 
easily compensated; it contains too much water, thereby overloading 
the heart; and its phosphates tax the kidneys. One to one and a half 
quarts of milk with a pint of cream, fats and carbohydrates (baby foods, 
sago, rice or potatoes) meet the needs of metabolism; over half of the 
phosphates can be precipitated in the intestine by calcium carbonate, 
gr. x, with the milk. It should be taken in sips, as it is a food, not a 
beverage. Milk was a favorite article of diet with the older masters of 
medicine; a short time ago we heard that it contained an excess of water; 
now it is excellent because it contains little salt! 

The present reaction in favor of meat is extreme, as it promotes uremia. 
The average daily amount is 100 gm. There is no difference between 
red and white meats as to extractives or purin bodies. Some meat is 
preferable to overloading the stomach with a bulky vegetable diet, save 
when uremia is imminent. Boiled meats contain less extractives. Game 
is interdicted. 

Raw eggs increase (perhaps induce) albuminuria; three cooked eggs 
are allowed. Substances excreted with difficulty include the following, 
according to von Noorden: Urea (in meat), creatinin (in meat broths, 
extractives and to a less extent in eggs), urinary pigments (in hemo- 
globin), hippuric acid (in cranberries, fruits with pits, prunes, plums and 
gages), phosphates (in milk) and inorganic sulphates (in meats); uric 
acid and alloxur bodies found in glandular organs — the thymus, sweet- 
breads, liver and kidney — in broths and coffee are eliminated readily. 



CHRONIC NEPHRITIS 635 

The chlorides and also sod. bicarb, and phosphate are especially avoided 
in parenchymatous nephritis with edema. As pointed out by Widal, 
Lemerre and Javal, in 1902, administration of salt (which is retained in 
the body) increases the body weight, induces edema and aggravates 
albuminuria, while " dechloruration" of the food reduces weight, edema 
and albuminuria. Salt probably raises arterial tension. The tissues 
ordinarily demand 2-3 gm., but most people take 10 gm. or more. Milk 
contains 2 gm. per liter and meat soups 6-8. The salt in bread and 
butter may be disregarded. Rice, potatoes, sugar and eggs may be 
given. In acute or early nephritis, salt is excreted in excess (polychlor- 
uria), as the tubules are oversensitive; later they are less sensitive and 
there is achloruria; the pot. iodide and phenolsulphonephthalein tests 
concern the same tissues. Widal differentiates two stages of edema, 
the deep or invisible and the obvious; the former is distinguished only 
by regularly weighing the patient. He designates the retention of chlo- 
rides as hydropic uremia and nitrogen retention as dry uremia. Irritants , t 
as cheese, relishes, horse-radish, onions, rhubarb, garlic, radishes, aspara- 
gus, spices, sauces, broths, beef-tea and alcohol, should be absolutely 
avoided; tea and coffee because they may aggravate or produce nephritis 
and tobacco must be limited. 

5. Water. — In regard to water, the same extremes of opinion are 
noted; fluids were once excessively restricted and later undue quantities 
were recommended; von Noorden states that flooding the vascular 
system with water overtaxes the heart; "water can only be excreted by 
the kidney if the blood-pressure is increased; many patients having weak 
hearts give a history of excessive water drinking; in such cases improve- 
ment is frequent if the ingestion of water is limited." The maximum 
elimination of waste substances occurs on about 1500 c.c. of fluids; 
500-1000 c.c. are given when there is edema. We consider the weight 
of the patient and the in- and output of fluid from the kidneys and 
bowels. The urinary output is 70 per cent, of the water ingested. 1500 
c.c. of water ingested (+ 500 in food) = 1500 c.c. of urine (+ 500 c.c. 
excreted by the lungs and skin). In early or acute nephritis, there is 
polyuria, due to increased sensitiveness of the bloodvessels, and loss of 
power to concentrate the urine; later there is normaluria and eventually 
oliguria or anuria (decreased sensitiveness of the glomeruli). 

The following therapeutic measures are but symptomatic: 

6. Diuretics. — Diuretin produces no renal hyperemia but acts directly 
on the epithelium and sometimes reduces the albuminuria (v. page 377). 
The use of diuretics is indicated by increase of hydrops, scanty urine and 
imminent uremia. Theocin is more efficacious, given well diluted to 
avoid nausea. Diuretics first increase, and then decrease the urine 
(fatigue of the kidneys); they are injurious when the organs have lost 
their power to secrete. The refrigerants (cream of tartar, 3j) or potas- 
sium citrate (gr. xx-xxx) are the safest diuretics; they are thought 
to abstract water from the tissues and facilitate the excretion of urea, 
uric acid and similar products. Basham's mixture (liq. ferri et ammonii 
acetatis) as a tonic and diuretic should be given in doses of 1 or 2 drams. 
Digitalis perhaps is a renal stimulant. 



636 



DISEASES OF THE KIDNEYS 



7. Hydrops. — Hydrops necessitates treatment because it prevents 
movement, threatens suffocation by pulmonary or laryngeal edema, 
increases the danger of secondary infection, as erysipelas or cellulitis, 
embarrasses the circulation by pressure on the afferent capillaries and 
efferent lymphatics and venules, interferes with digestion and increases 
the danger of uremia, (a) Though cathartics may eliminate fluids as 
well as solids, drastics must be given with due care for the digestion 
and nutrition; vegetable are better than saline cathartics. Purging 
in nephritics may increase the protein in the movements even to 30 per 
cent, (normally 10 per cent.). Watery stools are produced by pulv. 
jalapse co., 3,}\ or elaterinum, gr. yq, but not by cascara, rhubarb, aloes, 
senna or phenolphthalein; liq. magnes. citrat. contains an excess of water 
and Pluto, etc., an excess of chlorides; concentrated Epsom salts may in- 




Fig. 48. — Sweat bath employed in nephritis. 



duce fatal results, (b) Sweats. Though the functional relation between the 
skin and kidneys cannot be overestimated, profuse sweating eliminates fluid 
rather than solids (about 2 gm. each of CI and N per liter). When a 
patient sweats one quart (1000 c.c.) 7 to 15 grains (0.5 to 1 gm.) of urea 
are eliminated. Sweats do not concentrate the blood and predispose to 
uremia, but lower the blood-pressure 10 to 20 mm., by diverting blood from 
the splanchnic to the cutaneous vessels. The author has seen a fatal issue 
result from sweating and prefers the old-fashioned full warm bath of 
Osborne and Liebermeister, to the more active methods; an ice-bag is 
placed on the head to prevent brain congestion. Commencing with 
water at body temperature this is raised five or six degrees. After 
twenty or thirty minutes the patient is removed and wrapped — without 
drying — in blankets. A hot-air bath may be given by placing a lamp 
under one end of a stove-pipe which runs by an elbow into a tent built 



CHRONIC NEPHRITIS 637 

over the patient. In the alcohol sweat, hot bricks protected by flannel 
are placed around the heavily covered patient; equal parts of alcohol 
and water are poured on the bricks and the patient is covered again; 
the steam vapor is well tolerated unless the heart is weak, when fatal 
collapse may ensue. It is often unsafe to give pilocarpine, gr. \ (page 
623), because it may produce vomiting, diarrhea, syncope, pulmonary 
edema and sudden death, even when the heart appears strong, (c) 
Mechanical relief by means of incision is superior to all other measures 
which must first bring the fluid with all its urea and extractives into 
the circulation, with the danger of inducing uremia. The author makes 
deep incisions, three inches long, over the lower leg (not over the malleoli 
where infection from the feet is likely). In testing the fluid evacuated 
there has frequently been 0.1 per cent, urea, a measure for other retained 
products of kindred nature; quarts often seep out. Free incision is 
obviously less dangerous than punctures or Southey's capillary tubes. 
8. The Circulation. — Treatment often resolves itself into the care 
of the heart. Excitement, nervous strain, physical exertion, constipa- 
tion, tobacco, coffee, alcohol and exposure to heat must be avoided, 
as cardiac dilatation is the inevitable fate of hypertrophy. In the 
uremic seizures, with the same symptoms in other respects, the heart 
may beat strongly or weakly, (a) With cardiac overaction observed 
early in uremia, the high tension must be corrected by vasodilators 
(see pages 399 and 400). Iodides are beneficial when there is no urgency, 
grs. x, t. i. d.; iodism, especially salivation, may result from renal reten- 
tion. When extreme tension and imminent uremia exist, tr. veratri 
viridi, Tfl,v-x, every half -hour for three doses may be given; the author 
prefers spiritus glycerylis nitratis, Tfl,ij, until results are produced; vaso- 
dilators are often given to excess, as hypertrophy and increased arterial 
tension are less pathological than compensatory conditions. Chloral 
frequently operates better than any other remedy. Lowering the tension 
30-40 points, decreases elimination of solids and fluids. Bleeding may 
relieve the intracranial blood-pressure, lessen the molecular concen- 
tration of the blood {%. e., its toxicity), relieve the laboring heart, 
and avert for awhile the uremia; salines may be given afterward, 
either subcutaneously or by rectum; they "lavage the blood." An 
excess of salt may be given in the infusions (v. s.) and when they 
are repeated the salt should be left out, for it may induce edema of the 
lungs. Bouchard states that the abstraction of 32 gm. of blood removes 
more toxins than 280 gm. of fluid feces or 100 liters of sweat. Increased 
intracranial tension may be relieved by lumbar puncture; the normal 
pressure of 120 mm. is increased, sometimes to 600 mm.; the author 
remarked relief of the headache, vomiting, convulsions and coma, (b) 
When the heart is weak, rapid, irregular or galloping, cardiac stimula- 
tion by digitalis and strychnine is indicated. Infusion of digitalis by 
mouth may cause vomiting and TTlij-v of the fluidextract may then be 
given hypodermically or by rectum. Its combination with calomel 
may cause the most intense salivation and in one instance necrosis of 
the entire tongue. Cardiac unrest, palpitation or dyspnea should be 
relieved by a hypodermic of morphine, by application of ice to the heart 



038 DISEASES OF THE KIDNEYS 

or by champagne, nitroglycerin, bromides and valerian. Pilocarpine 
and sweats overtax or fatally depress the heart. Von Ziemssen gave 
champagne and digitalis by mouth as long as the patient could swallow 
and then digitalis by rectum and camphor subcutaneouslv. 

9. Vomiting. — Vomiting and diarrhea are as often vicarious as toxemic 
and should not be checked at once. Gastric lavage and colonic flushings 
are beneficial. If improvement ensues, a starvation diet should be insti- 
tuted. 

10. Convulsions. — Hypodermics of morphine should be given (though 
medical opinion is generally against it), with chloral (gr. xv every hour 
for not more than four doses). 

11. Operation. — Many cases of " decapsulated" kidney are not 
genuine nephritis, but albuminuria from floating kidney or ascending 
infection, and nephritis is .more than merely a renal disease, perhaps a 
result of a general blood condition. 

PASSIVE CONGESTION. EMBOLISM. 

I. Passive Congestion. — Venous hyperemia is an important lesion 
compared with arterial hyperemia, of which latter little is definitely 
known, though it occurs in renal inflammation, diabetes and after the 
administration of diuretics. 

Etiology — (a) Among the chief causes of general stasis are cardiac 
insufficiency from valvular disease, myocarditis and pulmonary emphy- 
sema, (h) Local stasis has scarcely any part in the renal pathology. 
Berkmann (1859) described renal stasis and thrombosis of the renal 
veins occurring in the newborn or nurslings after severe diarrhea; when 
unilateral there is renal pain, great albuminuria, some hematuria, swell- 
ing of the kidney and decreased urine; most cases of bilateral thrombosis 
die from uremia. Thrombosis of the cava and pressure by large tumors 
may cause passive congestion. 

Pathology. — The slowing of the arterial flow and to a less degree venous 
hyperemia, alter the integrity of the secreting renal structures, notably 
the glomeruli. In experiments, arterial insufficiency causes initial glome- 
rular alteration, while venous obstruction causes primary congestion 
in the medullary portion. 

Early Changes. — The kidney is swollen, dark and firm and the 
stellate veins are prominent. On section it expands beyond its close- 
fitting capsule, which is readily stripped off. The organ is very vascular 
and may drip blood. The glomeruli are seen as dark red points and 
the medullary bloodvessels are clearly defined. Microscopically the 
conspicuous changes are hyperemia, occasionally with punctate hemor- 
rhages, fatty and cloudy degeneration of the epithelium of the tufts and 
convoluted tubules, escape of albumin into them, forming hyaline casts 
in the tubules, and finally some thickening of the vessels. 

Late Changes. — Prolonged stasis leads to greater atrophy of the 
secreting structures and to increase of connective tissue; this "cyanotic 
induration" has been rather overdrawn in clinical descriptions, but may 
result from extreme and protracted stasis. The kidney becomes pale and 



AMYLOID DEGENERATION OF THE KIDNEY 639 

firm, the cortex shrinks and connective tissue develops in the medulla. 
Microscopically, fibrillar connective tissue, thickening of Bowman's 
capsule and epithelial degeneration are found. 

Symptoms. — The urinary findings are of chief interest. The urine is 
decreased and its amount directly follows the heart's activity. It is 
acid, dark, concentrated (specific gravity 1.025 to 1.030) and it has a 
lateritious sediment of urates and uric acid. Albumin and globulin are 
present in moderate amounts. Microscopically a few leukocytes, epithe- 
lial cells and hyaline casts are found; granular casts are seldom found; 
red cells indicate nephritis or infarction. 

Diagnosis. — The urinary findings are significant in association with 
the causal lesion; edema begins in the legs; the nutmeg liver, dyspnea, 
cyanosis and pulmonary stasis are present. The percentage of albumin 
runs parallel with the strength of the heart, increasing with its failure 
or decreasing if digitalis or strychnine improve its action. If cardiants 
increase the urine, and if abundant albumin and casts still remain, there 
is probably coincident nephritis. (See page 640.) 

II. Embolism. — Valvular disease of the left heart is its predisposing 
cause. Sixty-six to 75 per cent, of all embolisms are renal. Stoppage 
of a renal terminal artery causes the well-known wedge-shaped anemic 
infarct in twenty-four to thirty-six hours; the local ischemia causes 
fatty degeneration, necrosis and a finely granular transudation into 
the connective tissue and glomeruli. Fibrous substitution occurs with 
ultimate shrinkage and deformity. Repeated infarctions produce the 
irregular "embolic contracted kidney." The process may be innocent 
(mechanical) or less commonly suppurative. 

Symptoms. — In most cases there are no symptoms. Exceptionally a 
diagnosis is possible, based on (1) the valvular lesion; (2) sudden onset 
with fever, chills and vomiting; (3) lumbar pain and tenderness and 
(4) hematuria and albuminuria. Treatment is symptomatic. 

AMYLOID DEGENERATION OF THE KIDNEY. 

Etiology. — The etiology of amyloid kidney is that of amyloid liver 
(q. v.), i. e., ulcerative tuberculosis, protracted suppuration and inveterate 
syphilis. First described by Rokitansky (1842), its symptomatology 
was developed by Wilkes, Todd and Traube. 

Pathology. — Renal amyloidosis seldom occurs without amyloid of 
the liver and spleen. To the naked eye the kidneys generally appear 
enlarged, weighing together even as much as 870 gm.; when amyloid 
infiltration is slight, there may be no alteration in size or weight; in 
some cases the kidneys are large from coincident chronic parenchymatous 
or small from interstitial nephritis. The capsule strips readily, showing 
a pale, smooth surface. On section the cortex is enlarged, waxy and pale 
and its edge translucent; the glomeruli stand out as glistening points and 
become brown when treated with Lugol's solution. Microscopically 
the amyloid substance can be seen clearly; it is so named because of 
its starch-like reaction, though chemically it is an albuminoid. It is 
either deposited from the blood in the small vessels or more probably 



640 



DISEASES OF THE KIDNEYS 



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642 DISEASES OF THE KIDNEYS 

formed in situ, especially in the glomeruli, then in their afferent vessels 
and the straight vessels of the medulla. The renal inter stitium is involved 
secondarily; the membrana propria may be affected but the cells may 
suffer only secondary compression, degeneration and atrophy. 

Symptoms. — (a) Urinary symptoms are exceptionally absent. The 
urine is generally limpid and increased, but may be decreased when 
amyloid degeneration is associated with parenchymatous or greatly 
increased when associated with interstitial nephritis; some writers place 
undue importance upon variability in its amount. The specific gravity 
is 1.010 to 1.015 or higher in syphilitic cases. Albuminuria is usual, 
being absent only in exceptional cases which invade the vasa recta and 
evade the glomerular capillaries; albuminuria results from increased 
permeability of the glomerular vessels and may amount to 1 or 2 per 
cent.; Senator remarked the large amount of globulin in the urine. 
There is little change in the solids; indicanuria is not infrequent. Micro- 
scopically hyaline casts may be present and perhaps a few leukocytes 
and epithelia, but the sediment is scanty in most cases; the so-called 
waxy or amyloid casts found in severe nephritides have no relation to 
amyloidosis of the kidney, (b) Cardiac hypertrophy, uremia and retin- 
itis do not occur in renal amyloidosis, except when it is associated with 
nephritis, (c) Amyloid degeneration of both the spleen and liver and 
sometimes the alimentary tract is associated in 66 per cent, of cases; 
these and the causal disease are necessary for diagnosis, (d) Edema 
and anemia, which is almost cachexia, are usual in diffuse amyloidosis. 
Hydrops of the serous sacs, especially ascites, is less common than edema 
and usually occurs as a late or terminal event. Differentiation (v. p. 640). 

Prognosis. — Amyloid disease is incurable, though light grades may 
recede. Amyloid of the kidneys in most cases runs its course in a year 
or less, particularly when associated with parenchymatous nephritis. 
Cases may endure for several, even fifteen years, but these are generally 
complicated by contracted kidney. 

Treatment. — With modern surgical methods and early treatment of 
tuberculosis and syphilis amyloid disease is less common than formerly; 
for the developed disease there is no treatment. 

MALFORMATIONS OF THE KIDNEY. 

I. Malformations and Structural Anomalies of the Kidney.— : These 
are of little clinical importance. Complete absence or rudimentary 
development of both kidneys occurs only in unviable infants. 

One kidney may be absent or rudimentary, whereon the normal kidney 
vicariously hypertrophies and may be mistaken for malignant disease, 
whence its removal is fatal. In Ballowitz's 184 cases 61 per cent, occurred 
in males and in 63 per cent, the left kidney was lacking. Absence 
of one kidney is usually associated with unilateral malformation 
of the internal genitalia, but this is not true in unilateral renal atrophy 
or in horseshoe kidney. Before operation cystoscopy is imperative in 
doubtful cases to determine the presence of two ureters. Two ureters 
mav come from one kidney. 



MALFORMATIONS OF THE KIDNEY 043 

Fifteen cases of supernumerary kidneys are recorded (Graser) and in 
2 cases there were four kidneys. 

The "horseshoe" kidney (ren arcuatus) due to the fusion of both kid- 
neys, is fairly common ; it may cause pain. Errors in diagnosis are com- 
mon, especially if the kidney is dislocated and are inevitable if the renal 
pelvis is inflamed or dilated. The ren arcuatus has been mistaken for a 
tumor and extirpated. 

II. Movable Kidney. — Congenital dislocation occurs twice as frequently 
in males as in females and is usually left-sided, wherein it differs from 
the acquired form, and frequently coincides with congenital anomalies 
of the genitalia and intestines. The kidneys may lie one upon the other 
(dystopia renum cruciata), of which Chatelin could collect but 15 cases. 

Acquired dislocation, described by Rayer a century ago, is much more 
common and important. It is called movable or floating kidney, ren 
mobilis s. migrans, ectopia renis acquisita or nephroptosis. 

Etiology. — (a) Sex; 88 per cent, occur in women, (b) Age; most 
cases occur between the twentieth and fiftieth years. Comby reports 
18 and Abt 5 cases in children, (c) The kidney is supported by the fat 
around it, the peritoneum in front of it and by its own bloodvessels. 
Among the alleged causes are: atrophy of the perirenal fat; the presence 
of a mesonephron surrounding the kidney to a variable extent; weakening 
of the abdominal walls by pregnancy and other causes; alterations in 
the intra-abdominal pressure by malpositions of the uterus; pressure 
by corsets; congenital laxness of the supporting structures, in connection 
with which Stiller claims that the tenth rib is usually "floating" like 
the eleventh and twelfth ribs (costa fluctuans decima); tumors of the 
kidney, which drag it downward; and trauma or sudden efforts. Enterop- 
tosis is frequently observed with floating kidney. 

Symptoms. — Symptoms are absent, probably in most cases; they 
may date from the time when the physician incautiously remarks upon 
the presence of a " floating kidney." 

1. Pain. — Pain may be merely a dragging sensation or severe renal 
colic, from stretching of the renal nerves; it may be lumbar, abdominal 
or may shoot toward the chest, thigh or sciatic region; it may be constant 
or intermittent like a crisis (v. i.). 

2. Objective Kidney Findings. — On bimanual examination with 
one hand over the kidney in front and the other pushing it up from 
behind, the findings vary; (a) frequently the kidney is not painful or 
tender, but palpable, which condition has no significance, especially in 
women; (b) the kidney may be movable, descending on deep inspiration, 
maybe to the navel, where it can be retained by pressure during expira- 
tion; movable kidney is found in 20 per cent, of women; (c) the most 
extreme type is floating kidney, which may wander to the lower abdomen 
or pelvis, even into a hernial sac. In 76 per cent, of cases the right kidney 
is involved, in 11 per cent, the left and in 13 per cent, both kidneys 
(Kuttner); the right kidney has longer vessels, but the left renal vein 
is more firmly connected with the suprarenal vein and the pancreas. 
When the kidney is grasped a sickening sensation sometimes results, as 
when the testicle is compressed. The smooth tumor is recognized by its 



644 DISEASES OF THE KIDNEYS 

shape. In rare cases the pulsating renal vessels are felt. It may be felt 
only in the standing posture or in the left decubitus. Occasionally tym- 
pany can be found along the spine, over the dull area normally occupied 
by the kidney, which merges with the liver and spleen above and extends 
outward 2.5 inches on the left and 3.5 inches on the right side. In thin 
subjects the sinking-in of the back and the tumor in front may some- 
times be clearly seen. 

3. Complications. — (a) The same train of neurasthenic, hysterical 
or hypochondriacal symptoms are present as in enteroptosis. Nervous 
dyspepsia is particularly common, (b) Dietl (1864) described sudden 
severe pain and collapse known as " Dietl' s crises;" they are marked by 
fever, chill, vomiting, collapse, severe pain, sometimes with swelling and 
tenderness of the kidney, scanty urine containing blood, pus, uric acid 
and oxalates and in some instances peritonitic manifestations; Dietl's 
theory that the kidney became "incarcerated" between the connective 
tissue and peritoneum is now abandoned; in one of Sutton's cases the 
ureter was found twisted three times, causing acute renal retention and 
hydronephrosis. Perhaps the renal vessels suffer torsion or the crises are 
due to acute nephritis or peritonitis, (c) Dilatation of the stomach is 
only a coordinate and not at all a common coincidence, (d) Dysmenor- 
rhea, constipation and enteroptosis are common complications. Colitis 
mucosa, compression of the intestine, icterus, abdominal aneurysm by 
tugging upon the aorta and compression of the cava inferior are rare 
and questionable sequences. Albuminuria may occur periodically, on 
palpation of the kidney or when the patient stands (orthostatic type). 

Diagnosis. — The finding of the sensitive kidney-shaped movable tumor 
is most important. It may be mistaken for movable omental, gastric, 
intestinal and gall-bladder tumors or corset liver. Particular reserve is 
necessary in the diagnosis of left-sided floating kidney. Severe pain may 
be confused with a tabetic crisis, appendicitis or the passage of gall- or 
kidney-stones. 

Prognosis. — Death is an extremely rare occurrence. 

Treatment. — The patient should never be told of a movable kidney, 
because neurasthenic symptoms may date from the diagnosis, (a) A 
rest cure may develop adipose tissue and relieve the nervous symptoms. 
(b) A well-fitted bandage, with padding to prevent renal descent, is 
excellent in many cases, (c) In obstinate and extreme cases, nephro- 
pexy is indicated. Hahn's results are 75 per cent, complete recovery, 
15 per cent, decidedly improved and 10 per cent, failures; the mortality 
is under 1 per cent. Nephrectomy is seldom indicated, (d) The crises 
are treated by morphine, reposition and later by operation. 

ANOMALIES OF RENAL SECRETION. 

I. Albuminuria. — Albuminuria, discovered by Cotugno, in 1770, 
results (a) from leakage of albumin through the glomeruli and tubules 
(albuminuria vera, renalis) or (b) from blood, pus, semen or fluid of 
tumors (albuminuria spuria). The spurious or accidental form will be 
considered under Pyuria and Hematuria. 



ANOMALIES OF RENAL SECRETION 645 

The most common albumin is serum albumin (or simply albumin) 
with which serum globulin is frequently associated. 

Etiology. — (a) Its incidence in the diffuse renal diseases, the nephritides, 
amyloidosis and passive congestion has been discussed, (b) Blood 
alterations are frequent causes: (i) blood diseases proper, as anemia, 
leukemia, pernicious anemia, etc., in which the poverty of the blood or 
toxins induce renal degeneration; (ii) toxemic states, as acute and 
chronic infections, in which "febrile albuminuria" evidences the renal 
degeneration; this condition borders very closely on mild acute neph- 
ritis; (iii) diabetes, icterus and poisoning by lead, mercury, etc. (c) 
Nervous maladies possibly act by lowering the local blood-pressure, as 
epilepsy, exophthalmic goitre or migraine, (d) Affections of the diges- 
tive tract, as intestinal incarceration, hepatic disease and lead colic may 
produce albuminuria, (e) In the newborn it was first noted by Virchow. 
It is almost regular in the first week of life and occurs with hyaline casts, 
urates and epithelium. Bibbert holds that it is due to imperfect develop- 
ment of the glomeruli. (/) Pregnancy; it occurs in 40 per cent, of cases 
in the last few months of gestation (from increased tax on the kidneys 
and from pressure) and in the same percentage after delivery (from effort 
and strain), (g) Is there a ''physiological albuminuria' '? Various types 
are described, as Pavey's cyclical albuminuria, which appears and dis- 
appears; intermittent albuminuria; adolescent albuminuria, in young, 
anemic subjects, often with vasomotor disturbances, or orthostatic albu- 
minuria, also termed postural or lordotic, which appears only when the 
subject stands; the latter types give the euglobulin reaction, show a lower 
blood-pressure (by 10-20 mm.), when the patient sits than when he lies 
down and are harmless. Some bring under this caption albuminuria 
after heavy eating, severe exercise, coitus, mental strain or cold baths. 
Senator, Bradford and Grainger Stewart, whose names alone carry weight, 
insist that there is a physiological albuminuria, in which signs of neph- 
ritis, as casts or cardiovascular changes, are absent. The author regards 
most cases of albuminuria as pathological; its cause may be an insidi- 
ously developing nephritis, a receding nephritis, stasis or may be "con- 
stitutional," as Martius calls it, but it is always a sign of glomerular or 
tubular lesion (see Prognosis). The amount of albumin in this type 
rarely exceeds 0.5 per mille (Senator). 

Detection. — The urine must be clear and acid; if turbid it should be 
filtered and if it then remains turbid it should be cleared by shaking with 
magnesia; it must be acidulated, if necessary, with acetic acid; if very 
concentrated, dilution with distilled water is advisable. 

1. Boiling Test. — A test-tube, two-thirds filled with urine, is held by 
its lower part and the upper layers are boiled. Albumin produces cloud- 
ing, which may also result from phosphates and carbonates (dissolving 
when nitric acid is added), balsams (dissolving in alcohol) and uro tropin. 
Nitric acid should not be added before boiling, for a soluble acid-albumin 
may result. 

2. Nitric Acid or Heller's Test. — Urine, somewhat diluted, is 
placed in a test-tube and nitric acid is run under it by a pipette. Albumin, 
globulin, mucin and albumose are precipitated at once or after a few 



646 DISEASES OF THE KIDNEYS 

minutes at the contact point; albumose dissolves by heating, the others 
do not. 

3. Ferrocyanide Test. — To a test-tube half-full of urine 10 drops 
of acetic acid are added, which may precipitate uric acid, urates, oleo- 
resins or nucleo-albumin. These are filtered out and 5 c.c. of 10 per cent, 
potassium ferrocyanide is added. A precipitate indicates albumin, 
globulin or albumose; the latter dissolves on heating. 

4. Acetic Acid and Salt Test. — Adding to the urine acetic acid to 
an acid reaction and then an equal volume of saturated sodium chloride 
solution precipitates albumin and albumose. 

5. Spiegler's Test. — Nucleo-albumin is removed by adding 15 drops 
of dilute acetic acid and filtering. To the urine is added a quantity of 
Spiegler's reagent (bichloride mercury 8, tartaric acid 4, glycerin 20 
and distilled water 200) when albumin or albumose develops at the 
contact zone. 

Globulin occurs chiefly in renal congestion, acute and chronic nephritis 
and amyloid degeneration. It dissolves in an excess of acetic acid. It 
is precipitated by boiling. Flocculi of globulin are thrown down, when 
2 drops of dilute acetic acid are added to 1.6 ounces of filtered urine 
diluted ten times with distilled water. 

Nucleo-albumin (euglobulin, mucin) occurs in acute desquamative 
nephritis, icterus, poisonings causing necrosis of the renal cells and 
regularly in catarrh of the urinary passages. It is precipitated by boiling 
and by acetic acid but unlike globulin, does not dissolve in an excess of 
acetic acid. Shreds of mucus, voided with colic, have been observed by 
von Jaksch and Baumuller; the condition seems analogous to colica 
mucosa and spasmodic asthma. 

Albumose is albumin which does not coagulate by heat. When the 
urine is boiled the albumin is precipitated and filtered out. Albumose 
in the filtrate causes clouding and precipitation on cooling, (a) Bence- 
J ones' s albumose is rather a peculiar albumin than an albumose ; described 
by him in 1848, albumosuria has also been called Kahler's disease. De 
Castello, in 1909, collected 52 cases. It has been found in osteomalacia, 
multiple myeloma, leukemia and bone-marrow tumors. It is precipitated 
by cold nitric acid, dissolves on heating and reappears on cooling, (b) 
Albumose may be found in various acute infections, septicemia, peri- 
tonitis, empyema, etc. Albumin in the kidney, bladder or urinal may be 
converted by pepsin into albumose. 

Diagnosis. — Blood or pus may give albumin reactions (v. i.). 

Prognosis and Treatment. — These are etiological. The outlook is not 
favorable, though not necessarily bad. In seemingly "physiological" 
cases, the condition of the heart must be watched and casts carefully 
looked for. In youth and adolescence albuminuria may be "physio- 
logical;" Senator observed such a case develop contracted kidney after 
twenty years; in middle and later life it is usually nephritic. Shattuck 
and Osier, however, hold that "albuminuria is more common apart 
from Bright's disease than is commonly supposed, that it increases 
with advancing years and that a small amount of albumin with finely 
granular casts of small diameter in those over fifty years of age is of small 



ANOMALIES OF RENAL SECRETION 647 

importance." Life-insurance figures show that it entails double the 
average death-rate. Hawkins reported a case in which albuminuria 
lasted, without any unhappy symptoms, for forty-three years after 
Bright had given a fatal prognosis. 

II. Hematuria. — Etiology. — Like albuminuria, blood in the urine is 
only a symptom of many diverse conditions, (a) It is most frequently 
renal, (i) General conditions may cause it, as intoxications (by quinine, 
carbolic acid, turpentine or salicylic acid), acute infections (malaria, 
exanthemata, particularly hemorrhagic types, appendicitis) or blood 
diseases (hemophilia, leukemia and the anemias), (ii) Other causes 
are local renal conditions, as trauma, vascular maladies (thrombosis of 
the renal veins, infarct, aneurysm, varicose veins, arteriosclerosis and 
rarely passive congestion); inflammation (acute, chronic, hemorrhagic 
and suppurative nephritis) ; tumors; tuberculosis; calculous ulceration and 
pyelitis; rarely amyloidosis or parasites (distoma, filaria, nephrophages 
sanguinarius) ; sometimes floating and cystic kidney, especially after 
bimanual examination, (hi) Hematuria may be "idiopathic" or "essen- 
tial," occurring in very rare cases in "apparently healthy kidneys," 
to which phrase there has been a just objection; it has been called renal 
epistaxis, angioneurotic hematuria and renal purpura. Nephrotomy may 
give relief. In Eshner's 48 cases of unilateral renal hematuria nothing 
was found at operation in 33 per cent., floating kidney in 12.5, renal 
pelvic changes in 19, and diffuse renal disease in 24 per cent, (b) Of 
lesions in the lower urinary tract, the chief types are stone in the ureter 
or bladder; ruptured varices anywhere in the urinary tract; stasis from 
liver cirrhosis or thrombosis of the iliac veins; inflammation (pyelitis, 
ureteritis, cystitis, prostatitis or urethritis, sometimes called "Russian 
gonorrhea"); and tuberculous, malignant or other ulcerations. 

Symptoms and Diagnosis. — Hemorrhage may be macro- or microscopic. 
The urine may be clear or turbid, red or smoke-colored. It is usually 
acid, or alkaline from copious vesical hemorrhage. The color is brighter 
when the urine is alkaline. Confusion is possible with concentrated, 
icteric, carbolic, fuchsin, hematoxylin and senna urines. The presence 
of blood is positively determined (a) by the microscope; the red cells 
remain normal for a long time in acid urine, but may become pale in 
dilute and mulberry-form in concentrated urine; (6) by the spectroscope; 
if no red cells are present with positive spectroscopic findings it indicates 
hemoglobinuria (v. i.); and (c) by chemical tests, as Heller's, Almen's 
guaiac or Teichmann's test. 

Diagnosis of the origin and cause of hematuria is often most difficult. 
(a) In cases of renal origin, the blood is intimately mixed with the 
urine, as much with that first voided as with the last. The color is often 
that of water in which raw meat has soaked (" beef -water" color). Clots 
are infrequent in renal hematuria, save from trauma, tumors, aneurysm 
or varicosities. The red cells are seldom seen in rouleaux-form and 
are fragmented from action of the renal cells; this does not occur in 
vesical hemorrhage. If there is some other renal lesion, as nephritis, 
there is more albumin than the red cells would account for, and albumin 
is present after careful filtering; if there is albumin with a red cell count, 



648 DISEASES OF THE KIDNEYS 

by the hemocytometer, of less than 3000 per c.mm., the albuminuria is 
renal. Blood casts, granular casts and renal epithelium are indicative of 
renal origin, (b) Hematuria originating in the pelvis and ureter is more 
often marked by clots and possibly by caudate epithelium, (c) Blood 
from the bladder is more apt to clot and the last urine voided is more 
bloody than the first. Tenesmus and alkaline urine often indicate a 
vesical origin, (d) Urethral hemorrhage stains most deeply the first 
urine voided. Hematuria may be accidental, e. g., menstrual. 

Treatment. — The treatment is etiological. Rest, morphine and aside 
from the local treatment of vesical disease, urethritis and calculous 
pyelitis, tannic acid, thyroid extract, calcium chloride aa gr. v., t. i. d., 
normal horse serum and adrenalin 1 to 1000 (given by the catheter) may 
stop hemorrhage. In idiopathic renal hematuria, simple incision of the 
kidney is frequently efficacious. 

III. Hemoglobinuria. — This is hemoglobin in the urine without 
hematuria. Though first described by Dressier (1854), most of the 
early accounts are English (Pavy, 1855). 

Etiology. — The toxic form may follow transfusion of blood, poisons, 
organic and inorganic, as potassium chlorate, phosphorus, mercury, 
quinine (in malarial cases), phenol; burns, icterus, pernicious anemia, 
scarlatina, acute nephritis, WinckeFs disease and estivo-autumnal 
malaria. The paroxysmal form, of which Gilman Thompson collected 
206 cases, occurs largely in England, France and Germany; 96 per cent, 
are males, chiefly between thirty and forty years of age. (i) After some 
infection, notably lues, (ii) a hemolysin is formed, capable of dissolving 
the red disks of the subject or of other individuals; cold is important in 
anchoring the hemolysin to the red cells but does not produce this toxin; 
besides this type of Donath and Landsteiner (hemolysin in the blood and 
hemoglobinemia), there is another, characterized by abnormal fragility 
of the red cells; exercise, excesses or menstruation may precipitate an 
attack. It is observed in horses after cold and exertion, with hemoglobin- 
emia and hemoglobinuria, paresis of the hindlegs and death from dis- 
turbed circulation and respiration. In cattle and sheep epidemics, 
Babes and Krogius found a hematococcus. (iii) There is some renal 
disturbance and hemoglobin is excreted, chiefly by the convoluted tubules ; 
genuine renal hemoglobinuria (without hemoglobinemia) seems to occur 
in some cases of nephritis and from certain intestinal nematodes, (iv) 
Hemolytic icterus and splenomegaly may result. 

Symptoms. — Symptoms occur only after destruction of at least one- 
sixth of the blood. After a chill, fever, lumbar pain which radiates 
to the legs, cyanosis, oppression and gastric symptoms, the urinary 
findings appear; the urine is dark and contains clumps of blood pigment, 
peculiar granular (iron) casts and epithelium stained with hemoglobin, 
and albumin. In most cases the hemoglobin is already altered to 
methemoglobin, as shown by the spectroscope. There may be slight 
jaundice, edema or urticaria. The blood shows increased coagulability 
and diminution in the number and redness of the red cells, which do not 
form in rouleaux. There' may be swelling of the liver and spleen from 
hemoglobin deposits in them. The paroxysm lasts one-half to several 



ANOMALIES OF RENAL SECRETION 649 

hours and in the interval the general health is fairly good. The course 
is most chronic. No death is known from the paroxysm itself and very 
rarely from the disease. 

Treatment. — Prophylaxis in regard to cold and exertion may modify 
the attacks. Attacks are sometimes aborted by nitrite of amyl inhala- 
tions and warmth may modify the seizure. 

IV. Pyuria. — Etiology. — (a) Pus may occur intermittently, as in 
pyonephrosis or continuously, as in calculous or tuberculous pyelitis. 
The urine is usually acid in tubercle, colon and proteus infec- 
tions and in some infections ascending from the bladder; the staphyl- 
ococcus may render the urine less acid than normal or alkaline (v. i. 
Pyelitis). (b) In cystitis pyuria the urine may be acid or alkaline and 
contains ropy mucus and triple phosphates. Pus is seen especially in 
the last urine voided, (c) Urethral pyuria, usually gonorrheal, is greatest 
in the urine first evacuated, (d) Accidental pyuria from leucorrheal 
contamination is excluded by catheterization. In pyuria from rupture 
into the urinary tract of appendicular, pelvic or psoas abscess, much 
pus is voided at first, but it gradually lessens and disappears. 

Symptoms. — The urine is yellowish-white, turbid, with a ropy sediment 
becoming gelatinous when caustic potash is added ; it is often ammoniacal, 
from decomposition of the urea, by the proteus and staphylococci. Gas 
may be voided with the urine (pneumaturia) , particularly in entero vesical 
fistula and diabetic cystitis. Alkalinity was formerly thought character- 
istic of cystitic, and acidity of pyelitic pyuria, but this distinction has 
been dropped. Albumin is found, corresponding in simple pyuria with 
the number of pus cells. Albuminuria may be absent if there are not 
over 600-800 pus cells to the c.mm. It is less or may disappear when 
the urine is filtered. The question often arises whether the albuminuria 
is simply accidental or whether, for instance, cystitis is combined with 
contracted kidney; besides consideration of the amount of urine, its 
specific gravity, cardiovascular findings, washing out the bladder and 
ureteral catheterization — leukocytes coming from the renal parenchyma 
in nephritis are mononuclear and those from suppuration .are poly- 
morphonuclear; DeLint found that (a) when there is one part per 
mille of albumin and less than 7000 pus cells the albuminuria is renal; 
and (b) it results from the pus alone when there are more than 40,000 
pus cells; no conclusion can be drawn if the pus cells number between 
7000 and 40,000 per c.mm. 

Treatment. — The treatment is that of the fundamental tuberculosis, 
calculus, pyelitis, cystitis, etc. Phenylis salicylas and hexamethylen- 
amina, aa gr. x, t. i. d., are excellent antiseptics for the urinary tract. 

V. Chyluria. — The tropical form plugs the lymph vessels, which 
dilate and rupture in the kidneys, as proved by Mackenzie's autopsy 
(see page 314). The non-tropical forms are not understood and have 
rarely occurred in Europeans who have never been in the tropics; 
the rare autopsies have shown no marked renal alteration. Probably 
there is some communication between the urinary and chylous vessels. 

The urine resembles chyle, is weakly acid or neutral in reaction, may 
present a fatty, creamy surface and contains 2 to 10 per cent, albumin 



650 DISEASES OF THE KIDNEYS 

(serum albumin, globulin or albumose), cholesterin, lecithin, fat and 
stearic and palmitic acids. Sugar is seldom found. Microscopic findings 
are fat globules, leukocytes, sometimes red disks and the filaria parasites, 
usually in the fibrin clots, which sometimes occasion dysuria. Casts 
are never found. Chyluria is often intermittent; it occurs especially 
at night and in 66 per cent, of cases, it disappears in the recumbent pos- 
ture. In some cases there is free fat in the blood (lipemia). Its course 
is chronic. Recovery is the rule, though death may occur from anemia 
and marasmus. Treatment is unsatisfactory. Potassium picronitrate, 
gr. J, t. i. d., is said to accelerate recovery. Prophylaxis regarding 
drinking water must be considered in the tropics. 

VI. Lipuria. — Lipuria or adiposuria is symptomatic of (a) lipemia or 
fat in the blood. The clearest instances follow fractures, contusions 
of the liver or delivery (fat from the pelvic cellular tissue). Fatty foods, 
acute yellow atrophy, diabetes, disease of the pancreas and various 
poisonings are possible causes. (6) It is symptomatic of renal lesions 
(or fatty epithelial, degenerated tumor or pus cells). 

Under the microscope small fat globules are seen which stain black 
with osmic acid or red with the alcanna test. The fat may be saponi- 
fied by alkalies, emulsified by albumins or dissolved by alcohol, ether, 
xylol or chloroform. Lipuria is often simulated by bacteria or phosphates 
or by oil from catheters, suppositories or greasy urinals. 

VII. Phosphaturia. — Phosphoric acid is. chiefly excreted in com- 
bination, two-thirds with sodium and potassium, the alkaline phosphates, 
and one-third with calcium and magnesium, the earthy phosphates; 
it is chiefly derived from the food, but some is derived from decomposi- 
tion of lecithin, nuclein and protagon. It averages two to three 
grams daily. Amounts over 4 gm. or alteration of the normal relation 
of the phosphorus to the nitrogen (17 or 20 to 100) are pathological. 
An excessive deposit which occurs in dyspepsia is not synonymous with 
an actual increase. Phosphaturia may be observed in neurasthenia, 
pulmonary tuberculosis, diabetes (largely from the diet), acute yellow 
atrophy, leukemia and anemia; 8 gm. daily were reported by Teissier 
and Ralfe, who termed the condition diabetes phosphaticus. Earthy 
phosphates may cloud the last part of the urine, which is mistaken by 
the laity for " spermatorrhea." The addition of an acid rapidly clears 
the urine. The diet, recommended for this condition, consists of meat, 
fish, bread, potatoes and apples. Coffee, nux vomica, arsenic, cod-liver 
oil and ammonium benzoate (gr. x-xxx, t. i. d.) are also given. 

VIII. Lithuria. — No subject has occasioned more clinical absurdities 
than uric acid. It normally bears to urea a ratio of 1 to 70. Futcher 
has found a ratio of 1 to 300 or 500 (v. Gout). It is deposited in larger 
amounts than normal when the urine is very acid and the mineral salts 
or pigments are decreased. An increased precipitation as red granules 
resembling red pepper is far more common than an increased excretion 
of uric acid. Uric acid combines chiefly with ammonium and sodium, 
which form urates of the "brick-dust" color so frequently seen in febrile 
urine and urine of high specific gravity or excessive acidity (sedimentum 
lateritium). They are soluble when heated. 



ANOMALIES OF RENAL SECRETION 651 

IX. Oxaluria. — Oxalates first detected by Donne (1838) in the normal 
urine amount to less than 10 mg. daily. Larger daily quantities are 
pathological. Helen Baldwin decided that they are not formed during 
normal metabolism and are taken in with the food. Oxaluria is observed 
in gout, hyperacidity, increased intestinal putrefaction, neurasthenia, 
icterus and diabetes. Oxalates occur as octahedral and dumb-bell 
crystals, which, according to Klemperer, occur in 50 per cent, of renal 
calculi. Cantani maintains that oxaluria is associated with nervous 
depression, irritability, lumbar pain, sweats and nervous dyspepsia, 
though the consensus of opinion is against any definite clinical picture 
or diathesis. Klemperer advised a diet of meat, fat and vegetables 
(except spinach and cabbage); he excludes milk and eggs and adminis- 
ters magnesium sulphate 3ss. Nitromuriatic acid Tfljj, with tincture of 
nux vomica Tfl,x, is excellent. 

X. Indicanuria. — Potassium indoxylsulphate is present in small amounts 
in normal urine. It is colorless as a rule, but may be voided blue or violet 
in alkaline urine. When acid or some oxidizing substance is added it 
decomposes and frees indigo. The action of the pancreatic juice on albu- 
mins produces indol, which is absorbed, oxidized in the tissues to indoxyl 
and unites with potassium sulphate to form potassium indoxylsulphate. 
Its absence in some pancreatic diseases has been discussed. It is rarely 
found in urinary calculi. It is increased in cachexia? in which albu- 
minous substances are decomposed, in intestinal obstruction, carcinoma, 
suppuration and peritonitis. Boiling the urine and adding nitric acid, 
as in the ring test for albumin, gives a blue ring; adding chloroform and 
shaking brings down the violet- or blue-stained chloroform. 

XI. Other Anomalies. — Alkaptonuria was discovered by Badecker. It 
is a crystalline, aromatic body, probably derived from proteid decom- 
position, whose chief clinical significance is that (a) it reduces Fehling's 
solution, thereby simulating glycosuria, though negative to polarization 
and fermentation tests; and (b) it imparts to the urine a dark brown 
color, usually apparent only after it has stood or after caustic potash is 
added (by derivation, urine which "absorbs" an "alkali" freely). Add- 
ing a drop of a very dilute solution of ferric chloride causes a dull green 
color which at once disappears. It is said to be homogentisic or uroleu- 
cinic acid. Garrod collected 47 cases, 73 per cent, of which were 
males; in 32 congenital cases, 19 occurred in 7 families. Virchow 
(1866) described a case of ochronosis, a discoloration of the cartilages and 
ligaments; Osier described 2 cases associated with alkaptonuria, making 
11 in the literature; it may occur with pigmentation of the face, chronic 
arthritis and deformation of the lumbar vertebrae. Chronic phenol 
poisoning is a possible cause. 

Hydrochinon, from phenol poisoning, causes similar discoloration. 

Hematoporphyrinuria, discovered by Hoppe-Seyler, imparts a dark 
color to the urine. It occurs in tuberculosis, intestinal hemorrhage, 
sulphonal and lead poisoning, etc. Hematoporphyrin resembles hematin, 
save that it contains no iron. Barker reports a fatal familial form, with 
gastric dilatation, fits and polyneuritis. 



652 DISEASES OF THE KIDNEYS 

PYELITIS. PYELONEPHRITIS. SUPPURATIVE NEPHRITIS. 

I. Pyelitis. — Pyelitis and pyelonephritis are inflammation of the pelvis, 
and pelvis and kidney, respectively. They were first fully described 
by Rayer, though recognized by Hippocrates and Galen. 

Etiology. — Pyelitis is mycotic. The kidneys usually eliminate bacteria 
without injury to their structure, but when the general vitality or the 
local resistance of the kidneys is lowered, inflammation of the pelvis 
or kidney may result. Various bacteria may be found, including the 
tubercle bacillus, (a) Foreign bodies, as calculi, less often cancer or 
tubercle, and rarely parasites, promote infection, (b) Goodhart has 
shown that 50 per cent, of cases with obstruction (from urethral stricture 
or prostatic hypertrophy) to the flow of urine die of renal suppuration 
— ascending infection. When the bacteria causing cystitis decompose urea, 
.the ammonia evolved is an additional eroding factor; certain streptococci 
act in this way, but not the tubercle or colon organisms. Bacteria 
usually ascend from cystitis along the ureters, producing ureteritis, then 
pyelitis and perhaps a pyelonephritis, but usually reach the kidney along 
the lymph vessels, entering through erosions in the vesical mucosa, (c) 
Infection may be hematogenous, as in typhoid, etc. (d) Less common 
factors include traumatism, extension by contiguity from neighboring 
inflammations, pyelonephritis (usually an ascending process, in which 
the kidney is secondarily involved, and only rarely a process descending 
from the kidney to the pelvis), toxic factors, irritating diuretics, such as 
turpentine; hemorrhagic diseases; cold, venou's stasis and diabetes; 
arteriosclerosis induces a form of pyelitis attended by hemorrhage and 
fibrin coagula. 

Pathology. — Pyelitis may be solitary or combined with cystitis; uni- 
lateral or less often bilateral. Acute catarrhal forms present redness, 
edema, desquamation, mucopus and ecchymoses. Chronic forms show 
grayish to brown pigmentation. Croupous or diphtheritic inflammation 
or even gangrene may develop. Urates and triple phosphates may pre- 
cipitate. Small retention cysts may form in the pelvis or ureter; the 
small lymph nodes may enlarge and in rare cases the epithelium may 
hypertrophy, causing cholesteatoma. 

Symptoms. — (a) In the ascending type early vesical symptoms ante- 
date and often obscure the pyelitis, (b) The symptoms are most clear 
in primary pyelitis from calculus or hematogenous infection. 

Pyuria is the chief symptom. The amount of albumin is generally 
held to parallel the number of pus cells but often it exceeds the latter 
(the converse being true in cystitis). The pyuria varies; when the 
ureter is obstructed, pyuria is suspended and when the obstruction is 
removed the pus escapes in increased amounts. Polyuria and a low 
specific gravity are usual in chronic cases; the writer observed a case in 
which 6 quarts daily were voided, simulating diabetes insipidus; polyuria 
results from decreased absorption of water from the medullary portion 
or from compensatory hypertrophy of the sound kidney. In acute cases the 
urine is decreased. The often cloudy urine is usually acid but frequently 
alkaline from coincident or causal cystitis or from bacteria decomposing 



P YE LI TIS—P YELONEPHRITIS—S UPP URA TI VE NEPHRITIS 653 

the urea. Large, caudate, club-like epithelial cells, often overlapping 
like shingles, are present in moderately severe pyelitis, but they occur, 
though less frequently, in ureteritis and cystitis. When pyelitis extends 
to the papillae or higher (pyelonephritis), cylindrical plugs of pus cells, 
epithelium, but chiefly of cocci, are seen. Red cells (calculus), triple 
phosphate or uric acid crystals, fibrin (croupous or diphtheritic pyelitis) 
and various bacteria (the colon bacillus, in 90 per cent., perhaps the 
tubercle bacillus) may occur. Pain over the kidney is usually dull, but 
in acute cases may suggest stone. The desire — probably reflex — to 
urinate frequently, may lead to an erroneous diagnosis of cystitis. Fever 
and rigors are common, especially in severe calculous, colon bacillus or 
tuberculous types or those invading the kidney substance. Tempera- 
ture is sometimes sudden and high, at other times intermittent from 
septic absorption. 

Complications. — (a) There may be extension to the renal substance 
(pyelonephritis) which may be reduced to a pulpy, inspissated and even 
calcified mass, (b) Prolonged inflammation may lead to fibrosis — the 
"ascending contracted kidney." (c) Plugging of the ureter may occasion 
distention of the pelvis by retained urine (hydronephrosis) or pus (pyo- 
nephrosis), both of which are described below, (d) Anuria, described 
by Morgagni, is occasioned by reflex suppression of the sound kidney 
or by extensive lesions in both kidneys, (e) Amyloidosis may develop. 
(J) Intoxication may occur by bacterial toxins and renal inadequacy 
resembling uremia in some respects; Senator described a dyspnea like 
that of diabetic coma. Treitz and v. Jaksch ascribe intoxication to 
absorption of ammonia (ammoniemia) from decomposed urea, (g) 
Perforation outward causes the paranephritic abscess (v. i.). In some 
cases a "spinal paraplegia" is described, probably resulting from an 
ascending neuritis. 

Prognosis. — The prognosis is influenced by the basic simple, tuber- 
culous or calculous infection and by the complications. In acute cases 
the outlook is generally good. Chronic cases without much necrosis 
may last many years and may even recover. 

Diagnosis. — Much depends on careful analysis of the pyuria (q. v.). 
Cystitis may be confused or combined with pyelitis; no absolute reliance 
can be placed on the reaction, acidity or alkalinity, though pyelitic 
urine is more often acid. The tailed, clubbed or shingle-like epithelia 
are more common in pyelitis, though not pathognomonic. Thorough 
vesical irrigation and gentle compression of the suspected kidney to 
force pus or cells into the bladder and into the catheter is easier but less 
certain than cystoscopy and ureteral catheterization. In nephritis the 
leukocytes are mononuclear and casts and cardiovascular changes are 
decisive. 

Treatment. — Prophylaxis involves care in the use of catheters or 
irritating diuretics, the expectant treatment of gonorrhea, etc. Water, 
milk and mineral waters should be used freely to flush out the urinary 
tract. Pain is relieved by hot applications to the kidney; opium is 
seldom indicated. For pyuria, phenylis salicylas and hexamethylenamine, 
aa gr. x, p. c, are most efficient. Methylene blue, gr. j-ij, t. i. d., may 



654 DISEASES OF THE KIDNEYS 

induce digestive disturbances. Colon vaccines are less efficacious than 
pelvic irrigation. Surgical interference may be necessary when ureteral 
drainage is incomplete. Nephrotomy is the best operation, nephrectomy 
being seldom indicated. 

II. Suppurative Nephritis. — Its etiology is partly that of pyelitis. 
The microorganisms encountered are the staphylo-, strepto- and pneu- 
mococcus, gonococcus, proteus, colon, typhoid and tubercle bacilli, 
actinomyces, etc. (a) The embolic form from suppurative processes 
elsewhere represents one phase of septicopyemia; suppurative foci are 
chiefly bilateral and cortical; the glomeruli are filled with microorganisms 
and, as the foci enlarge, they show as yellowish areas through the cortex; 
some deposits may also occur in the medulla. Clinically, pyuria, hema- 
turia and cylindruria are seldom seen and a diagnosis seldom can be made; 
anuria or oliguria may result from multiple glomerular involvement. 
(b) The ascending type is essentially a cystopyelonephritis, the so-called 
"surgical kidney"; infection and urinary obstruction are its usual 
antecedents; pyuria, polyuria and albuminuria its usual symptoms; 
and suppuration in the medullary rays its usual anatomical evidence; 
very rarely necrotic renal tissue is evacuated, (c) Suppuration of the 
kidney may result from its invasion by contiguity from adjacent pus foci 
as appendicular, periuterine or vertebral foci; much pus may be voided 
at once, with later gradual cessation of the pyuria. 

The diagnosis is uncertain, save when sequestra come away. In 100 
nephrotomies, 17 died, 27 recovered and 53 were not benefited (Kiister). 

PERINEPHRIC ABSCESS. 

A distinction is made between perinephritis, inflammation of the fibrous 
capsule and paranephritis, inflammation (suppuration) of the fatty capsule 
and surrounding tissue. 

Etiology. — (a) The most common cause is suppurative disease of 
the kidney, as pyelitis, pyelonephritis, pyonephrosis and tuberculosis, 
from which extension occurs by actual rupture or along the blood. or 
lymph vessels, (b) Extension by contiguity may occur from vertebral 
caries, appendicular, hepatic, pelvic or pancreatic suppuration, etc. (c) 
It may result from trauma plus infection, (d) The so-called idiopathic 
abscess is probably embolic. Most cases occur between thirty and forty 
years of age and 70 per cent, occur in males. 

Symptoms. — (a) The onset is acute, with a rigor and sudden fever 
in the embolic (so-called primary), but it is insidious in the secondary 
group, (b) Fever of a continuous or remittent type is usual, (c) Pain 
and tenderness are experienced over one kidney, more often the right. 
Sometimes, with coincident involvement of the kidney, pain shoots 
along the ureter to the pubes or thigh. To relieve tension the patient 
lies on the back with the knee flexed and the thigh rotated outward. 
Pain may also arise from simple perinephritis, relieved by nephrotomy. 
(d) Local findings. In some patients there are lumbar edema, redness 
and swelling, as suppuration usually occurs behind the kidney. The 
surgeon finds a diffuse phlegmon and less often diffuse serous infiltration 



H YDRONEPHROSIS 655 

or circumscribed abscess; the pus may be odorless; it may smell of 
urine when the abscess has arisen from perforation outward of a pyelitic 
lesion; a fecal odor results from infection (without perforation) from 
the bowel or appendicular abscess. Necrotic fat and sometimes altered 
blood are voided, (e) The urine 'is negative, unless there is a pyelitic 
origin or rupture of the abscess into the urinary tract. (/) The chief 
complication is rupture, which occurs in about a quarter of the cases, 
twice as often upward into the lung and pleura, as downward, chiefly into 
the intestine. Burrowing occurs along the ureter toward the pelvis, 
when the abscess is anterior to the renal fascia, and toward the lumbar 
region or iliac fossa, when the abscess is behind the fascia. Amyloidosis 
from neglected or obscure cases of paranephritis, pleurisy, subcutaneous 
emphysema, portal compression, icterus and septicemia may result. 

Diagnosis. — Diagnosis depends on local pain, edema or swelling, 
fever and exploratory aspiration. Psoas abscess, appendicular abscess 
behind the kidney or rupture downward of empyema are more often 
etiological factors than separate questions for differentiation. 

Treatment. — The only treatment is incision and drainage. In Kuster's 
230 cases 66 per cent, recovered. 



HYDRONEPHROSIS. 

Definition. — Hydronephrosis is a sac-like dilatation of the pelvis 
and calices, with accumulation there of a watery fluid; obstruction to 
the urinary flow is its cause and atrophy of the renal substance is its 
result. It was first described by Tulp (1674) and named by Rayer. 

Etiology and Pathology. — (a) The congenital form is most often due to 
anomalies in the ureters; these include atresia, stenosis, valve formations, 
twists, compression by peritonitic bands, vestiges of Muller's or Gartner's 
ducts, abnormal bloodvessels, imperfect insertion into the bladder or 
insertion too high into the pelvis, in the lower part of which the urine 
accumulates; of the latter form the author observed 2 cases. When 
there are double ureters, one may end blindly in the bladder wall and 
dilating, may compress its fellow of the same side. Hydronephrosis may 
occasion dystocia and is commonly associated with other congenital 
malformations; 65 per cent, of congenital cases are bilateral, (b) The 
acquired form may be bilateral or unilateral; its cause may, in rare cases, 
be in the kidney itself, producing partial hydronephrosis. One or both 
ureters may be compressed by malignant pelvic growths, as uterine cancer, 
and this explains the large proportion (67 per cent.) of bilateral hydro- 
nephrosis in autopsy figures; in clinical cases 62 per cent, are unilateral. 
Ureteral obstruction may arise from calculus, tumors, tuberculous 
detritus, ulceration, cicatrization, floating kidney or rarely clots from 
trauma or parasites. Large sacs are usually caused by affections of the 
ureter. Other possible types are obstruction from urethral stricture, 
enlarged prostate, phimosis and atresia of the hymen. 

Cohnheim contended that a slow development with intermissions is 
more potent in the production of large sacs than is acute obstruction. 



656 DISEASES OF THE KIDNEYS 

The writer has seen G. D. Scott's experiments which prove that acute 
obstruction rapidly produces marked hydronephrosis. 

The results of urinary accumulation are (a) distention of the pelvis, 
(6) flattening of the papillae, (c) renal atrophy and (d) the formation of a 
fibrous sac. 

Symptoms. — The chief finding is a fluctuating renal tumor, (a) It 
is located at first in the renal region but later assumes an abdominal 
importance. (6) Its size varies, being largest when the ureter is ob- 
structed and in slowly developing cases becoming as large as the head 
and even simulating ascites; Peter Frank's case contained 60 quarts. 

(c) The chief causes of intermittent hydronephrosis are valve formation, 
stenosis or abnormal insertion of the ureter into the renal pelvis. The 
amount of urine is (i) normal from hypertrophy of the sound kidney, 
(ii) decreased in bilateral disease or from increased pressure in the diseased 
kidney, reflexly lessening the secretion from the sound kidney (Israel) ; 
or (iii) when the sac evacuates, suddenly very abundant and then the 
tumor disappears; this point is often volunteered in the patient's history. 

(d) Its form, on bimanual palpation, is irregularly oval; in moderately 
severe cases the kidney itself may be palpated, as well as its irregularly 
protuberant calices and sometimes the dilated ureter, (e) The ballotte- 
ment renal is a repercussion shock obtained by tapping the tumor with 
one hand while the other is spread broadly over it. (/) Small tumors 
are covered by the colon, which imparts a modified tympanitic note on 
percussion. Distention of the colon by air brings out tympany over the 
tumor. Very large sacs push the colon aside. The ren saccatus may 
develop in a floating or horseshoe kidney, (g) Its contents are albumin, 
paralbumin, mucus, urea and other urinary constituents, which are 
usually absorbed only after a long time. Diagnostic puncture is not 
always safe, (h) Sometimes pain may arise from torsion of the ureter. 
The author noted hematuria and renal colic in hydronephrosis due to an 
insertion of the ureter high up in the renal pelvis, (i) Complications 
include rupture, infection (pyonephrosis) or anuria and uremia if both 
kidneys are implicated. 

Diagnosis. — Diagnosis is easy (a) by recognizing the cause, if possible, 
as stone or tumor; (b) by careful bimanual palpation and (c) by cysto- 
scopic proof that urine does not flow from one ureter. Differentiation 
concerns especially: 

1. Other Renal Tumors. — (a) Pyonephrosis, a dilatation of the pelvis 
and calices by purulent fluid, is caused by obstruction plus infection, 
especially from pyelitis with obstruction. It occasions the same kind of 
tumor as to location and physical examination, but it is generally smaller 
and more irregular than hydronephrosis; its walls are thicker and more 
tender from infection; there is more renal necrosis; systemic septic 
symptoms prevail; its contents are pus, pulpy detritus, triple phosphates, 
bacteria, disorganized blood, fat, cholesterin, fetid ammonium compounds 
and even gas. Puncture in doubtful cases is more dangerous than 
operation. Its prognosis also is clearly more unfavorable, (b) Cystic 
kidneys, (c) malignant renal growths and (d) echinococcus (v. ?'.). 



RENAL CALCULUS G57 

2. Other Abdominal Tumors. — (a) Ovarian tumor is connected with 
the uterus and grows upward. Ovarian tumor with a long pedicle may 
deceive, but it pushes the cecum backward. The dulness is greater, 
though in large renal sacs the colon is pushed aside. Confusion is 
likely when hydronephrosis develops in a floating kidney. Exploratory 
puncture is an unsafe procedure; when made, the fluid from ovarian 
cysts shows a high specific gravity (1.020); much paralbumin is present, 
also cylindrical epithelium, colloid or chocolate-colored material and no 
urea, (b) A scites and pregnancy are readily differentiated, (c)* Encapsu- 
lated peritonitis may be harder to differentiate, but the urinary condition 
and sac-like distention are usually decisive, (d) Splenic and hepatic 
tumors are more flat on percussion, encroach more upon the lungs and 
are above or anterior to the gas-distended colon. In a renal growth a 
furrow and tympanitic loop of bowel may lie between it and the liver 
or spleen. 

Prognosis. — The prognosis is generally unfavorable, as_ the cause is 
often inaccessible or the process well advanced. The prognosis is 
better in cases of renal stone than in cancer or in the generally inviable 
congenital forms. The course is often intermittent and protracted. 

•Treatment. — Nephrotomy is indicated; nephrectomy is poor surgery 
since Ayrer proved that some sound renal tissue nearly always remains. 
The mortality resulting from nephrectomy for hydronephrosis is 5.7 
per cent., for pyonephrosis 15.3 per cent. (Schmieden); Rosving reports 
per cent, and 19 per cent, mortality in his cases of nephrotomy for 
hydro- and pyonephrosis, respectively; 34 per cent, of his cases recovered 
completely, 27 per cent, recovered, though with fistula, and secondary 
operation was necessary in 20 per cent. Fenger advised conservative 
operation in partial hydronephrosis. Israel and Rosving prefer to cut 
down on both kidneys before extirpating either one, to tests of the renal 
function. 

RENAL CALCULUS (NEPHROLITHIASIS). 

Etiology. — Stone in the kidney or its pelvis results from deposition 
of the solid constituents of the urine. Probably bacteria, especially 
colon and typhoid bacilli, form the nucleus of stones. An albuminous 
cement substance is found even in slight urinary deposits or renal sand. 
Renal stone was described by Hippocrates. 

The predisposing factors are obscure, (a) A sedentary life and over- 
indulgence in food and alcohol are apparently predisposing factors. 
Galen noted the coincidence of gout and renal calculus. Stones are said 
to be uncommon in very active persons, (b) Most cases occur between 
thirty and sixty years of age; in the extremes of life vesical calculus is 
more common, (c) Seventy-five per cent, of cases are in males. Stones 
are passed more easily, and therefore are possibly less often detected, in 
women, (d) Renal calculus occurs most frequently in Asia and there are 
certain foci, where it is particularly frequent, as central Russia, Holland, 
Italy, Altenberg, Munich, Hungary, Scotland, west France and southeast 
England, (e) Other possible factors are heredity, especially formation 
of uric acid and cystin calculi; paraplegia (Muller reported 10 cases of 
42 



658 DISEASES OF THE KIDNEYS 

spinal fracture with calculus formation) and foreign bodies in the renal 
pelvis, as blood clots from trauma and parasites. 

Chemistry and Pathology. — According to their size, urinary deposits 
are spoken of as sand, gravel or stones; sand and gravel consist of uric 
acid or its salts. They may range from the size of a pea to that of a hazel- 
nut. The heaviest recorded stone weighed thirty-six ounces. Though 
most often round, oval or cylindrical, they may be dendritic or coral- 
shaped. A number of them may exist, perhaps 15 to 20; 1000 to 2000 
may be found, (a) The uric acid and urate stone constitutes 66 per cent, 
of renal stones. It is hard, smooth or slightly uneven, sometimes facetted 
or lamellated and consists of uric acid, ammonium and sodium urates 
and a small amount of xanthin. Its broken surface is amorphous. Its 
color is yellow, red or brown, depending on the amount of urinary pig- 
ment. It may contain some oxalates and phosphates. Under the micro- 
scope needles are seen. Uratic calculi turn carmine-red on adding nitric 
acid and ammonia. They dissolve in caustic potash. They are deposited 
in acid urine, but the exact reason is not known; a decrease of the urinary 
pigments is considered of great importance; disturbed metabolism or 
indigestion may occasion uratic deposits, though little is known of the 
"uric diathesis." (6) Oxalate stones are next in frequency; they are very 
hard, warty or prickly (the mulberry calculus); for this reason they 
cause more pain and hematuria than the uratic stones and are more often 
removed surgically. They are usually single and gray, but may be dark 
colored from the bleeding they induce. Lamellation is never observed. 
Uric acid, calcium carbonate or xanthin may also enter into their com- 
position. No effervescence occurs on adding acetic acid unless carbonates 
are also present. They dissolve in mineral acids and oxalate of lime 
crystals gradually precipitate on the addition of ammonia. Oxalates 
precipitate from acid urine, (c) Phosphatic calculi are formed in alkaline 
or neutral urine. They are usually calcium salts, but if the urine is 
ammoniacal triple phosphates may be formed. Admixture of bacteria, 
calcium carbonate and xanthin may be noted; phosphatic stones are 
small, soft and clay-colored. They are infrequent and usually only form 
a coating to calculi of other composition, (d) Other forms are rare. 
Calculi of (i) calcium carbonate and more rarely ammonium or magnesium 
carbonate may occur in the aged; they are white and dissolve with 
effervescence in mineral acids, (ii) Cystin calculi are smooth, yellow and 
waxy, never exceed the size of a pea, are soluble in acids and alkalies and 
deposit hexagonal crystals when dissolved in acetic acid and ammonia. 
Only 60 cases are reported, (iii) Xanthin stones occur almost exclusively 
in children; only 10 cases are recorded; they are smooth, yellow or brown, 
dissolve in nitric acid and on evaporation leave a residue which turns 
red on adding caustic potash, (iv) Only 3 indigo stones are on record. 
(v) Urostealiths probably result from fatty substances deposited in the 
bladder; they are 85 per cent, fat and are soft, rubber-like and com- 
bustible. 

Symptoms. — Stones may be first discovered accidentally at autopsy 
or, very exceptionally, may pass without symptoms. Gravel or renal 
sand is more often latent than is stone. 



RENAL CALCULUS 659 

1. Pain. — Pain, the most common symptom, is of two kinds: (a) 
The dull pain in the loin, often associated with local tenderness over the 
kidney; localized pain without any urinary changes, may indicate stone 
in the medullary substance. Pain may be felt over the opposite kidney. 
(b) The renal colic, which arises from incarceration of the stone as it 
attempts to leave the pelvis; it is often preceded by pain in the loin 
and may be initiated by exercise or indigestion; Eichhorst's patient 
had renal colic every time he drank white wine. The pain begins over 
the kidney and radiates down the ureter to the testis, labia, bladder or 
urethra; the testicle is retracted (in the descent of the testis, its envelopes 
receive a twig from the first lumbar nerve) . It may rarely radiate to the 
chest, heart, shoulder, epigastrium or to the opposite side. During the 
colic, the kidney is sensitive; when it is not so, Israel hesitates to diag- 
nosticate stone. The pain is cutting and very severe; it often occasions 
reflex nausea and vomiting, sometimes chills, sweats and fever or in 
children convulsions and rarely collapse or even death in most exceptional 
cases. If the stone passes, the pain is greatest as it enters the bladder. 
It lasts, with intermissions, a few hours, rarely days; movement may 
excite recurrence. The patient lies on his back with the leg drawn up 
and the abdominal wall rigid. After the attack there may be dull pain 
(v. s.), which may be caused by large, numerous or sharp stones. 

2. Ukine. — The urine is almost invariably altered, (a) Hematuria 
occurs independently of pain and colic, as well as after them. Absence of 
hematuria after a renal colic argues strongly against stone (Israel). 
It is often macroscopic and red disks are found with the microscope, 
except in the rare cases when stone is imbedded in the renal tissue or 
there is permanent occlusion of the ureter. At the time of the colic the 
scanty, bloody urine is frequently voided with considerable tenesmus. 
In exceptional cases early profuse hematuria may result from vascular 
erosion, (b) Anuria (suppression of urine) is not common. Legeau 
collected 30 autopsied cases of calculous anuria; there was stone in one 
kidney and the opposite kidney (a) contained a calculus in 14 cases, (/3) 
was hypoplastic in 3, (7) sclerotic in 6, (8) its ureter was stenosed by 
calculi in 6 and (e) in one case the opposite kidney was absolutely normal 
(Morgagni's reflex suppression via the splanchnic). The urethra may be 
plugged with a calculus. The resulting symptoms are called "latent" 
uremia. However, in 41 cases collected by Herter convulsions were 
present in but 12 per cent., headache in 14 per cent, and vomiting in 29 
per cent.; consciousness is usually preserved and the temperature is 
low; 11 cases of anuria persisted over four days, 18 cases seven to 
fourteen days and 7 cases over fourteen days. Russel records recovery 
after twenty-eight days of anuria. With its relief large quantities of 
urine are voided, (c) Pyuria results in protracted cases from pyelitis, 
secondary to the calculus; infrequently a renal intermittent fever is 
observed, resembling the hepatic intermittent fever of gall-stones. 
Pyelitis may be catarrhal, suppurative, ulcerative or perforative, (d) 
Crystals of pointed uric acid and oxalates are considered important in 
diagnosis, (e) Stones in the urine are not frequently found. 



660 DISEASES OF THE KIDNEYS 

3. The X-rays. — Oxalate stones throw a shadow in every instance; 
uric stones often are invisible. Leonard reports but 3 per cent, of 
errors; he found calculi in the ureter twice as often as in the renal 
pelvis. Kummel insists that 90 per cent, of stones cast a shadow. 

4. Physical Findings. — The physical findings as tenderness (v. s.) 
are less important than the urinary findings and the colic. Palpation of 
the stone in the ureter is rarely possible, either from without or by the 
rectum or vagina; once the writer felt a calculus at McBurney's point. 
Stones have been felt to crepitate in the renal pelvis (Piorry). Cysto- 
scopic examination and catheterization of the ureters are most valuable 
methods. 

Complications. — Ulcerative pyelitis may lead to perforation, pyeloneph- 
ritis and paranephric abscess. Hydronephrosis results from mechanical 
occlusion of the ureter and pyonephrosis from obstruction with infec- 
tion. Injury to one kidney may be compensated by hypertrophy of its 
fellow. Amyloid degeneration, renal tuberculosis or even cancer may 
develop. The ureter may rupture from ulceration or tension. Troja 
instances a pregnant woman in whom abortion occurred after each 
of fourteen attacks of colic. 

Diagnosis. — The diagnosis is based on (a) the colic, particularly after 
exertion, (b) hematuria, (c) pyelitic pyuria, (d) x-ray findings and (e) 
less often, the anuria and swelling of the kidney. If the x-rays are 
negative stone is not excluded. A diagnosis of stone is found correct 
in only 60 per cent, of the cases operated on. 

1 . Pain and Colic. — Pain and colic may rarely occur in renal embolism ; 
also in passage of blood clots, parasites, echinococcus vesicles, malignant 
tissue or tuberculous detritus; renal aneurysm and floating kidney. 
In one case pain, colic and hematuria resulted from high insertion of the 
ureter. Confusion may result with vertebral disease, the crises of tabes 
or angioneurotic edema, herpes zoster, gall-stones, appendicitis, dia- 
phragmatic pleurisy or hysteria. 

2. Hematuria. — Associated with pain, it may cause errors in diag- 
nosis, usually corrected only at operation; thus acute congestion, or 
capsular fibrosis may be found; Israel describes a unilateral nephritis 
(a) with colic, (b) with albumin and without casts; (c) with casts and 
without albumin; (d) with hemorrhage, simulating tumor; but (e) the 
bleeding never causes the colic. Hematuria from cancer and tuber- 
culosis does not improve with rest in bed, while calculous hematuria 
usually does. Hematuria and renal colic may develop in ordinary 
chronic nephritis from acute renal congestion. 

Prognosis. — The course is usually chronic and relapsing, yet the author 
knows of four physicians who passed calculi without symptoms after- 
ward. Rupture of the ureter, collapse during the colic, pyelitis becoming 
pyelonephritis, anuria and uremia must be considered in the prognosis. 
Pyuria is more ominous than hematuria. 

Treatment.— 1. Prophylaxis. — Little is known regarding the patho- 
genesis of renal calculus, It is usually stated that regulation of the diet 
concerns moderation in both proteids and carbohydrates; foods rich 
in nuclein, acid foods and alcohol are interdicted, water given freely 



TUMORS OF THE KIDNEY 661 

and exercise insisted upon; vegetables may be allowed. In uric acid 
calculi, the alkaline waters are valuable, as those of Karlsbad, Vichy, 
Marienbad, Saratoga, Bedford, Poland and Mountain Valley. Sodium 
phosphate, gr. x, or bicarbonate, 3 ss, t. i. d., is indicated. Lithium carbon- 
ate, piperazin and glycerin possess no proved solvent powers. In localities 
where calculi develop very frequently, the drinking water must be used 
with caution. Stones once formed cannot be dissolved by drugs. 

If the oxalates are deposited, treatment is the same as in oxaluria 
(q. v.). In alkaline urines from which phosphates are precipitated, the 
urine must be made acid by phenylis salicylas, gr. x, t. i. d.; acid waters, 
as Seltzer or Apollinaris, may be employed; meats should be restricted; 
hexamethylenamine, gr. x, t. i. d., is excellent in bacteriuria. 

2. Colic. — The colic is treated as in gall-stones. 

3. Surgical. — Intervention is indicated by (a) anuria; (b) severe 
pyelitis; (c) septic or aseptic obstruction of the ureter;- (d) exhausting 
hematuria and (e) repeated attacks of colic. The ideal operation is 
myelotomy; next is nephrolithotomy (nephrotomy), closing the renal 
wound if there is no infection; operation on the aseptic kidney entails 
a mortality of 3 per cent., and operation in the presence of infection 10 
per cent. (Albarran) ; in these cases the pelvis should be drained (nephros- 
tomy). Tenny collected 134 cases of ureteral calculus; 122 were operated 
on, with a mortality of 19 per cent, or of 47 per cent, if pyelitis was 
present; anuria is a serious complication, for 52 per cent, of the operated 
cases die; without pyelitis or anuria the fatalities were 6 per cent. 

TUMORS OF THE KIDNEY. 

I. Cancer. — Etiology. — The etiology is obscure. It constitutes but 
2 per cent, of all cancers and but 1 per cent, of primary cancers in adults 
(Rubinstein); 62 per cent, occur in males and 32 per cent, in the first 
ten years of life. Its frequency in children was noted by Bright. Weigert 
observed 1 case in a newborn child. Cancer in the renal pelvis may 
result from stone. In the Albarran and Imbert series of 380 renal tumors 
cancer constituted 50 per cent. 

Pathology. — The primary form is usually infiltrating and the second- 
ary form consists of nodules. Medullary cancer is more common than 
scirrhus, colloid and other forms. It usually begins in the convoluted 
tubules of the cortex, and is limited by the renal capsule. The average 
kidney weight in children is 8 \ pounds and in adults 10 to 15 pounds 
(or even 50). The opposite kidney and the sound parts of the affected 
viscus may show compensatory hypertrophy. Hemorrhages into the 
neoplastic tissue, invasion of the renal veins, ureter, cava, pancreas, 
adrenals or intestine and metastases (58 per cent.) in distant organs 
sometimes develop. 

Symptoms. — Some, particularly secondary, cancers are latent. 

1. Renal Tumor. — Renal tumor occurs in 97 per cent, of cases. It 
begins in the renal region, but, resisted by the firm lumbar tissues, it 
grows forward. Bimanual palpation demonstrates its origin. If large, 
it may fall forward. It is tender and firm. The form of the kidney 



662 DISEASES OF THE KIDNEYS 

is usually preserved, though nodules may be palpated. It attains large 
dimensions (v. s.), compressing and dislocating the liver and spleen up- 
ward, crowding the abdominal viscera and even pushing the heart up to 
the clavicle. On tapping, a repercussion wave is sometimes noted (ballotte- 
ment renal). Percussion gives a dull note, except so far as the colon 
overlies the kidney, running from left to right, from above downward; 
on the left side this relation is more clearly distinguished; on inflation 
of the colon with air its tympanitic note in some degree obliterates the 
renal dulness, in less than 50 per cent, of large renal tumors; in tumors on 
the right side the colon is often dislocated laterally or even downward. 
There is but little if any respiratory excursion. In rare instances the 
tumor may pulsate and by pressure on the aorta produce a systolic 
murmur, which, as in Richard Bright's case, may simulate aneurysm. 
If the tumor grows into the ureter hydronephrosis may augment the 
swelling. 

2. Pain. — Dull pain is an early and frequent symptom, from pressure 
on the lumbar plexus, which also may cause some sensory disturbance 
in the legs. Only rarely is the pain colic-like, due to passage of clots or 
bits of tumor {v. L). 

3. Hematuria. — According to Guillet it occurs in 50 per cent, and 
is the first symptom in 25 per cent, of cases; Israel holds that it occurs 
in 92 per cent, and is the first manifestation in 70 per cent.; it is less 
frfequent in children (16 per cent.) . Sometimes worm-like clots are passed, 
with great colic; they sometimes measure one-half to one inch; clots 
in a clear urine are almost pathognomonic (Israel). The cystoscope and 
ureteral catheterization prove that the hematuria is unilateral. The 
hemorrhage usually originates in the diseased kidney, rarely from the 
opposite hyperemic kidney. Albarran asserts there is more albumin 
than the blood accounts for. Very rarely bits of cancer tissue pass. The 
urea is increased as in all cancers. Pyuria is no part of renal cancer. 

Complications. — Compression symptoms include paraplegia dolorosa, 
constipation, intestinal obstruction, edema from compression of the 
iliac veins and ascites; varicocele, first noted by Guyon, is due to late 
compression of the spermatic vein by the tumor or contiguous lymph 
nodes. Metastases, enlarged glands, rarely perforation into the lumbar 
muscles, skin, peritoneum or intestine with fatal hemorrhage, uremia, 
fever from cachexia or terminal infection may be observed. According 
to Israel, tumor of the renal pelvis causes greater hematuria, more 
hydronephrosis and therefore greater variations in the size of the tumor; 
it sometimes grows down the ureter and with the cystoscope is seen to 
project into the bladder; particles of tumor tissue and cells are more 
often obtained. 

Course and Prognosis. — Death is invariable without operation; it 
usually results from cachexia, in two years in adults and in eight months 
in children; 6 cases lived over ten and 1 case seventeen years. 

Diagnosis. — The following are important: renal tumor, pain, hematuria 
and cachexia. Imbert speaks of the complete type (tumor and hematuria), 
the hematuric type (without tumor, 6 per cent.) and the tumor type 
(without hematuria, 23 per cent.). 



TUMORS OF THE KIDNEY 663 

Differentiation. — (a) Liver tumor encroaches much more upon the 
diaphragm and is characterized by its respiratory excursion, location of 
the tumor within the edge of the liver, icterus and ascites. There are 
no suggestive urinary findings. Bimanual palpation clearly differentiates 
uncomplicated cases. Between a kidney tumor and the liver a furrow 
and loop of resonant intestine are frequently found. (6) A splenic tumor 
maintains the form of the spleen, lies above the colon (whose distention 
does not modify the splenic dulness), moves on inspiration, shows the 
characteristic notches and seldom causes confusion except when it so 
rotates that only its convexity can be felt, (c) An ovarian tumor projects 
upward from the pelvis, with which its connection can be demonstrated, 
save when it has a long pedicle. It is more central and sustains no char- 
acteristic relation with the colon, (d) Retroperitoneal growths are much 
more difficult to differentiate, especially enlarged lymph glands and 
lymphosarcoma. They are generally more central and less movable. Of 
perirenal retroperitoneal lipoma 50 cases are reported, (e) Cystic degen- 
eration (v. i.) is usually bilateral and runs a most chronic course. 
Sarcoma cannot be differentiated. In hydro- or pyonephrosis the tumor 
varies and presents characteristic urinary changes. Tuberculosis is 
distinguished by pyuria and tubercle bacilli in the urine. 

II. Sarcoma. — Sixty-six per cent, occur under ten years and most in 
the first two years of life. Sarcoma constitutes 20 per cent, of renal 
growths. It is slightly more common in girls than in boys and in the 
left than in the right kidney. Cohnheim's theory of embryonal inclusion 
is supported by the occasional presence of cartilage, bone, striated 
and unstriated muscle and even carcinomatous tissue. Sarcoma is 
of the round-, spindle-cell or melanoid type and may weigh 6000 gm. 
Secondary sarcomata may develop by metastasis from other organs or 
by invasion by contiguity. 

Its symptoms are essentially those of carcinoma, from which an intra 
vitam diagnosis is rarely possible, except when sarcomatous tissue is 
passed in the urine or excised at operation. Hematuria and cachexia 
are infrequent; age and glandular involvement are of no diagnostic 
value. A remarkable overgrowth of the pubic and axillary hair and 
pigmentation of the skin may be observed. Operated cases live on an 
average sixteen, and non-operated, eight months. 

III. Hypernephroma. — This " struma lipomatodes aberrans renis" of 
Grawitz develops from aberrant (included) particles of adrenal tissue. 
Lately their origin is considered Wolffian. Small tumors are not a rare 
autopsy finding. They constitute 20 per cent, of renal tumors and consist 
of a scanty vascular stroma, containing fatty cells like those of the adrenal 
bodies. Hemorrhage, cystic degeneration, a tendency to invade the 
veins and a large proportion of glycogen are considered characteristic. 
Fatty cells may be found in the urine. Hematuria occurs in 80 per cent, 
of cases. Bone metastasis is the first symptom in 16 per cent, but may 
develop as a late symptom only. Fever is noted in 57 per cent.; it 
occurs in but 1 to 2 per cent, of other tumors of the kidney (Israel). 

IV. Other Tumors. — Fibroma, lipoma, myxoma, angioma, endothe- 
lioma and rhabdomyoma are very rare; 33 cases of tumor of the capsule 
are on record. 



664 DISEASES OF THE KIDNEYS 

Treatment of Renal Tumors. — Symptomatic therapy concerns the pain. 
Surgical treatment alone is of value. Thirty-three recoveries after 
radical operation are on record, one patient being alive after eighteen 
years. Israel in 43 cases reported a mortality of 18.6 per cent., of which 
two-thirds died of heart paralysis; 19 per cent, enjoyed perfect health 
for three and a half to fourteen years. Schede in 18 operations obtained 
22 per cent, apparent recoveries after four to nine years. Recurrence 
after two years is very exceptional. Advanced cachexia, large or 
bilateral tumors, metastases and growth into the cava are contra- 
indications. 

CYSTIC DEGENERATION. 

Various renal cysts are observed, (a) The most frequent occur in 
chronic interstitial nephritis from snaring-off of the tubules and glomeruli. 
(6) Parasitic cysts are next in frequency (v. i.). (c) But three dermoid 
cysts are on record, (d) Cysts of the fatty capsule, retroperitoneal 
cysts and degenerated lymph glands are very rare, (e) Hydrops renum 
cysticuSy degeneratio renum polycystica was first separated by Rayer from 
the above-mentioned varieties and constitutes cystic degeneration, as it 
is generally understood. 

Etiology. — Over 50 per cent, are observed in mpn between forty and 
fifty years of age. Cystic kidneys are observed in later fetal life, at birth 
and in the adult. Probably they are congenital and remain latent until 
middle life. 

Pathogenesis. — Three main theories obtain; (a) that they are retention 
cysts, (b) new formations, i. e., neoplastic (cystadehomata), the most 
acceptable hypothesis, and (c) malformations. 

Pathology. — Congenital cases are usually bilateral; Lejars found 1 
unilateral case in 67 and Luzzatto 41 in 226 cases. The kidneys may 
contain innumerable small cysts, when the shape of the kidney is pre- 
served, or it contains larger cysts, when its contour is more irregular. 
The kidneys may be the size of a child's head and weigh twenty-one 
pounds. On section the kidney is honey-combed. The cyst walls consist 
of fibrous tissue. The cysts contain thin, yellow, transparent fluid, 
less often milky, gelatinous or brownish contents (altered blood). They 
are multilocular, are lined with cells like the urinary tubules or with flat 
polygonal cells and contain albumin, oxalate of lime, leucin-like crystals, 
red disks, epithelial detritus, fat granules and rarely urea. According 
to Englander, only 23 unilocular cysts are on record. Between the 
cysts are found vestiges of renal tubules or glomeruli, which may be 
vicariously hypertrophied. Cysts may occur in the pelvis, ureter, pan- 
creas and liver (v. i.). Other congenital deformities are sometimes 
found, particularly in the genitals, brain and fingers. 

Symptoms. — In congenital forms the cystic kidneys may obstruct 
delivery; if the infant is born alive death from asphyxia is usual, for the 
diaphragm is crowded upward. Adult forms generally come to autopsy 
undiagnosticated or with the diagnosis of nephritis. The symptoms 
may be classified as follows: (a) Renal cysts are detected clinically in 
20 per cent, of cases only. Their general characteristics are those of 



RENAL PARASITES 665 

solid kidney tumors, but they are bilateral (v. s.). Fluctuation seldom 
is elicited. In 2 cases which the author demonstrated, the individual 
cysts could be clearly palpated. Echinococcus cysts, hydro- and pyo- 
nephrosis, sarcoma and cancer of the kidney are only distinguished by 
their unilateral occurrence, (b) The urine may be normal, increased or 
decreased. The urinary findings are typically like those of interstitial 
nephritis, i. e., the urine is abundant, with few solids, low specific gravity 
and traces of albumin. Red disks are found in 20 per cent., sometimes 
in great numbers. In 2 of the author's cases many red cells appeared 
each time the kidneys were palpated. Leucin-like bodies may appear 
in the urine or in exploratory punctures; Beckmann first described 
these small colloid bodies ("rosettes") with structureless centres and one 
to five concentric rings and clearly radiating striations. (c) Cardio- 
vascular changes (left ventricular hypertrophy and sclerosed arteries) 
are common and heighten the resemblance to contracted kidney, (d) 
Uremia is the common cause of death. The clinical course is very 
chronic and is broken by attacks of periodic uremia; digestive disorders 
are very frequent. Patients may live fifteen and twenty years after the 
cysts are found. 

Diagnosis. — The diagnosis can be made when there are (a) bilateral 
(perhaps palpably cystic) renal swellings; (b) the cardiovascular and 
urinary findings of contracted kidney, with hematuria and colloid 
"rosettes," obtained in the urine or by puncture; (c) uremia and (d) 
perhaps renal pain like calculus, tenderness, or congenital cysts in the 
liver (in 28 per cent., Lejars); in a case of Dr. W. F. Dickson renal 
cysts were found with cystic liver, atrophic heart and pain resembling 
appendicitis. (See Echinococcus of the Livek.) 

Treatment. — Operation is permissible only in the exceptional, uni- 
lateral cases; about one-third of the operated cases die immediately 
and in few only are any lasting results obtained. The treatment is that 
of chronic nephritis. Multiple punctures are advocated. 

RENAL PARASITES. 

Echinococcus Cysts. — Renal cysts occur in 9 per cent, of echino- 
coccus disease (Neisser's 900 cases). In 970 cases (Vegas and Cranwell) 
the liver was diseased in 64 per cent., the lungs in 7 per cent., the spleen 
in 3 per cent, and the kidneys in 2 per cent. Baradulin in 1906 collected 
142 renal cases (see page 305). 

Symptoms. — (a) A renal tumor is found in 50 per cent, when the 
cyst attains large dimensions. Without the exploratory puncture and 
the urinary findings, it is easily confused with other cysts, hydroneph- 
rosis, cancer or tuberculosis. Fluctuation and the hydatid thrill are not 
often found (see Liver Echinococcus). The cyst begins in the cortex, 
usually in either pole of the kidney; it is unilateral in 96 per cent, of 
cases and is left-sided in 62 per cent. If the cyst calcifies it may be seen 
by the x-rays. The opposite kidney may hypertrophy, (b) Exploratory 
aspiration may show (i) fluid or pus containing urinary constituents, 
cholesterin, succinic acid, much sodium chloride and a reducing sub- 



666 Diseases of the kidneys 

stance; (ii) vesicles, hooklets or particles of lamellated membrane, (c) 
The urine may contain vesicles, hooklets, membrane, pus from pyelitis 
and blood from rupture. As many as 100 vesicles have been passed. 
(d) Passage of vesicles is attended by severe colic, fever, chill and vomiting. 

Complications. — Seventy-five per cent, rupture, chiefly into the renal 
pelvis; perforation may occur into the intestines, lumbar muscles, 
lung or pleura; the patient may feel the rupture. The toxic substances, 
liberated by rupture or puncture, may cause urticaria, severe heart 
symptoms or even fatal syncope. Adhesions to the liver, spleen and 
intestine may form. Suppuration or gangrene may develop (pyonephrosis 
or paranephritis). Obstruction of the ureter causes hydronephrosis; 
vesicles plugging the lower end of the ureter have been seen with the 
cystoscope. 

Prognosis and Treatment. — The course is chronic, covering even twenty 
to thirty years. Suppuration may cause pyemia. The cyst may shrink 
or calcify. Bilateral involvement makes the prognosis unfavorable. 
Spontaneous recovery by rupture into the urinary tract occurs in 32 
per cent. Extra-peritoneal nephrotomy is indicated, as there is seldom 
more than a single cyst. In 30 nephrotomies by Schede there were no 
fatalities; 87 per cent, completely recovered and 10 per cent, recovered 
but had fistula?. Nephrectomy entails a higher mortality (8 per cent.). 



SECTION VI. 

DISEASES OF THE BLOOD. 



Anemia is a reduction in the blood as a whole or more often a reduc- 
tion of its important constituents, as the red corpuscles, their number, 
hemoglobin or albumin. Every anemia has a cause, yet in our present 
ignorance we adhere to the older division of anemia into primary and 
secondary forms. Primary anemia includes chlorosis and pernicious 
progressive anemia. 

CHLOROSIS. 

Definition. — Chlorosis is a disease of hemogenesis, occurring in women, 
chiefly in the developmental years, in which the cardinal symptom is 
anemia ; the red cells are reduced but the hemoglobin is disproportionately 
reduced; chlorosis responds to therapy by iron. Chlorosis is a disease, 
while anemia is but a symptom. 

Etiology. — Its etiology is uncertain, (a) All cases occur in women, 
especially in girls who menstruate before the pubes and mammae develop 
(Niemeyer). It is more common in blondes than brunettes, (b) Chlorosis 
occurs largely between the fourteenth and seventeenth years, rarely after 
the twenty-fourth year, (c) Heredity, chlorosis, tuberculosis and hys- 
teria are not infrequently associated in the family history, (d) Malnu- 
trition, lack of hygiene, working in dark quarters, insufficient or excessive 
exercise, wearing of corsets and emotional or sexual factors are indirect 
causes. Various theories are advanced as to the nature of the disease, 
as adynamia of the blood-making organs at puberty, insufficient absorption 
of iron, auto-intoxication from the internal genitalia and intestines. 

General Symptoms. — Among the early frequent symptoms are rapid 
tiring, dyspnea and palpitation. Pallor is the earliest and most constant 
sign, the skin being of a yellowish-green hue (chlorosis, as named by 
Varandel in 1670). Sometimes the face is flushed, probably from per- 
ipheral vasomotor irritability (chlorosis rubra) ; hence the mucous mem- 
branes should be examined also. The eyes are often brilliant. Lack 
of mental and muscular energy is noted, associated with headache, which 
may be dull or sharp, sometimes migraine-like or increased at the time 
of menstruation, spots before the eyes, tinnitus, vertigo and syncope, 
especially from standing, travel and exposure to the sun. Menstrual 
disturbances are frequent, the flow being often decreased in younger 
subjects. Digestion is very often disturbed. The hands are cold, the 
skin dry and the peripheral circulation sluggish. Circulatory symptoms 



668 DISEASES OF THE BLOOD 

appear, as the bruit de diable in the neck veins, anemic heart murmurs 
and rapid pulse. 

Special Symptoms. — 1. The Blood. — The blood is fluid and its coagu- 
lability is increased. The red blood cells are decreased (oligocythemia) and 
average 3,000,000 to 4,000,000; as few as 900,000 have been observed. 
In rare cases they are not decreased. Formation of rouleaux is poorly 
marked. The red cells appear pale and their average size is reduced. 
Irregularity in contour (poikilocytosis) , megalocytosis and microcytosis 
are rare; normo- and megaloblasts are found in the severest cases, or 
in "blood crises." More suggestive than the oligocythemia is the reduc- 
tion of hemoglobin (oligochromemia) , which is reduced more than the red 
cells (Duncan, 1867) ; the hemoglobin averages 30 to 40 per cent. This 
reduction in the color index to one-half or less always suggests chlorosis, 
and is less conspicuous in relapses and in older individuals. The white 
cells are essentially normal, therein differing from many other forms of 
anemia; occasionally lymphocytosis and eosinophilia occur. The iron 
and nitrogen of the blood and its specific gravity are reduced proportion- 
ately to the decrease in hemoglobin. 

2. The Vascular System. — (a) Rokitansky and Virchow observed 
hypoplasia of the aorta and vessels, which may coexist with hypoplasia 
of the genitalia, muscles and bones, but cannot be regarded as causative. 
(b) Palpitation is almost constant on exertion ; the apex-beat is strong to 
compensate for the poverty in hemoglobin, (c) Heart murmurs occur in 
two-thirds of the cases; they are functional and caused by insufficient 
tension of the mitral valve, relative mitral insufficiency, weakened heart 
muscle (producing a muscular murmur in place of the tone) or vibration 
of the pulmonary artery. The murmurs are largely systolic; undoubted 
diastolic venous bruits have been heard, (d) Dilatation of the heart may 
occur from anemia or myocardial degeneration, though usually it is not 
real but apparent, retraction of the lungs away from the heart, because of 
insufficient lung expansion being seen by the .T-rays. (e) The pulse may be 
rapid, throbbing or excitable. Dicrotism and capillary pulsation are 
frequent and double tones have been noted in the crural vessels from de- 
creased tension and diastolic recoil. (/) A venous bruit de diable in the 
neck occurs more frequently than in other anemias (in over 50 per cent, of 
cases and in two-thirds of the cases over the right jugular vein, because it is 
more vertical). It is increased by turning the head and deep inspiration. 
It is referred to change in the tonus of the vessel, waves in the veins above 
their valves or change of the blood plasma, (g) Arterial murmurs may be 
heard, as over the subclavian artery; pulsation in the peripheral veins, 
angiospasm and erythromelalgia have been observed, (h) Edema is 
seen in 12 per cent, of cases and is usually slight, occurring chiefly about 
the ankles and eyes. 

3. Respiratory Tract. — Dyspnea is common, explained as a hema- 
togenous respiratory insufficiency. The respiration-rate is 26 to 30. 
Sometimes a paroxysmal cough develops. 

4. Digestive Tract.— The digestive tract is involved in one-third of 
the cases, (a) Pain is frequent near the ensiform with tenderness, 
especially in nervous individuals. Vomiting and perversity of appetite 



CHLOROSIS 669 

are occasional, (b) Dyspepsia may be purely nervous. Exceptionally 
the stomach is dilated and atonic, (c) The hydrochloric acid is often 
increased, probably from nervous irritability, id) Constipation is no 
more frequent than in the average case; intestinal fermentation is not 
the cause of chlorosis. 

5. Sexual Sphere. — Menstruation is decreased or absent in 80 per 
cent.; menstrual disturbance, the uterus infantilis or small ovaries are 
neither the cause nor result of chlorosis, but result from some common 
factor. Conception is unlikely to occur. Chlorotics are first treated by 
the gynecologist for leucorrhea in 22 per cent, of cases. 

6. Special Senses. — The usual symptoms of anemia, as spots before 
the eyes and weakness of accommodation, are observed. The retinal 
vessels may be transparent or pulsating; retinitis and neuroretinitis 
or " choked disk" exceptionally simulate brain tumor. Retinal hemor- 
rhage is rare. 

7. Skin. — The skin is usually anemic; angiospasm, coldness and 
paresthesia occur. In chlorosis rubra the cheeks are flushed. Seborrhea 
and acne are very common. Sweats, urticaria, eczema, purpura, chloasma 
and trophic disturbance' of the hair and nails may occur. 

8. Nervous System. — Chlorosis often brings out a latent neurosis — 
especially hysteria — and psychosis. 

9. Metabolism. — Metabolism is not essentially disturbed. Usually 
the body weight is maintained, less from decreased, oxygenation than 
from inactivity. The urine is clear, of low specific gravity, often alkaline 
with decrease of urea and uric acid and sometimes albuminuria. Leube 
found fever frequently in mild chlorosis. When present, we may suspect 
" tuberculous pseudochlorosis." 

Complications. — Chlorosis may favor acute infections and render their 
course severe. Venous thrombosis complicates 2 per cent, of cases and is 
probably inflammatory. In Quensted's series 67 per cent, involved the 
veins of the leg and 25 per cent, the cerebral sinuses; pulmonary embol- 
ism occurred in 19 per cent. Virchow emphasized the frequency of septic 
endocarditis. Rheumatic endocarditis with organic valvular lesion is 
frequent, as also are ulcer of the stomach, tuberculosis and Basedow's 
disease. The spleen is enlarged in 16 per cent, and often the thyroid 
gland. Hemorrhages are not infrequent from the nose, stomach or intes- 
tine, although less than in severe secondary or pernicious anemia. 

Clinical Course and Prognosis. — Chlorosis develops abruptly and runs a 
short course of two to four months. The prognosis is generally good. The 
tendency to recurrence is great, especially in unmarried or childless women ; 
the blood may not return absolutely to normal, shown by persistent pallor 
or irregular menstruation. Acute chlorosis is observed in young girls 
after their first menstruation; it is attended by severe headache, nervous 
symptoms, weakness and optic neuritis or "choked disk," which may be 
confused with brain tumor. The periodic type occurs in the higher classes 
and in those who acquire the disease in their seventeenth to nineteenth 
year. The disease may last for years with chronic chlorotic blood, men- 
strual, dyspeptic, muscular and nervous symptoms, with alternate exacer- 
bation and amelioration ; there is poor development of the bones, muscles, 



070 DISEASES OF THE BLOOD 

genitalia, mammae and adipose tissue; marriage, pregnancy and iron 
often benefit these cases, but they may last until the menopause. 

Diagnosis. — The diagnosis is made by the grouping of symptoms, 
positive and negative, for no single symptom is pathognomonic. The 
obtrusive symptom is anemia, especially when there is disproportionate 
reduction in the hemoglobin, when the color index is less than one and the 
white cells are normal. Rhomberg described exceptional cases in which 
the blood was normal. The age, rapid development, periodic manifesta- 
tion and successful treatment with iron are important features. Second- 
ary anemia is most difficult to differentiate and is usually attended by 
some leukocytosis (v. page 677). Hemorrhage from latent ulceration 
of the stomach, early pregnancy in unmarried girls, the anemia of heart 
disease, etc., must be considered. Splenic anemia, especially in children, 
requires differentiation; cases of chlorosis with enlarged spleen are a. 
transitional form between chlorosis and splenic anemia proper. Malig- 
nant disease and incipient tuberculosis are important. 

Treatment. — 1. Prophylaxis. — General hygiene and development of 
adipose tissue to a reasonable extent are prophylactic. More albumin 
should be given to growing children than to adults, together with fruit 
and vegetables, for their iron, and butter, cream and oils, rather than 
animal fats. Physical culture and trips to the country are valuable. 
Children at this age are confined too much to the school-room; they 
should be kept children as long as possible. In society or in the struggle 
for existence young girls too often overtax their strength. 

2. Specific Therapy. — Iron exists in the hemoglobin of the blood 
cells as an oxygen carrier and is a food as well as a medicine ; it is found 
in blood, meat, oatmeal, peas, spinach and beans. 

Physiological Action of Iron. — (a) The nervous tonus is increased; 
an excess produces frontal headache from constipation; some persons 
exhibit a peculiar intolerance of iron, as shown by headache, vertigo and 
palpitation, (b) It increases the number of red disks and the hemoglobin, 
(c) Iron stains the teeth because of the acid it contains. Small doses stimu- 
late digestion, improving, by their astringent action, the tone of the 
tissues. Hydrogen is generated and from it sulphuretted hydrogen, which 
causes eructations. Small doses constipate but large doses relax the 
bowels; diarrhea sometimes follows small doses. Sulphide of iron 
darkens the stools, (d) The amount of urine is increased. Iron is found 
in the urine in very small quantities. The kidneys may be irritated by 
very large doses, (e) It is absorbed from the stomach and intestines 
as an albuminate, reaches the blood and is deposited first in the spleen 
and then in the liver, by which, and the intestines chiefly and kidneys, 
it is eliminated. 

Administration. — Soluble would seem to be better than insoluble prepa- 
rations, but Quevenne has shown that they are precipitated by the gastric 
juice. Headache is obviated by using laxatives, or ferrous salts, which 
derange digestion less than ferric salts, and can be reduced; chlorotics 
cannot reduce the ferric salts. Iron is said to be best absorbed when some 
gastric catarrh exists, hence Brunton gives large doses at first to improve 
absorption. There are only 38 to 45 grains of iron in the body; the ordinary 



CHLOROSIS 071 

daily diet contains but one-sixth of a grain of iron, but while sufficient as 
food, does not stimulate the blood-making centres. The doses should not be 
too small. Statements of the patient that she has previously taken iron 
should not be regarded, for its administration may have been irregular. 
In the first week the dose should be gradually increased; for three weeks 
the maximum dose should be given and for the last two weeks it should 
be gradually decreased. If iron is not beneficial it should not be repeated 
but other methods tried. Relapses are less easy to treat than the first 
attack. Idiosyncrasy, as gastro-intestinal disturbance, is only a relative 
contra-indication. The administration should then be subcutaneous. At 
mineral springs hygiene is more important than iron; the water should 
be taken on an empty stomach, for the gas promotes absorption of iron. 
When bottled it is precipitated as a carbonate. 

Preparations. — Ferrum reductum (reduced iron) is iron gray (if it is 
black it is impure) and tasteless; it is least astringent, but may cause 
eructation; gr. j. (See formula on page 377.) Pilula ferri carbonalis, 
a ferrous salt nearly free from astringency; grs. ij-v. Ferri sulphas 
(green vitriol), a ferrous salt which is very astringent, whence its use 
in chronic diarrhea. It stimulates digestion, but in large quantities 
it causes vomiting or diarrhea; gr. ij may be given with 1 dram of 
magnesium sulphate p. c. 

1$ — Ferri sulphatis exsiccati, 

Potassii carbonatis aa 3ij 

Syrupi : q. s. 

M. et fac pilulas no. 1. 

S. — One to three pills after meals (Blaud's pills). 

Liquor ferri et ammonii acetatis (Basham's mixture) is diuretic and 
excellent for chlorosis in the obese, 3j _ iv given after meals, well diluted. 
Tinctura ferri chloridi is the chloride of iron plus hydrochloric acid and 
alcohol, which develop hydrochloric ether. It is yellowish-red, astringent, 
somewhat corrosive and diuretic, increasing the amount of urine and 
frequency of micturition. It is used to best advantage when the tongue 
is white, flabby and indented. In weak, anemic girls, with vomiting, neural- 
gia and epigastric pains, full doses should be given ; when poorly tolerated, 
one drop in a full glass of water is more beneficial than chalybeate waters. 
Iron and iodine given separately are usually more beneficial, but the 
syrupus ferri iodidi may be given in doses of 30 to 40 drops in adults and 
of 5 to 10 in children. Ferri citras in doses of gr. v, is efficacious in 
delicate stomachs ; for hypodermic use it is painful ; ferri arsenas, gr. y 1 ^, 
or ferri cacodylas, gr. J to j, is better. Most organic irons are useless. 
Arsenic alone seldom increases the red cells or hemoglobin; ferri phosphas 
solubilis, gr. v, is almost free from astringency and taste. Arsenic is 
given as in pernicious anemia (q. v.) uninterruptedly, with gradually 
increasing doses, sustained doses and then decreasing doses for a period 
of four to six weeks. 

High altitude increases the red cells and hemoglobin. 

3. Dietetic Treatment. — The amount of albumin should be increased 
and the heavy English breakfast is indicated. Equal parts of milk and 
cream should be given but with care lest the appetite be spoiled, too much 



672 DISEASES OF THE BLOOD 

fat be deposited and the stomach suffer atony. Alcohol is indicated in thin 
rather than in obese individuals. Patients should rest before and after 
eating and retire early. In thin subjects the diet should be concen- 
trated, consisting of albumin, vegetables, fats, alcohol, and milk at 
breakfast and at bed time, but without increase of the carbohydrates. 
Iron produces better results in such cases after limiting the amount of 
water to about one quart. Sweats may produce the same results. Gas- 
tric disturbance disappears after administration of iron, and meals at two- 
hour intervals— fluid and solid meals being alternated. Hydrochloric 
acid, strychnine, belladonna, exercise in convalescence (during chlorosis 
the patient should rest in bed) and cool rubbings early in the morning 
are advantageous; cold baths produce chills, insomnia and digestive 
disturbances. Marriage may help mild cases, but is injurious in the 
severe type. 

PERNICIOUS ANEMIA. 

Definition. — A primary anemia with progressive diminution of the red 
cells and reduction in the hemoglobin; due to hemolysis and defective 
hemogenesis; characterized by pallor, adynamia, edema and cardiac 
symptoms and resulting in death from vomiting, diarrhea, hemorrhages 
and fever. It was described by Combe (1822) and Andral (1826) ; Addi- 
son (1855) gave the best early description and it is sometimes called 
Addison's anemia. Since Ehrlich drew the blood picture, little has 
been added to our knowledge of the disease. 

Etiology. — The disease occurs in 0.2 per cent, of cases, especially in 
the fourth and fifth decades of life; six-sevenths of the cases occur after 
the thirty-fifth year (Cabot). Baginsky could collect but 16 cases in 
children. Sixty per cent, occur in males. The ultimate cause is to be 
sought in some hemolysin, as yet unknown. Although called a primary 
or essential anemia, some undoubted secondary cases may be included 
under this head because the symptom-complex is the same. Bothrio- 
cephalus and ankylostoma anemias present identical blood findings, 
symptoms and pathology. Talquist found a lipoid substance in the 
alimentary mucosa and in tape-worms. Pregnancy, the puerperium, 
syphilis, typhoid, malaria, and diarrhea, vomiting and oral or gastro- 
intestinal sepsis have been considered factors. 

Symptoms. — 1. The Blood Changes (Sorenson, 1874). — The amount 
is decreased, several punctures often being necessary to obtain enough 
for the blood count; it is often watery. The specific gravity is low, even 
1.027. There is an increase in the albumin in the individual red cell 
(hyperalbuminemia rubra, von Jaksch). The serum does not contain 
free hemoglobin. If injected into normal individuals the serum has a 
hemolytic action. In contrast to chlorosis and secondary anemias, the 
coagulability of the blood is decreased and the blood may remain fluid for 
some time after death. Dropped on filter paper, there is a white zone 
outside the blood stain (Talquist). The hemoglobin is rarely more than 
50 per cent, and may be reduced to 10 per cent. In 90 per cent, of cases 
and in contrast to other anemias, the hemoglobin per corpuscle is propor- 
tionately increased, i. e., the color index is more than 1 (even 2.25). 







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PERNICIOUS ANEMIA 673 

Laache's explanation is that certain red cells, especially giant forms, 
contain a large compensatory individual amount of hemoglobin, which is 
also true of the microcytes, but less so of normal-sized red cells. Free 
hemoglobin, acting on the white cells, possibly produces a fibrin ferment, 
which causes fever, hemorrhage and capillary embolism. The red blood 
corpuscles are greatly reduced in number, even to 100,000, the average 
being 1,200,000. Patients often die when this figure is reached. Poikilo- 
cytosis is marked, the irregularity in form and size of the corpuscles being 
great, as Litten's horseshoe or pessary-shaped corpuscles. In 90 per 
cent, the red corpuscle is above the average size, i. e., 11, even 18ju, instead 
of 5 to Sfi, the highest normal measurement. Polychromatism is frequent. 
Megalocytes may be observed in numbers, with less marked or absent 
umbilication; they probably indicate megaloblastic degeneration of the 
bone-marrow. (See Plates XVII and XVIII.) Megaloblasts are rarely 
found in large numbers ; in rare cases they may be abundant, as just before 
death, whence their generally ominous significance; they may be absent 
for months or weeks at a time. Normoblasts occur in nearly all cases, 
especially in the u blood crises" but are not numerous; they are immature 
cells and indicate activity of the blood-forming organs. Microblasts 
are frequently absent; their teleological significance lies in the increase 
of the respiratory surface of cells thus afforded. Cell divisions are found. 
Granular deposits (staining with basophilic dyes) in the protoplasm are 
noted; according to Ehrlich, they are not due to polychromatophile 
degeneration but to nuclear degeneration. The cells may stain only at 
their margins. Decreased formation of rouleaux is observed as well 
as ameboid movement of the red cells. The white corpuscles are decreased 
absolutely, the lowest record being 1500; the polymorphonuclears are 
decreased. Leukocytosis is a distinct complication, is often ominous and 
indicates inflammation or suppuration. The lymphocytes are relatively 
increased, even to 62 per cent, of the total white cells. Marked decrease 
of the eosinophiles is an unfavorable sign. Pernicious anemia due to 
parasites shows increase in the eosinophiles to 6, 36 and even 50 per cent. 

2. Subjective Symptoms. — The most marked are weakness, muscular 
adynamia, vertigo, palpitation and dyspnea. 

3. Skin.- — The skin presents a peculiar pallor, often of a somewhat 
characteristic lemon tint Slight icterus is not infrequent. The skin is 
usually dry. Edema is invariable, especially about the ankles and eye- 
lids. It is obstinate and may produce pronounced general anasarca; it 
is due to degenerative vascular permeability. Hemorrhages, usually 
punctate, are frequent in the skin and mucosa?. Large hemorrhages occur 
in 25 per cent, of cases. Pigmentation is sometimes as marked as in 
Addison's disease. The author observed herpes zoster and crural herpes. 

4. Metabolism.— The nutrition is maintained in 61 per cent, of cases 
because tissue waste is lessened and water is retained in the tissues; 
in 39 per cent, the weight and strength finally decline with persistent 
vomiting and diarrhea (Cabot). In the urine indican, putrescin, cada- 
verin, leucin and sometimes tyrosin, acetone and albumose are found. 
Albuminuria, due to tubular degeneration, is frequent. Urobilin is fre- 
quently increased and indicates hemolysis. The chlorides are decreased. 

43 



074 DISEASES OF THE BLOOD 

The iron in the urine and uric acid are sometimes increased and the phos- 
phates are greatly increased. Irregular fever, present in 80 per cent, of 
cases, bears no constant relation to the severity of the disease. It may 
rise considerably; the temperature may fall below normal in the ante- 
mortem coma. It is probably due to a ferment from the destroyed red 
cells or from the leukocytes (v. page 073). 

5. The Circulation. — Palpitation, precordial anxiety and dyspnea are 
observed, sometimes only on exertion. The heart impulse is fallaciously 
strong to the palpating hand. Its outlines are usually normal, save that 
dilatation of the right heart may develop. Almost always a blowing 
systolic murmur is heard, usually with a clear diastolic tone; the murmur 
is rarely presystolic or diastolic. No parallelism exists between the 
degree of anemia and the loudness of the murmur. Leube reports cases 
of chlorosis and pernicious anemia in which there was relative tricuspid 
insufficiency with a positive venous pulse but no cyanosis. A venous 
hum in the neck, carotid pulsation and thrills, a loud, clear systolic tone 
and murmurs or double tones over the peripheral arteries are often 
present. The pulse is collapsing, decreased in tension and increased in 
rate, usually between 90 and 120. Anatomically, vestiges of hemorrhage, 
atrophy and the fatty, "tabby-cat heart" are almost constant. 
Degeneration in the smaller vessels is noted, especially in the brain. 

0. Digestive Tract. — Anorexia, distaste especially for meats, pain 
and sensitiveness throughout the alimentary tract are noted. The 
tongue and gums often exhibit circumscribed hemorrhages. Pain in the 
mouth (50 per cent.) and esophagus is due to the anemia or administra- 
tion of arsenic. The gums may ulcerate; erythema bullosum and other 
eruptions may occur. Vomiting is frequent and often incoercible; the 
vomitus consists of food, greenish mucus and sometimes traces of blood. 
The writer has observed profuse hematemesis and cyclic vomiting as the 
first symptoms. Crises of abdominal pain occur in 00 per cent., and the 
writer observed simulation of gall-stones by the pain and subicterus. Epi- 
gastric pulsation, abdominal distention and achylia are observed. The 
author saw expansile abdominal pulsation, diagnosticated as aneurysm. 
The glands in the gastro-intestinal tract may atrophy, which probably 
toxemic condition is coordinate with and not causal of pernicious anemia. 
The mesenteric glands are not infrequently enlarged. Paroxysmal 
diarrhea occurs in 50 per cent., constipation in 35 per cent, and an alter- 
nation of these conditions in 15 per cent. The stools are not characteris- 
tic; parasites or their eggs may be noted. Leucin and tyrosin crystals 
are frequently caused by diarrhea, but are not characteristic of the 
disease. Fermentation, indicanuria, edema, hemorrhage and follicular 
swelling in the bowel are frequently observed. Some ascites is found 
in the terminal stage. A deposit of iron (siderosis) in the liver, in 
the outer and middle zones of its lobules, especially in acute types, in 
the spleen, bone-marrow, kidneys and lymphatic glands is usual and 
results from hemolysis; it is very unusual in other anemias. The liver 
is slightly swollen and tender in one-third of the cases. 

7. Blood-making Organs. — The lymph glands are not usually en- 
larged. In the prevertebral hemolymph glands Warthin found their 
sinuses dilated and evidences of hemolysis, shown by increased phago- 



PERNICIOUS ANEMIA 675 

cytosis and sometimes hyperplasia. The bones are tender, especially the 
sternum and tibiae, and sometimes painful; the fatty marrow may become 
lymphoid (leukoblastic degeneration), as in other anemias, cachexia or 
fevers; in pernicious anemia the red cells of the marrow are abnormally 
large, abnormally dark from increase of the hemoglobin and are oval 
rather than round; the megaloblastic degeneration develops at the 
expense of the other elements in the bone-marrow. These probably 
secondary bone changes were first described by Wood, Pepper and 
Tyson (1875). The spleen is not enlarged save from accidental causes; 
in it are found phagocytosis and evidences of hemolysis. 

8. The Nervous System. — The psychical functions are depressed, the 
memory is weak and psychoses, delirium, hallucinations, mania and 
insomnia may develop temporarily or antecedent to the terminal coma. 
The pupil reflexes sometimes disappear. Paresis, apoplectiform attacks, 
cramps, convulsions, paresthesia, aphasia or vertigo may develop. The 
cord is more frequently involved (in 84 per cent, of cases) than the brain. 
The weakness may amount to paresis, not due simply to muscular 
adynamia but to spinal changes. The picture may resemble tabes as 
concerns the pupils, patellar reflexes, ataxia, bladder and rectal changes, 
crises, pains, anesthesia and paresthesia; or, less often, the symptoms of 
spastic spinal paralysis prevail, as increased reflexes and spastic paresis. 
In one group of cases the nervous symptoms are slight, and in a second 
they are so conspicuous as to overshadow the anemia itself. Early 
paresthesia occurs in all cases, usually in the hands and feet, sometimes 
in the mouth; sometimes there is hyperesthesia or disturbance of the 
temperature sense. The sexual function is decreased in males and amen- 
orrhea is regular in women. There is a sclerosis of the posterior (which 
rarely wholly escape) and lateral columns, most marked in the lower 
cervical and upper dorsal segments, oftener diffuse than focal, and 
involving chiefly the white substance, but not the entire neuron. Small 
foci of degeneration with secondary connective-tissue growth occur 
about the bloodvessels, which foci may fuse into small plaques with 
secondary degeneration, whence the symptom-complex of a system 
disease. 

The discrepancy between the anatomical and clinical findings is re- 
markable, i. e., there may be many symptoms with few autopsy findings, 
and conversely; probably the nervous symptoms are less sequences of 
anemia than coordinate toxic manifestations. The peripheral nerves 
present few symptoms. 

In the eyes the general symptoms of anemia occur; hemorrhages in 
the retina are found by Hasse in 94 per cent, of cases but not in other 
anemias requiring differentiation. Occurring on a pale background, 
with tortuous veins and a strong light reflex from the vessels, the punctate 
hemorrhages form a striking picture (see Plate VI, Fig. 9) . Labyrinthine 
hemorrhage with vertigo is recorded. 

Clinical Course and Prognosis. — The initial pallor and weakness increase 
insidiously and later dyspnea, weak heart action, edema, complete 
anorexia, languor, spinal and gastro-intestinal disturbance and finally 
capillary hemorrhages and fever develop; the vomiting and diarrhea 
may resemble acute poisoning. In other instances remissions may occur 



676 DISEASES OF THE BLOOD 

with treatment or independently of it, perhaps after violent gastro- 
enteric manifestations. In Ehrlich's case, the red cells in seventeen 
days rose from 1,340,000 to 4,115,000. The disease with remissions may 
cover a period of years, the longest duration being seventeen. Death 
usually occurs within half a year. The writer observed recovery for 
fourteen years after a count of 400,000. 

The prognosis is usually poor when many megaloblasts are present 
or when the color index is over one. 

Cabot recognizes two forms: 

The Severe, Rapidly Fatal Type — and the Less Severe, Slow Type. 

(a) Extreme progressive anemia. Remissions. 

(6) Color index high. Normal or low. 

(c) Red cells increased in size. Normal. 

(d) Degenerative changes. None. 

(e) Many megaloblasts. Many normoblasts, few megaloblasts. 
(/) Lymphocytosis. Normal ratio of the various white cells. 

Emerson distinguishes three groups, according to the blood count: 
(i) With 1 . 000 000 reds, weakness and shortness of breath on exertion; (ii) 
with 1,000,000 to 2,000,000 reds, alimentary symptoms; and (in) in higher 
counts, various, perhaps severe, but particularly nervous, symptoms. 

Death usually occurs in coma. There are only 6 recoveries, according 
to Cabot, yet he found 27 cases which lived eight or more years. The 
mortality in the parasitic form is 17 per cent. 

Diagnosis. — No single finding is absolutely characteristic, though the 
pallor, apathy, adynamia, edema, weak heart, retinal hemorrhages, 
maintained nutrition and the blood findings are highly suggestive. The 
yellow color is very often mistaken for icterus. Ewing states no impor- 
tance should be attached to the increased diameter of the red cells unless 
33 per cent, of the red disks show it. 

Differentiation. — (a) From metastatic bone tumors, in which the 
white cells are increased (the polymorphonuclear, neutrophile and 
eosinophile marrow cells); (b) from parasitic anemia, for w T hich the 
stools should be examined for parasites and their eggs; (c) fever, if 
dominant, may suggest typhoid, meningitis or acute endocarditis; (d) 
from latent carcinoma; the gradual cachexia, anorexia, nausea, vomiting, 
hematemesis and absence of hydrochloric acid may suggest gastric car- 
cinoma, but the blood examination determines the point; (e) spinal 
disease, Addison's disease and hemorrhagic pleuritis are usually excluded 
with ease; and (/) from other anemias. The table on page 677 is 
constructed after Cabot's table. 

Aplastic anemia, generally regarded as a type of pernicious anemia, 
is characterized by its low blood count and reduced hemoglobin. It 
was so named by Ehrlich because the bone-marrow was aplastic; there- 
fore in the blood there are no evidences of regeneration, such as nucleated 
red cells, the red cells are small and the color index is low. The white 
cells may number only 200 per c.mm. and SO to 90 per cent, of them are 
lymphocytes. Two-thirds of the cases are women. There may be 
hemorrhages, especially purpura, fever or hyperplasia of the spleen and 
lymph glands. The outcome is rapidly fatal, 80 per cent, dying within 
three months. 



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OSIAtV/V BY U/» 'Z CMASf 



PLATE XVIII 

BLOOD. 

(Ehrlich Triple Stain.) 
(Prepared by Dr. I. P. Lyon.) 

Fig. I.— TYPES OF LEUKOCYTES. 

a. Polymorphonuclear Neutrophile. b. Polymorphonuclear Eosinophile. c. Myel- 
ocyte (Neutrophilic), d. Eosinophilic Myelocyte. e. Large Lymphocyte (large 
Mononuclear). /. Small Lymphocyte (small Mononuclear). 

Fig. II.— NORMAL BLOOD. 
Field contains one neutrophile. Reds are normal. 

Fig. III.— ANEMIA, POSTOPERATIVE (secondary). 

The reds are fewer than normal, and are deficient in hemoglobin and somewhat 
irregular in form. One normoblast is seen in the field, and two neutrophiles and one 
small lymphocyte, showing a marked posthemorrhagic anemia, with leukocytosis. 

Fig. IV.— LEUKOCYTOSIS, INFLAMMATORY. 

The reds are normal. A marked leukocytosis is shown, with five neutrophiles and 
one small lymphocyte. This illustration may also serve the purpose of showing the 
leukocytosis of malignant tumor. 

Fig. V.— TRICHINOSIS. 
A marked leukocytosis is shown, consisting of an eosinophilia. 

Fig. VI.— LYMPHATIC LEUKEMIA. 

Slight anemia. A large relative and absolute increase of the lymphocytes (chiefly 
the small lymphocytes) is shown. 

Fig. VII.— SPLENOMYELOGENOUS LEUKEMIA. 

The reds show a secondary anemia. Two normoblasts are shown. The leukocytosis 
is massive. Twenty leukocytes are shown, consisting of nine neutrophiles, seven myelo- 
cytes, two small lymphocytes, one eosinophile (polymorphonuclear) and one eosinophilic 
myelocyte. Note the polymorphous condition of the leukocytes, i. e., their variations 
from the typical in size and form. 

Fig. VIII.— VARIETIES OF RED CORPUSCLES. 

a. Normal Red Corpuscle (normocyte), b, c. Anemic Red Corpuscles, d-g. Poikilo- 
cytes. h. Microcyte. i. Megalocyte. j-n. Nucleated Red Corpuscles, j, k. Normo- 
blasts. I. Microblast. m, n. Megaloblasts. 



PERNICIOUS ANEMIA 



677 





Pernicious anemia. 


Chlorosis. 


Secondary anemia. 


Red Cells 


Average number 
1,000,000. 


Rarely under 
2,000,000. 


Findings as in chlorosis. May be 
1,000,000 or less, though rarely. 


Shape. 


Poikilocytosis great, sau- 
sage-shape, etc. 


Somewhat deformed. 




Size. 


Average increased, some 
dark. 


Diminished, light col- 
ored. 


Various, not increased. 


Hemoglobin. 


Increased per corpuscle. 


Reduced per cor- 
puscle. 




Staining. 


Polychromatophile cells. 






Nuclei. 


Micro-, megalo-. normo- 
blasts. Megaloblasts 
constitute majority of 
nucleated red blood cells. 


Megaloblasts rare. 
Normoblasts more 
than megaloblasts. 


Normoblasts far more than mega- 
loblasts in malignant diseases. 
Normoblasts common (more than 
in chlorosis). 


Rouleaux. 


Not present, or decreased. 






Color Index. 


High color index (not in 
chronic or mild cases) . 


Index less than 1; 
lower than in sec- 
ondary anemias. 


Relatively low (this rule does not 
hold positively). 


Leukocytes. 


White blood cells decreased, 
except in blood crises, 
hemorrhage, etc. 


Usually normal. 


Polymorphonuclear leukocytosis 
in malignant disease; when red 
blood cells are low, e. g., 
1,000,000, speaks for second- 
ary anemia. 


Lymphocytes. 


Lymphocytosis (relative) . 


Lymphocytosis. 


Rarely increased (no decrease). 


Myelocytes. 


Small number only. 


Rare; less than in 
pernicious anemia. 


Myelocytes very rare. 


Adult 

Leukocytes. 


Usually decreased. 


Decreased. 


Usually increased. 


Coagulation. 


Slow. 


Rapid. 


Often rapid. 



Treatment. — 1. Hygienic. — The patient should have absolute rest in 
bed, if possible in a warm climate. A full, nitrogenous diet increases 
tissue waste and produces diarrhea. Patients display a distaste to 
nitrogenous foods. A vegetable diet is better tolerated, with bread, 
zwieback, beef-tea, peptones, milk, honey or porridge. Nutrient enemata 
are indicated in the gastric crises. In pregnant women labor should not 
be induced. 

2. Hematinic. — (a) Transfusion of human blood is seldom beneficial. 

(b) Lepine recommends the physiological salt solution, based on Marag- 
liano's findings that the serum in pernicious anemia has a globulicidal 
action on the red blood cells (the blood of a patient clears in a test-tube 
on standing). (Following Talquist's experiments, Vetlesen employed 
glycerin with success to neutralize the hemolytic oleic acid in the blood.) 

(c) Phosphorus is without value and iron is often injurious, (d) Arsenic, 
recommended by Bramwell, is said to have cured the disease, and is 
the best remedy known, probably acting upon the blood-forming centres. 

Physiological Action of Arsenic. — (a) The smallest dose increases the 
appetite. (6) Small doses stimulate the appetite by gastric irritation, 
increasing secretion and stimulating peristalsis; tissue waste is lessened. 
It is an alterative, increases the muscular strength and endurance, 
improves the quality of the blood, the complexion, sexual powers and 
lung capacity, (c) Continuous administration produces constitutional 
effects, as puffiness of the eyes, first seen in the morning (Wier Mitchell) ; 



678 DISEASES OF THE BLOOD 

this may be followed by general edema, due to vascular and sometimes 
renal alteration, (d) Large doses result in nausea, diarrhea, abdominal 
colic, sympathetic headache, and neuritis. Arsenic is absorbed by the 
bloodvessels. The circulation, respiration and digestion are stimulated 
by small and depressed by large doses, although some deny the stimulant 
action of any dose. Elimination is very rapid and mostly by the kidneys 
and intestinal mucosa, but also by the skin, bile, lungs, saliva and mother's 
milk. 

Administration. — Children tolerate large doses, while the aged stand 
the drug poorly and their digestion suffers; after the fifth year adult 
doses are given; girls tolerate the drug better than boys. When sus- 
ceptibility is marked a few drops of laudanum may be added, but its 
administration should always be stopped when the eyes become puffy or 
itch, the tongue becomes furred or colic develops. It may be given in 
the following forms: (i) Arseni trioxidum, gr. -^ p. c, with ext. glycyr- 
rhizse and piper (black pepper) aa gr. iv (" Asiatic pill"). (See formula on 
page 377.) (ii) Liquor potassii arsenitis (Fowler's solution, 1786); for 
hypodermic use it must be sterilized, because fungi are likely to grow 
in it. Even with great care abscess may develop. Minims v equal gr 3^ 
of arseni trioxidum. Treatment should commence with TTLiij and each 
day the dose should be increased a drop until Tfl,xij are given; rarely 
can larger doses (Tfl,xv-xxv) be given, (hi) The cacodylate of soda pill 
(gr. J) may be given one to five times daily; it is seldom toxic. 

3. Symptomatic Treatment. — Opiates for diarrhea, cardiants for weak 
heart, dilute HC1 for gastric achylia, colonic flushings, salvarsan and 
splenectomy are recommended. 



SECONDARY ANEMIA. 

1. Acute Posthemorrhagic Anemia. — Etiology. — It may result (a) from 
trauma of large vessels: (b) from postpartum hemorrhage, abortion or 
tubal pregnancy; (c) from hemoptysis, aneurysm or cardiac disease; 
(d) from carcinomatous ulcerations in the uterus, gastro-intestinal tract, 
etc.; (e) from peptic ulcer; (/) from varicosities, as in the leg, stomach, 
esophagus and liver cirrhosis; (g) from blood conditions, hemorrhagic 
states or constitutional diseases. 

Symptoms. — 1. The blood is (a) hydremic, the loss of fluid being sup- 
plied by the tissues, and its specific gravity is lowered, (b) The red 
disks are reduced to 50 or even 20 per cent., are often irregular in contour, 
pale and poor in hemoglobin; generally there are some normoblasts. 
(c) The hemoglobin is lessened even more than the red cells, (d) The 
leukocytes show a moderate increase; the polymorphonuclears are 
decreased and the mononuclears increased. In anemia with rapidly 
resulting death the red cells are seldom nucleated and there is no 
leukocytosis, because the bone-marrow makes no effort to regenerate 
the blood. (See Plate XVIII, Fig. 3.) 

2. There is marked anemia of the skin and mucovs membranes. Some 
edema results from changes in the blood or increased permeability of the 



SECONDARY ANEMIA 679 

vessel walls. The vasomotor system accommodates itself to a loss of 
one-quarter of the blood volume; a greater loss produces cardiac weak- 
ness. Sometimes the heart action seems more violent and respiration 
deeper and more rapid than normal. 

3. Albuminuria is due to permeability of the renal vessels. 

4. Amblyopia and amaurosis, known to Hippocrates, are at first func- 
tional, but usually later degeneration of the retina develops; as the 
blood-pressure rises, retinal hemorrhages may follow. The patient 
sees spots before the eyes. Occasional nervous manifestations include 
aphasia or vertigo; delirium and hallucinations are chiefly terminal 
events; sometimes lasting psychoses develop. 

5. The autopsy findings are fatty degeneration, particularly of the 
heart, endothelium of the vessels, liver, brain, stomach and kidney cells, 
which is usually caused by imperfect oxygenation. Hemorrhages in 
the uterus, gums and retina are due to impaired nutrition of the vessel 
walls. The bone-marrow changes from a yellow to a red color and abounds 
in normoblasts. 

Prognosis. — The patient may survive the loss of one-half of the blood; 
Hayem reports recovery after the number of red cells fell to 550,000. 
Men stand hemorrhage better than women and young children; the loss 
of a pint may cause death in arteriosclerotics. Recovery is more rapid 
in acute than chronic hemorrhage; water and albumin are readily 
yielded to the blood by the tissues; the red cells regenerate more slowly 
and the hemoglobin is the last element to reach normal. Increase in 
the coagulability of the blood is a favorable prognostic. According to 
Bierfreund, a loss of 10 to 15 per cent, of the blood is restored in eight 
days; of 16 to 20 per cent., in twenty days; of 21 to 25 per cent., in 
twenty-two days and of more than 25 per cent., in thirty days. 

Treatment. — This has been considered under gastric ulcer and intestinal 
hemorrhage in typhoid, viz., absolute rest, morphine to insure quiet 
and salt infusions only in extreme cardiac failure. 

II. Chronic Secondary Anemia. — Etiology. — Its possible causes are 
numerous; the chief types are (a) hemorrhages like those listed under 
Acute Posthemorrhagic Anemia, but frequent and persistent, as chronic 
hemorrhoidal bleeding, (b) Poor hygiene; overwork, long hours in 
poorly ventilated, sunless offices or factories; insufficient food or food 
poor in iron, (c) Exhausting discharges or loss of albumin, as frequent 
pregnancies with prolonged lactation, albuminuria, respiratory or ali- 
mentary catarrh or protracted suppuration, (d) Acute infections, as 
typhoid, diphtheria or malaria, in which the activity of blood-making- 
centres is diminished and food is poorly assimilated; chronic infections, 
as syphilis and tuberculosis, (e) Gastro-intestinal and possibly other 
intoxications. (J) Neoplasms acting as mechanical obstructions (as those 
of the esophagus or pylorus), affecting sometimes the bone-marrow 
by metastases deposited there, sometimes causing repeated losses of 
blood or elaborating toxins, which break down the tissue albumins; in 
neoplasms the red cells and hemoglobin average 55 to 66 per cent, of 
normal, (g) Parasites (uncinaria, etc.); and (h) poisons (alcohol, lead, 
arsenic or phosphorus). 



680 DISEASES OF THE BLOOD 

Symptoms. — -The blood is pale and its specific gravity is lowered. The 
red disks and hemoglobin are reduced in rather close parallelism. The 
hemoglobin may fall even to 14 per cent, of normal and the red cells 
may, in rare instances, approach the count of pernicious anemia. The 
red cells stain unequally and their umbilication is clearer, so that the 
hemoglobin may appear only as a slight peripheral ring; many of them 
are undersized; they show less poikilocytosis and less of nucleated 
erythrocytes than in the acute posthemorrhagic form. The white cells 
vary with the causal conditions; the polymorphonuclear neutrophiles 
are increased and the eosinophiles decreased. The latter are often 
increased in parasitic anemias, up to 10 or even 50 per cent. In some 
chronic anemias the leukocytes are diminished. 

It may be doubtful whether the general symptoms result from the 
anemia or from its cause. An anemic skin, muscular adynamia, irritable 
weakness, edema and hemorrhage into the skin, mucosae and serosse may 
be noted. There may be anorexia, tenderness over the stomach, nausea 
and decrease or increase of the HO. The intestinal functions are normal. 
The aromatic sulphates are frequently increased. Exceptionally per- 
nicious symptoms may develop, as alteration of the bone-marrow, fatty 
heart, cerebrospinal degeneration, atrophy of the gastro-intestinal cells 
and retinal hemorrhage. For differentiation see page 677. 

Treatment. — The treatment depends upon the cause, for which thor- 
ough and repeated search should be made. The hygiene of the home 
and place of work should receive consideration. Fresh air, sunlight 
and proper food are often difficult to obtain for the lower classes. Iron 
and arsenic are valuable in simple types (v. pages 670 and 677). 

LEUKEMIA. 

Definition. — Leukemia (leukocythemia) is a disease of hemogenesis, 
characterized by an increase of the circulating leukocytes, hyperplasia 
of the leukoblastic tissues (bone-marrow, lymph glands and spleen) 
and by secondary infiltration into various tissues. It was discovered 
by Bennett and Virchow (1841). 

Classification. — The older classification embraced (a) the splenic, (6) 
glandular and (c) medullary form (and also a gastro-intestinal and a 
dermal variety). This classification is clinical, but that of Ehrlich is 
based on the blood findings: 

I. Lymphatic leukemia, (i) Acute lymphemia. (ii) Chronic lym- 
phemia. 

II. Myelogenic leukemia with great polymorphism in the blood. 

I. Acute Lymphatic Leukemia. — Acute lymphemia includes nearly all 
acute leukemias. This infrequent disease occurs at any age, but especially 
in children, and 66 per cent, in males. The bacteriological findings are 
inconstant. The lymph glands are not necessarily the cause; there is 
evidence that the bone-marrow may be the seat of the causal change 
and that it may contain a parent cell for both leukocyte and lymphocyte. 
The chief pathological finding is hyperplasia of the lymphadenoid tissue. 
The course is that of a rapid infective disease, usually with an acute onset, 



LEUKEMIA 681 

lymphemic blood findings, asthenia and often fever; it is fatal in a few 
days to a few weeks. 

Symptoms. — The prodromal symptoms may be headache, pain in the 
neck, spleen, joints or head, epistaxis, mental obscuration, dyspnea or 
stomatitis, after which four cardinal findings develop: 

1. Lymphadenoid Changes. — Lymph gland intumescence is very fre- 
quent and usually moderate. Reed published a case without glandular 
enlargement. Splenic enlargement occurs in 66 per cent, and is of slight 
degree; in children it may be enormous; tonsillar hypertrophy occurs 
in 50 per cent., sometimes with hemorrhage and necrosis. The bone- 
marrow is constantly involved, especially in the long bones; "the lymphoid 
marrow" is red and jelly-like, more rarely reddish-gray or hemorrhagic. 
The typical granular neutrophile myelocytes are few, while large and 
small lymphocytes abound as in the circulating blood. Opinions vary as 
to whether the lymphatic or the medullary lesions are the primary change. 

2. Hemorrhages. — Hemorrhages are most characteristic and fre- 
quent (in areas of lymphemic infiltration) , (a) in the skin, as petechia? or 
larger effusions, with necrosis or ulceration; (b) in the mouth, gums, 
palate and pharynx, as petechias, erosions or extensive necrosis; (c) in 
the retina in 100 per cent.; (d) in the viscera, brain, cerebral nerves, 
labyrinth and spleen; (e) mucous surfaces, the vagina, urinary passages 
and intestines; and (/) the serous membranes. 

3. Necrosis — Necrosis in the infiltrated foci of the mouth occurs 
in 70 per cent, and is per se highly suggestive of acute lymphemia. 

4. Lymphemia. — Lymphemia is the crucial finding. The lymphocytes 
may reach 918,000 to the cubic mm.; in general, the increase is less than 
in the splenomedullary form and averages 350,000. The polymorphonu- 
clears are decreased, the eosinophiles constitute about 1 per cent, of the 
white cells, a few myelocytes may be found, but the larger lymphocytes 
may constitute 90 or even 99 per cent, of the leukocytes. Very large 
primordial cells are found, from which the red and white cells are probably 
derived. The red cells vary between 1,000,000 and 3,000,000 and exhibit 
some nucleation. The hemoglobin falls below 50 per cent., or much 
lower in peracute cases. (See Plate XVIII, Fig. 1, Plate XVII, Fig. 2, 
and Plate XVIII, Fig. 6.) 

Other findings are pallor, frequent pulse, priapism, exophthalmos, 
swollen, infiltrated liver, increased flow of urine, with increased urea and 
uric acid (increased nuclein destruction) ; albuminuria and nephritis are 
sometimes observed. Lymphomatous masses may cause dyspnea. The 
fever is irregular, both in type and occurrence. Intercurrent sepsis reduces 
the splenic and lymphatic enlargements, the white cells decrease even to 
normal and sometimes an ordinary polymorphonuclear leukocytosis 
replaces the lymphemia. Lymphatic deposits occur in the mouth, 
stomach, intestines (simulating typhoid ulcers), muscles, liver, kidneys 
and thymus. In a personal case the teeth were hidden by the infiltrated 
gums. The patient emaciates. Fatty and degenerative changes in the 
viscera are observed. 

Diagnosis. — Though the splenic and lymphatic enlargements, stomati- 
tis, fever, ulceration and hemorrhages are most suggestive, the blood 



682 DISEASES OF THE BLOOD 

findings alone differentiate from typhoid, purpura, scurvy, trichinosis, 
diphtheria, septicemia, severe acute anemias, etc. 

II. Chronic Lymphatic Leukemia. — This type is rarer than acute 
lymphemia and runs a clinical course of years, with lymphadenoid 
hyperplasia and lymphemia. 

Etiology. — No constant bacteriological cause has been proved. 

Symptoms. — The symptoms begin insidiously and the disease may 
be first detected by (1) swelling of the lymph glands, usually in the neck, 
which may reach enormous dimensions. The axillary glands are more 
massive than the inguinal; glandular swelling, as a rule, extends from 
above downward. Sometimes the internal glands alone are swollen and 
in rare cases the lymphatics are not enlarged., The glands are discrete, 
without periadenitis, oval and softer than in pseudoleukemia. Some- 
times moderate pain is experienced and there may be compression of 
vital structures, as the vagus, trachea and portal vein. The glands 
grow until death, unless an intercurrent affection, as erysipelas, causes 
temporary shrinkage. 

2. Splenic hyperplasia and intumescence are practically constant, 
though not extreme. The spleen protrudes beyond the costal arch an 
inch or so; it is usually proportionate to the duration of the disease. 
Intercurrent sepsis, cholera, erysipelas, etc., may cause the splenic 
tumor, lymphemia and the lymph nodes to disappear temporarily, but 
these findings may persist in such infections. Diarrhea and arsenic 
may likewise effect splenic reduction. Perisplenic adhesions and thick- 
ening are common and the organ is hard, in cases of long standing. The 
tonsils are often swollen, in which hemorrhages, with or without necrosis, 
are frequent. 

3. The changes in the bone-marrow seldom cause pain. The essential 
character of the marrow alteration is undetermined. 

4. The blood reveals an absolute and a relative lymphemia. The red 
and white cells may have a ratio of 100 to 1, yet the small lymphocytes 
constitute 90 to 99 per cent, of all the white cells, whereas the larger forms 
occur in the acute lymphemia. Many of them are degenerated or swollen. 
The polymorphonuclears are reduced to 10 or even 1 per cent. Myelo- 
cytes are usually absent. The red cells average 4,000,000, and seldom fall 
lower than 2,000,000. The lymphocytosis may temporarily disappear 
during infection and in one instance this was permanent. (See Plate 
XVII, Fig. 1.) 

5. The skin may be the seat of papular eruptions, or lymphomata, 
sometimes of considerable size; they may precede the lymphemic 
blood findings. Edema occurs, while hemorrhages are rarer. Facial 
growths are observed similar to chloroma {v. i.) or to Mikulicz's 
disease. 

6. The heart is degenerated, as are the vessels, from which hemor- 
rhages may occur. Intraperitoneal hemorrhage from ruptured adrenals 
is reported. The nerve trunks may degenerate with bulbar, spinal and 
nerve-trunk symptoms. Retinitis leukemica or optic-nerve involvement 
may impair vision. The liver is swollen from degeneration and lymphatic 
infiltration. Dyspnea is most common, from anemia, mechanical com- 



LEUKEMIA 683 

pression of the air tubes, vessels or nerves or from leukemic changes in 
the follicles of the throat and air passages. Renal infiltration is frequent. 

Course. — The disease develops gradually and passes slowly into cachexia, 
though now and then extension in the glands is "explosive." Remissions 
of weeks or months are not uncommon. Intercurrent disease may be 
fatal, and mechanical stasis, suffocation and acute exacerbations of the 
disease itself may hasten the course. 

Diagnosis. — The diagnosis, suggested, perhaps by the skin lesions, 
lymphomata, splenic enlargement or hemorrhagic tendency, is positively 
made only by the blood examination. 

III. Myeloid Leukemia. — Myelemia or myelogenic leukemia is the 
most common form and occurs for the most part between the twentieth 
and fiftieth years; 67 per cent, of cases occur in males. The disease is 
frequent among the Polish Jews and the poorer classes. A history may 
be obtained of malaria, syphilis, typhoid, stomatitis, tonsillitis, digestive 
disturbance, pregnancy, the climacteric and trauma, though they are 
only accidental occurrences. The disease has been noted in three 
generations. Leukemia also occurs in animals. 

Symptoms. — 1. Blood. — The specific gravity is decreased from 1.055 
to 1.045-36; it is watery or sometimes chocolate-colored; it coagulates 
slowly. Large white clots (leukemia) are observed at autopsy and 
Virchow thought he had incised an abscess when he opened the left 
ventricle in his first autopsy. The white cells are enormously increased, 
even as much as 2.5 whites to 1 red cell. In the highest count the 
author has seen the whites and reds numbered 1,200,000 each. Ameboid 
movement is greatly decreased (Plate XVII). 

The characteristics of the white cells are: (a) The large mononuclear 
neutrophiles ("mark cells," myelocytes) amount to 30 to 50 per cent, of 
the leukocytes. They are also found (in small numbers) in pneumonia, 
uremia, chlorosis, skin diseases, syphilis and normal blood, (b) Mono- 
nuclear eosinophiles occur in other diseases, but in myeloid leukemia are 
absolutely increased and are necessary to the diagnosis, (c) The "mast 
cells" are constantly increased; they are polymorphonuclears with 
basophile granulations which do not show with the tri-acid stain. Often 
they are relatively increased from 0.28, the normal percentage, to 1 or 
indeed 18 per cent, (d) The polymorphonuclear neutrophiles and eosino- 
phils constitute 30 to 60 per cent, of the leukocytes, (e) The lymphocytes 
are increased. (/) Atypical leukocytes, dwarf forms and white cells 
containing mitoses, fat globules or red cells mav also be found. (See 
Plate XVIII, Fig. 2.) 

The red cells are decreased to 3,000,000 or 2,000,000 and toward the 
end may decrease to even 300,000. The reds may exhibit degeneration 
necrosis, polychromatism, ameboid movement, mitoses and nucleation 
(more frequently than in any other anemia, normoblasts being found 
regularlv). The color index is 1 or less than 1. (See Plate XVII, Fig. 1, 
and Plate XVIII, Fig. 7.) 

2. Splenic Enlargement. — This is usually the first symptom to 
attract attention and appears with the blood findings; spleniculi, if 
present, are enlarged. Instead of a weight of 5 to 7 ounces, 18 to 28 



684 DISEASES OF THE BLOOD 

pounds are reported; from the normal measurements, 3 to 5 inches, 
dimensions of 15 inches are frequently observed. The form of the organ 
is preserved, the notches are palpable and the edge plump, rounded and 
hard. It may extend into the pelvis, displacing other organs. The 
size varies during intermissions, from administration of arsenic and from 
diarrhea or hemorrhages. A systolic murmur or pulsation is sometimes 
detected. Crackling under the fingers and tenderness indicate soft 
adhesions (perisplenitis). Firm adhesions may develop and the capsule 
may thicken. Though at first soft, it later becomes very firm; the 
pulp and trabecular hypertrophy and new lymphoid deposits are clearly 
marked against the reddish pulp (myeloid metaplasia). The author has 
seen 3 cases of leukemic floating spleen, 2 of which had been operated 
on as uterine tumors. Rupture is a rare complication. 

3. Glands. — Enlargement occurs in 33 per cent. The glands are 
heteroplastic, due to new-formed myeloid tissue, "metastases" from the 
bone-marrow. Soft at first, they later become hard. Caseation and 
suppuration are most infrequent. As in the other types of leukemia, 
recurrent compression of the vagus, trachea, portal vein and bronchi and 
retrosternal dulness have been observed. 

4. Bones. — In the spongy and long bones (ribs, tibise, sternum and 
vertebrae) , the bone is mostly rarefied and there may be tender or yielding 
areas. The histological changes in the marrow are (a) the lymphoid 
(Neumann), in which the reddish marrow resembles currant jelly and 
consists of small lymphocytes; it is sometimes hemorrhagic; the normal 
fatty appearance disappears. (6) The pyoid, which is seen mostly in 
the myelogenic type; the marrow is not transparent, but gray, its cells 
are rich in protoplasm with one or many nuclei. In both forms nucleated 
red cells, eosinophile cells and large cells with neutrophile granules and 
large nuclei abound. 

5. Vascular System. — The heart is distended with white clots and 
the muscle is pale, fatty and displays nodules of leukemic infiltration 
and foci of hemorrhage. Cardiac dislocation from pressure by enlarged 
glands and spleen, anemic bruits, venous pulsation, bruit de diable, palpi- 
tation, systolic murmurs from pressure by the glands on the vessels 
and centripetal venous pulse are observed. The radial pulse is rapid. 
Dyspnea results from weak heart, vagus pressure, nodules in the lung, 
bronchitis, hydrothorax, pressure of the spleen on the heart and com- 
pression by the glands. 

6. Respiratory Tract. — Nodules are frequently seen in the larynx, 
trachea, thyroid and thymus, often with hemorrhage and sometimes 
with tracheal, bronchial or laryngeal stenosis. In the lungs lymphoid 
nodules may necrose and form cavities like those of caseous tuberculosis; 
small myeloid foci of leukocytes may resemble miliary tuberculosis. 
Bronchitis with many eosinophile cells in the sputum and pleural hemor- 
rhage or exudation are observed. 

7. Fever. — Fever occurs in the majority of cases. It is rarely high; 
it may resemble recurrent fever, typhoid, sepsis or malaria. 

8. Digestive Canal. — Stomatitis or pharyngitis with ulceration of 
the lymphoid deposits, dysphagia from glandular pressure on the 



LEUKEMIA 685 

esophagus, eructations and vomiting are occasional symptoms. Diarrhea 
is very common, with leucin and tyrosin in the stools. In the enteric 
type the bowel symptoms are conspicuous, the lymphadenoid structures 
in the ileum prominent and Friedreich once confused this form with 
typhoid on account of the ulceration, enlargement of the spleen and 
hemorrhage from the bowel. The abdominal lymph glands may be 
enlarged alone. The liver is much enlarged and may weigh 13 to 25 
pounds. Its surface is smooth, its consistence increased and its edges 
plump. Myeloid deposits occur in the liver and deform the rows of 
liver cells. The portal lymph nodes may be enlarged. Icterus is infre- 
quent and ascites is common from cachexia or leukemic peritonitis. The 
fluid contains many myelocytes. 

9. Kidneys. — Frequently there is myeloid infiltration and cloudy, fatty 
and amyloid. alteration. The urine is decreased, pale and strongly acid. 
The uric acid may amount to 20 or 105 grains. Normally uric acid is as 
1:50-80 of urea, but in leukemia it is 1:16. The xanthin bodies are 
increased. Albuminuria is usual only in the last stages. The amount 
of urea depends on the degree of cachexia. Priapism occurs from nervous 
lesions or thrombosis of the dorsal vein. Amenorrhea is frequent. 

10. Nervous Symptoms. — These complications include delirium, neu- 
ralgia, headache, vertigo or mania or rarely bulbar palsy, facial paralysis, 
apoplexy or symptoms like those of brain tumor. 

The Eye. — Lymphoid nodules may develop in the orbit, possibly 
with exophthalmos. The retinitis leukemica, purely a leukemic infiltra- 
tion, occurs in 33 per cent.; the retina is pale, its arteries small and 
veins large; the papilla is "washed" and yellow spots with red borders 
and hemorrhages appear (Plate VI, Fig. 9). 

The Ear. — Vertigo, deafness, tinnitus and an atactic gait may result 
from growths in the labyrinth; the author saw T within one year 3 cases 
of sudden deafness from hemorrhage. 

11. Skin. — There may be acne, pigmentation, edema, pruritus, 
lymphoderma perniciosa (diffuse or tumor-like infiltrations) or sweats. 

12. Hemorrhages. — Cabot found them in 80 per cent. Epistaxis is 
the most common and may be fatal. Stomach and bowel hemorrhages 
rank next and those from the respiratory and genito-urinary tracts, the 
skin, joints, muscles, or brain are rarer. The writer has seen three 
massive hemorrhages under the skin of the thorax. Death has followed 
the extraction of teeth in a leukemic subject. The writer saw Kolisko 
autopsy a slow ascending paralysis following hemorrhage between the 
spinal pia mater and arachnoid. 

Complications. — Complications are nephritis, pneumonia, endocarditis, 
amyloid degeneration, diabetes and gangrene. Dock could collect but 
27 cases of complicating tuberculosis; the author saw a case in which 
tuberculous pleurisy developed; tubercle bacilli were recovered from the 
blood-stained fluid. 

Diagnosis.— Formerly the difference between leukemia and leukocytosis 
was made one of degree only and various limits were placed, beyond 
which leukocytosis w T as said to cease and leukemia begin. The mere 
number of white cells is no criterion, because a ratio of 1 to 20 may be 



686 DISEASES OF THE BLOOD 

leukocytosis (as in gastric cancer), and on the other hand, 1 to 200 may 
be leukemia. Leukocytosis from digestion, fasting, marasmus, pregnancy, 
acute infections or in the death agony is of the ordinary polymorphonu- 
clear neutrophilic type. (Plate XVIII, Fig. 4.) Leukocytosis is a symptom, 
but leukemia is a disease. The polymorphism of the blood is striking; 
there must be (a) mononuclear leukocytes with granulations (myelocytes) ; 
(b) increased mono- and polynuclear eosinophiles ; (c) absolute increase 
in the "mast cells," and (d) nucleated red cells. The gross splenic, med- 
ullary or lymphatic lesions are of presumptive value in diagnosis but the 
polymorphic blood picture alone differentiates from pseudoleukemia, 
typhoid, purpura, anemia, sepsis, etc. 

Caution should be exercised (a) during remission; in one of the author's 
cases the leukocyte count dropped from 1,250,000 to 9000 in a week, 
though the myelocytes still constituted 33 per cent, of the white cells. 
(b) The leukemic characteristics may disappear during typhoid, acute 
miliary tuberculosis, influenza or sepsis, (c) The blood findings may 
become atypical before death. 

Similar Conditions. — 1. Chloroma is considered a malignant type of 
leukemia or a "neoplastic hyperplasia of the red bone-marrow/' by 
Dock and Warthin; 80 cases are on record. Lymphomata form, causing 
orbital pain, tinnitus, deafness, temporal and orbital swellings and 
exophthalmos, strabismus, disturbed vision and retinal infiltration and 
hemorrhages. The lymphomata are greenish, whence the name chloroma. 
Other findings are ataxia, pallor, sternal tenderness, hemorrhages, 
greenish urine and greenish lymphomatous infiltration of the bone-mar- 
row, periosteum, liver, lungs and glands. The hemoglobin and red cells 
are reduced, even to 15 per cent, and 500,000 respectively. The leuko- 
cytes number about 50,000, even 500,000; they are chiefly lymphocytes. 
This form is called lymphoid, to differentiate from the rarer myeloid 
type, in which the leukocytes are myelocytes; Jacobaeus collected 10 
myeloid cases (1909). Chloroma is always fatal, usually within six 
months. 

2. Letjkanemia is a severe blood disease in which the myelogenous 
formation of both the red and white cells is disordered, i. e., it combines 
some features of both leukemia and pernicious anemia, e. g. (a) a pro- 
gressive anemia, waxy color and asthenia ; (b) numbers of normoblasts, but 
especially megaloblasts ; (c) no abnormal pigments in the urine, no adenop- 
athy and no siderosis of the tissues; (d) no true leukemic blood findings, 
but considerable myelocytosis and lymphocytosis; (e) firm connective 
tissue in the bone-marrow and (/) enlargement of the spleen and preverte- 
bral hemolymph glands. 

3. Secondary Cancer in Bone. — There are instances in the literature 
in which cancerous bone metastases have produced blood findings rather 
like those of pernicious anemia and increase of the leukocytes (of which 
the myelocytes constituted 4 to 17 per cent.). 

Prognosis. — Leukemia may last five or even ten years, but a little over 
one year is the average course. The beginning is insidious and enlarge- 
ment of the abdomen, dyspnea, anemia and adenopathy are the cause for 
seeking medical treatment. Sudden death may occur from hemorrhage 



PSEUDOLEUKEMIA (587 

of the brain, hematemesis, marasmus, anasarca, diarrhea, pleuritis, 
peritonitis, deep coma or pneumonia. Remissions occur, but the blood 
findings persist. Twelve acute cases were collected by Gordinier (1904); 
they resemble an infection with hemorrhages, moderate splenic and 
lymphatic hyerplasia, severe anemia, necrosis of the throat and jaw and 
low fever. A permanent cure after erysipelas was reported by Richter. 
Treatment. — Fats and carbohydrates cause dyspepsia, whence we give 
eggs, milk, raw, chopped meat, koumyss, oysters, zwieback, spinach, etc. ; 
an ice-bag to the spleen may mitigate pain. Benzol causes an initial rise 
in the leukocytes, especially after small doses but a decrease after two or 
three weeks, e. g., from 988,000 to 1720; an aplasia of the bone-marrow, 
spleen and lymph glands ensues. Given with olive oil, aa TUvij, the dose is 
pushed toTfl,xv (5j daily); larger doses produce burning in the stomach, 
eructations, bronchitis, vertigo or necroses in the liver and kidneys. 
Acute exacerbations may follow its exhibition. The drug is discontinued 
when the white cells reach 20,000. Splenectomy is irrational, for leu- 
kemia is a primary disease of the bone-marrow; 94 per cent, of Bissel- 
Hagen's group of 35 died, chiefly from hemorrhage. Caution must be 
observed in using purges, which, as in Addison's disease, may cause sud- 
den collapse and death. Inhalations of oxygen, blood infusions, spleno- 
or organotherapy and iron are inferior to arsenic, which decreases the 
number of white blood cells and the size of the spleen, and inhibits 
hemorrhage. In tapping an ascites, peritonitis is prone to develop. The 
x-rays may prove beneficial; in 1 case already alluded to, the patient 
lived nineteen months after the day he seemed to be dying. The .T-rays 
produce a leukolytic substance. Wendell thinks 90 per cent, are benefited. 
The exposure to the .T-rays should average fifteen minutes daily, carefully 
avoiding any toxic reaction. In some cases the glandular and splenic 
enlargements and the blood findings wholly disappear. 

PSEUDOLEUKEMIA. 

Definition. — A disease resulting in chronic anemia or cachexia, with 
enlargement of the spleen or lymph structures. The definition of the dis- 
ease as "leukemic appearance without leukemic blood findings" no longer 
holds, as it would include glandular tuberculosis, lymphosarcomatosis, 
etc. It is also called Hodgkin's (1832) disease, pseudoleukemia (Cohn- 
heim), adenia (Trousseau), malignant lymphoma (Billroth) and anemia 
lienalis or lymphatica (Wilkes) . 

Etiology. — The etiology is obscure. Like chloroma and leukemia, 75 
per cent, of cases occur in males between twenty and thirty years of age. 
The disease often occurs in the lower animals. Local lymphatic disturb- 
ances in the neck (following otorrhea, coryza or tonsillitis), malaria, 
syphilis, scrofulosis, alcoholism, rhachitis, typhoid, measles and scarla- 
tina are often noted in the patient's history, but their relation, if any, is 
obscure. Bunting and Yates cultivated a pleomorphic diphtheroid 
organism. The disease has no established relation to leukemia, yet tran- 
sitions from pseudoleukemia to leukemia have been observed. Neumann 
held that the leukemic blood changes depended solely on the hyperplastic 



688 DISEASES OF THE BLOOD 

marrow changes and that as long as the hyperplasia involves only the 
spleen and glands pseudoleukemia results. Sternberg's contention that 
it is tuberculosis, is disproved. 

Symptoms. — Its types are (a) lymphatic, (b) lienal, pseudoleukemia 
splenica, splenomegalia, (c) mixed and (d) myelogenic. 

1. Lymph Glands. — Swelling of the lymph glands is generally the 
earliest symptom; the cervical glands enlarge first, then the axillary, 
later the subpectoral, inguinal and other groups. They are soft and 
elastic; at first the glands are oval, discrete and smooth; later with 
increasing size, they fuse into harder, irregular masses as large as the fist 
or a child's head, particularly those in the neck. They may be painful 
from periadenitis, but never transcend the gland Capsule and seldom 
caseate or suppurate. From the neck, where the jugular veins may be 
compressed, the glandular enlargement often passes to the mediastinal 
glands, which are more often enlarged than the other internal nodes; 
this often occasions dyspnea, compression of the superior cava (whence 
the development of a large collateral circulation on the chest wall), 
dysphagia, bronchi compression and recurrent laryngeal or vagus par- 
alysis. The veins of the arm may be compressed, causing edema. In 
the abdomen the retroperitoneal, mesenteric, periportal, iliac and other 
groups may enlarge greatly; according to their location, abdominal pain, 
edema of the legs, paraplegia, hydronephrosis, ascites and jaundice may 
ensue. Histologically, the.lymphadenoid changes are (a) increase in the 
endothelial and reticular cells; (6) hyperplasia of the lymphoid cells; 
(c) formation of peculiar giant cells; (d) fibrosis and chronic inflammation 
and (e) great increase of the eosinophile cells (Dorothy Reed). 

2. Spleen. — The spleen, enlarged in 75 per cent, of cases, reaches dimen- 
sions rarely attained in leukemia, but maintains its form, is hard and 
tender and presents the same histological appearance as in leukemia, 
viz., nodes of lymphoid cells in a fibrous reticulum. The greatest spleno- 
megaly is observed when the lymphatic glands are large and hard; soli- 
tary splenomegaly with relative increase in the lymphocytes, is classed 
as Hodgkin's disease by Pinkus. 

3. Bone-marrow. — The bone-marrow is- not frequently involved. A 
myelogenous pseudoleukemia has been recorded, but its status is 
doubtful. The eosinophiles abound in the bone-marrow. 

4. The Blood. — The hemoglobin is decreased and the color index is 
usually 1. There is moderate anemia, especially in advanced cases. 
Poikilocytes and microcytes often occur, megalocytes rarely and normo- 
blasts sometimes, but the eosinophiles are not increased. The blood 
plates are increased. There is a relative increase of lymphocytes but no 
total increase in the leukocytes. The polymorphonuclear neutrophiles 
are decreased. Leukocytosis generally occurs in the death agony or in a 
terminal infection. 

5. Other Organs. — (a) Lymphatic growths in the skin occur more 
frequently than in leukemia; the lymphoderma perniciosa of Kaposi 
may be considered pseudoleukemic in cases with an absolute lympho- 
cytosis. Erythema, purpura, furuncles, pemphigus, prurigo from 
irritation of the lymphatic deposits around the sweat glands and pig- 



PSE UDOLE UREMIA 689 

mentation have been observed; severe sweats are frequent, (b) Symp- 
toms of anemia occur, as vertigo, syncope, palpitation, dyspnea, edema, 
hemorrhage, dyspepsia and diarrhea, (c) Local pain over the liver or 
spleen indicates perihepatitis or perisplenitis. Swelling of the liver is 
due to lymphoid deposits. Severe muscular pain has suggested trichin- 
osis, (d) Gangrenous stomatitis or pharyngitis may occur in degener- 
ated lymph nodes in the mouth, tonsils, tongue and throat. Gastric 
and intestinal ulcerations and sometimes perforation are noted less 
frequently than in lymphosarcoma. Neusser noticed gastric crises like 
those of tabes, (e) Ross and Osier described lancinating pains in the feet 
and edema from involvement of the spine and cava by the lymph nodes. 
(/) Amyloidosis, bronchial catarrh and pulmonary phthisis have been 
noted, (g) The uric acid in the urine is not increased, (h) The lymphatic 
hyperplasia may also involve the tonsils, circumvallate glands, mammae, 
eyelids, thyroid, thymus, lungs, heart, pleura, brain, genitalia and 
pelvis. 

6. Fever. — Fever is common. Gowers and Murchison observed a 
chronic recurrent type, later described by Pel and Ebstein, but also 
observed in chronic malaria, lymphosarcoma, cancer and glandular and 
splenic tuberculosis. The urine may show the diazo reaction. When 
the disease involves the internal glands only, the fever may simulate 
typhoid. Fever is rather indicative of glandular tuberculosis or of inter- 
current (terminal) infections. 

Course. — The clinical course is long. The glandular swelling sometimes 
decreases with or without therapeutic measures. The extension from the 
cervical to other lymphatic glands is generally gradual, but may occur 
explosively, as in Trousseau's case. An acute form of Hodgkin's disease 
is not well established; many are sepsis, tuberculosis or acute sarcoma- 
tosis. Death most frequently results from chronic cachexia, but also 
from obstruction of the air passages, twisting of the pedicle of the spleen 
or from hemorrhages from the nose, uterus, stomach, intestines or larynx, 
which sometimes resemble purpura hemorrhagica. It is a question 
whether well-developed types ever recover. Pleural effusions, diarrhea, 
dysentery and vomiting from pressure of the splenic tumor are unfavor- 
able complications. 

Differentiation. — There are two criteria; (a) the lymphadenoid hyper- 
plasia and chronic inflammation observed when an excised node is 
examined histologically; and (6) an absolute lymphocytosis, with a 
practically normal number of white blood cells. 

1. Glandular Tuberculosis. — Hodgkin's disease may be confused 
with tuberculosis ; in pseudoleukemia the typical structure of the tubercle 
is lacking, but in tuberculous adenitis there may be an accumulation of 
large endothelioid cells between which lie tubercle bacilli, without casea- 
tion. Of late the reports of glandular tuberculosis simulating Hodgkin's 
disease have increased enormously. The author examined two supposed 
pseudoleukemias in which tubercle bacilli (without anatomical tubercles) 
were found in the spleen and lymph nodes. In the neck tuberculous 
adenitis is more often in the submaxillary than in the anterior and posterior 
glands, in the latter of which pseudoleukemia is more common. Tuber- 
44 



690 DISEASES OF THE BLOOD 

culosis is more frequently attended by secondary suppuration. Fever 
and glandular tenderness indicate tuberculosis and node-like swellings 
of the lymph vessels in the mouth are symptomatic of pseudoleukemia. 

2. Anemia Infantum Pseudoleukemia. — This disease was first 
fully described by von Jaksch; it is known in Italy as anemia splenica 
infettiva dei bambini; it is called " pseudopernicious anemia of children" 
by Ehrlich. It is a profound anemia in which the blood findings suggest 
pernicious anemia; there are normoblasts, megaloblasts, decrease of the 
red blood cells (1,500,000 to 3,000,000) and sometimes poikilocytes or 
polychromatophilia; the leukocytes rarely exceed 50,000. It occurs in 
infants from nine. to eighteen months of age; the convalescence is very 
slow or death may result. Its other symptoms are firm enlargement of the 
spleen, swelling of the liver and hemorrhages into the skin, nose, mouth 
stomach or intestines. The status of the disease is not yet determined. 
The diagnosis is especially difficult when it occurs in syphilitic children; 
syphilis, rickets and dyspepsia are common antecedents. 

3. Anemia Splenica. — It is doubtful whether it should be classed as 
an essential anemia, liver cirrhosis, chronic splenitis or as a splenic form 
of Hodgkin's disease, (a) The spleen is enlarged, its capsule thick, its 
stroma increased and the endothelium of the lymph sinuses sometimes 
proliferated (endothelioma). The cause is possibly toxic. (6) There 
is an anemia of the secondary type; the red cells average 3,500,000, the 
hemoglobin is even more reduced and the whites are decreased to 3000 
or 4000. (c) Hemorrhages, particularly from the stomach, occur in 
one-third to one-half the cases, (d) In many cases there is a terminal 
liver cirrhosis, with icterus and ascites (Band's disease), (e) Its course 
is very chronic. In some cases there are profound alterations of nutrition, 
stunted growth, clubbed fingers or pigmentation of the skin. In several 
cases Dock and Warthin found portal thrombophlebitis and hyperplasia 
of the hemolymph glands. Of Armstrong's cases 23 recovered and 9 
died. 

4. Lymphosarcomatosis. — According to Kundrat, lymphosarcoma is 
largely a local glandular involvement, especially of the cervical glands, 
leading to infiltration of the throat by contiguity; the disease may begin 
in the tonsils, air passages, portal glands, etc. Lymphosarcoma ulcerates 
and transgresses the gland capsule; this never occurs in leukemia or in 
pseudoleukemia; though the glands may compress neighboring structures 
they never actually invade them. Unless lymphosarcoma extends beyond 
the capsule of the glands it cannot be distinguished by physical examina- 
tion unless it lies in parts which can be easily inspected, as the mouth. 
The spleen may enlarge enormously. According to Pinkus, the leuko- 
cytes are increased in pseudoleukemia, while in lymphosarcoma they are 
decreased. 

5. Other Splenic Enlargements. — The most common are the spleen 
of cirrhosis, malarial spleen, chlorosis with enlarged spleen, chronic 
polycythemic cyanosis and rarer forms, as miliary tuberculosis of the 
spleen, actinomycosis, syphilis, etc. 

6. Multiple Myeloma. — This is characterized pathologically by 
lymphoid hyperplasia of the bone-marrow, in the ribs and body ends of 



ERYTHREMIA 691 

the long bones chiefly and more often in the proximal than distal bones; 
no mestastases occur. Clinically, it occurs in males over forty-five years 
and is characterized by severe, deep-seated pain in the body, chest, spine, 
neck and more rarely in the extremities. Prominences in the bones, 
spontaneous fractures, especially of the sternum and ribs, and kyphosis, 
from softening of the vertebrae, may result. The growths may pulsate 
or rupture externally. The x-rays may clearly define them. Severe 
anemia without leukocytosis; motor and sensory paralyses, which develop 
late and involve the opticus, hypogiossus, facialis, cord (paraplegia 
dolorosa) and sciatic nerve; fever and Bence- Jones's albumosuria are 
observed. To call this disease a myelogenic form of pseudoleukemia 
or myelogadenia there must, according to Pinkus, be a lymphocytosis. 

7. Other Affections. — Syphilitic lymphatic glands; Mikulicz's lym- 
phoma of the lachrymal and salivary glands and secondary carcinoma or 
sarcoma must be differentiated. Difficulties of diagnosis are met when 
the enlarged glands in internal parts produce topical symptoms, thus 
simulating hypertrophic cirrhosis, etc. 

Treatment. — 1. Local Applications. — These are useless, excepting the 
x-rays; two cases, seen by the author eleven years ago, wholly recovered. 
In some cases the rays have no influence on the spleen and glands and in 
others the cachexia increases, though there may be improvement in the 
local findings. Inunctions of green soap, once or twice daily, are some- 
times beneficial. 

2. Drugs. — Arsenic is most efficacious (v. page 677) ; it acts on the glands 
more than on the spleen. Some believe that the fever which it sometimes 
produces, reduces the adenopathy. Winnewarter and Billroth recom- 
mended its parenchymatous injection into the glands, but the results 
are not very encouraging. Iodides are injurious. 

3. Surgical Treatment. — Extirpation of the glands is seldom bene- 
ficial. The removal of the spleen is attended by constantly decreas- 
ing mortality; the average mortality in splenomegaly was 61 per cent, 
before 1891 and since then 13 per cent. Carstens, 1905, collected 739 
cases of splenectomy; 72 per cent, recovered. 



ERYTHREMIA. 

Vaquez's disease (1892) is a syndrome including polycythemia, spleno- 
megaly and cyanosis. Lucas collected 189 cases (1912). The etiology 
is obscure; lienal tuberculosis is reported in the earlier cases, but the cause 
is probably excessive erythroblastic activity of the bone-marrow, (a) The 
red cells are increased, even to 9,000,000 or 15,000,000 (polycythemia rubra 
or polyglobulism) ; the hemoglobin may exceed 200 per cent. ; the white 
cells number from 4000 to 31,000, with increased polymorphonuclears. 
The viscosity, specific gravity and volume of the blood (plethora) are 
increased, (b) There is chronic cyanosis, or intense redness of the face, 
in 75 per cent, and (c) splenomegaly. The retinae exhibit congestion, 
even choking. There may be vertigo, headache, dyspnea, enlarged 
liver, mental and physical weakness, albuminuria, constipation, vomiting, 



692 DISEASES OF THE BLOOD 

pigmentation and a hemorrhagic diathesis. The arterial tension is 
increased and the heart hypertrophies. 

The prognosis is unfavorable and therapy uncertain — arsenic, benzol, 
arrays, iodides, nitrites, phlebotomy and splenectomy. 

THE HEMORRHAGIC DISEASES. 

The hemorrhagic diseases may be classified as follows: 

(A) Acquired types. j 2 * g^vy? 

(B) Congenital (hereditary) type. 3. Hemophilia. 

Purpura. — Purpura includes a number of affections, more or less 
similar and differing chiefly in degree, some symptomatic, others inde- 
pendent. 

I. Symptomatic Purpura. — Purpura may be symptomatic of: (a) 
Various infections, as endocarditis, scarlatina, measles, smallpox, rheu- 
matism, sepsis, syphilis, etc. (b) Toxemias, as nephritis, cholemia, 
snake-bites and drug poisoning (copaiba, ergot, belladonna, quinine, 
mercury, iodides, bromides or arsenic), (c) Cachexia; old age, mal- 
nutrition, carcinoma, sarcoma, leukemia, pseudoleukemia or pernicious 
anemia, (d) Nervous states; tabes, neuroses (bloody stigmata of hysteria) 
or neuralgias, (e) Mechanical conditions, as trauma, embolism or stasis. 

II. Purpura Simplex. — In purpura simplex (Zeller, 1684) cutaneous 
hemorrhages are the chief symptoms. Its etiology is obscure. It develops 
most often in middle-aged males. As in the other forms, whose descrip- 
tion follows, there is no constant or characteristic pathology, though 
vessel thickening, hyaline and fatty degeneration, thrombosis, and 
pigmentation sometimes occur. In the blood itself no change is observed 
other than its tardy coagulation, in 10 to 30 minutes instead of 3 to 5, 
which is the normal time. The blood platelets are decreased. The 
eruption begins as small red spots, which gradually become green and 
black; they occur largely on the extensor surfaces of the limbs and more 
often on the legs than on the arms or trunk. They do not fade upon 
pressure. The initial eruption may be macular, papular or urticarial 
(purpura maculosa, papulosa or urticans), but soon becomes blood- 
tinged. Constitutional symptoms are usually absent; there may be 
slight fever, gastric disorder or diarrhea. The course, sometimes with 
relapses, is 1 to 2 weeks, the prognosis good and the treatment hygienic. 

III. Purpura (or Peliosis) Rheumatica. — Purpura rheumatica, described 
by Schonlein, is somewhat arbitrarily listed by itself because of its 
articular symptoms, although joint symptoms also occur in Werlhof's 
disease (v. i.), scurvy and hemophilia. Most cases develop in males 
between fifteen and thirty years of age. It has no relation to rheumatism, 
being a pseudorheumatism. Its pathology is obscure. 

Symptoms. — (a) As prodromes, indisposition, muscular pains, colic and, 
particularly, sore throat may be noted. (6) The purpura may occur as 
simple hemorrhages of the skin, which vary from red to greenish-black, 
according to their age, or as urticaria, erythema, pemphigus or edema, 



PURPURA 693 

which becomes stained with blood; the legs are most often involved, 
largely on the extensor surfaces, (c) Articular symptoms are most com- 
mon in the knees and ankles, less frequent in the elbows and rare in other 
joints; there may be only stiffness and pain, or actual swelling; if the 
joints are first involved their symptoms frequently abate with the appear- 
ance of the purpura, (d) Other symptoms are inconstant, as fever, which 
may rise to 102° or 103°, splenic tumor, albuminuria or nephritis. The 
author had 3 cases at one time in the Cook County Hospital, in which 
there was severe sloughing of the tonsils. Osier (1904) described 29 
cases in which visceral lesions occurred with purpuric, urticarious and 
erythematous symptoms, chiefly in children and often with relapses; 
(i) digestive complications occurred in 25 cases; vomiting in 15; colic 
in 8 (resembling renal stone or appendicitis); blood in the stools in 8 
and diarrhea in 15; (ii) acute nephritis occurred 14 times and 5 cases 
died of uremia; (iii) arthritis occurred in 17 cases; (iv) swelling of the 
fauces, edema of the larynx, aphasia, transient hemiplegia and least often 
endocarditis may occur. 

Diagnosis. — The diagnosis chiefly concerns affections characterized 
by hemorrhages of the skin, articular symptoms and fever. Acute 
leukemia, septicopyemia and endocarditis must be excluded. Genuine 
rheumatic polyarthritis is differentiated with ease by the earlier migrat- 
ing, inflammatory arthritis, the fever, sweating, characteristic cardiac 
complications and the later, accidental and wholly secondary purpura. 

Prognosis. — The prognosis is generally good, relapses are common, 
perhaps periodic and its course rarely exceeds two weeks. 

Treatment. — The joint symptoms yield somewhat to acetanilide, 
though the salicylates exert no specific influence. 

IV. Purpura Hemorrhagica. — Morbus maculosus Werlhofii (Werlhof, 
1775) closely resembles the above types, but differs in that not only 
are the skin and joints the seat of hemorrhage, but also the mucous 
membranes, serous membranes and perhaps the viscera. 

Etiology. — Of this little is known; staphylo-, strepto- and pneumo- 
cocci and Bacillus pyocvaneus and coli have been found. It occurs 
oftener in young, weakly women than in robust adults. Exposure ot 
cold or dampness and malnutrition seem predisposing causes. It usually 
develops as an apparently primary affection. 

Symptoms. — (a) Hemorrhages appear on the extremities; the face is 
not often involved; they occur as spontaneous petechia?, blood-stained 
bullae or vibices or may result from slight trauma, as by pinching the skin. 
(b) Of the mucous membranes the nose and mouth bleed most often; 
less frequently there is hemoptysis, hematemesis, enterorrhagia, hema- 
turia or metrorrhagia in various combinations, sequences and degrees. 
The conjunctivae may be blood-stained. The writer saw in one rapidly 
fatal case hemorrhage from the middle ear. (c) The joints, particularly 
the knees, ankles and elbows, are less often implicated. Ecchymoses 
in the endo- and pericardium, pleura, peritoneum and meninges are com- 
mon autopsy findings, (d) Hemorrhage into the retina, brain, cord or 
testis is far less common. The connective tissues, fasciae and bones are 
practically exempt. 



694 DISEASES OF THE BLOOD 

General Symptoms and Complications. As to the blood, there is delayed 
coagulation and moderate anemia; some nucleated red cells may be 
found, as well as leukocytosis, reduction in the blood plates and methe- 
moglobinemia. Fever is inconstant and atypical. The pulse-rate may 
be raised; palpitation, delirium, vertigo, albuminuria, hepatic enlarge- 
ment, splenic tumor, subicterus, intestinal ulceration or perforation 
and nephritis occasionally occur. 

Diagnosis. — Most mistakes result from confusion with purpura 
symptomatic of sepsis, hemorrhagic exanthemata or blood affections. 
The difficulties in diagnosis are often great; in an anemic old man, who 
suddenly vomited blood and passed bloody urine, the diagnosis of purpura 
was made; the autopsy revealed a round ulcer of the stomach and a papil- 
loma of the bladder. Scurvy is distinguished by its gingivitis and muscular 
hemorrhages, and hemophilia by reason of its hereditary facts. Henoch's 
purpura (1874) occurs chiefly in children and is characterized by (a) 
cutaneous lesions, which resemble erythema nodosum rather than purpura; 
(b) hemorrhages from the mucous membranes; (c) gastro-intestinal crises 
of vomiting, diarrhea and abdominal pain; (d) pains in the joints and 
(e) relapses, often extending over a number of years. Of chronic purpura, 
Bensaude and Rivet collected 34 cases (1905). 

Prognosis. — The prognosis is uncertain; 50 per cent. die. Unfavorable 
factors are high temperature, nephritis and cerebral hemorrhages. 
Recurrence is not uncommon. Purpura fulminans, of which C. A. 
Elliott (1909) collected 56 cases, may be fatal in 24 to 48 hours; it was 
described by Guelliot, 1884. 

Treatment.— Werlhof s therapy was dilute sulphuric acid, ITtx, and 
quinine, gr. v, after meals. Everything of a supportive nature, as suffi- 
cient nourishment, rest in bed, iron and arsenic, is helpful. The hemor- 
rhages are arrested with difficulty and the author doubts the value of 
drugs in their control. Adrenalin solution to the nose and mouth, 
gelatin by mouth, calcium lactate, gr. xv, t. i. d., to increase the 
coagulability of the blood and antitoxin or simple, fresh serum are 
indicated (v. Hemophilia). 

Hemorrhagic Diseases of the Newborn. — Syphilis Hemorrhagica Neo- 
natorum. — It appears soon after birth. In some instances the syphilitic 
child may be born with hemorrhages in the skin, mucosae, internal organs 
and from the navel. Occasionally deep jaundice develops. Mracek 
found a causative endartertitis, especially of the capillaries, in 14 per 
cent. In other cases an added sepsis apparently cooperates. 

Winckel's Disease. — Winckel's disease, epidemic hemoglobinuria, is 
(a) an affection of the newborn in the first four days of life; (b) it appears 
epidemically in hospitals; (c) it is characterized by fever, gastro-intestinal 
symptoms, icterus, dyspnea, cyanosis, albuminuria, methemoglobinuria 
and large mortality, and (d) pathologically by internal hemorrhages, 
fatty degeneration (Buhl's disease) and splenic tumor; it is doubtless 
a hemolytic sepsis. 

Morbus Maculosus Neonatorum. — It is no clearer etiologically than Werl- 
hof s disease in adults; some cases are congenital syphilis; others with 
fever, jaundice and epidemic occurrence are infections (pyogenic cocci, 



SCURVY 695 

pneumococci, pyocyaneus and colon bacilli) ; and still others seem embolic, 
thrombi forming in the auricles when the heart is weak. Injuries to the 
head, causing hemorrhages in the fourth ventricle and cerebral peduncles, 
and other vasomotor disturbances are questionable causes. It occurs 
•once in 500 to 1000 births. 

Symptoms. — In the first week of life hemorrhages occur from the 
navel and mucous membranes; in Townsend's 50 cases they occurred 
in the following frequency: from the bowel (melena), 40 per cent.; navel, 
36 per cent. ; mouth, 28 per cent. ; stomach, 28 per cent. ; and nose, 24 per 
cent. Death occurs within a week in 63 per cent. Dusser, in 78 cases, 
found the mortality was 55 per cent. 

Treatment. — Iron, ergot and adrenalin are useless. Diffuse stimu- 
lants should be given when there is a weak, rapid pulse. Injections of 
gelatin are dangerous, for it possibly contains some ptomaine; fresh 
serum or direct transfusion is most reliable. 

Scurvy. — Definition. — A general disease, characterized by gingivitis, 
hemorrhages, inflammations, cachexia and chronicity of course. 

Etiology. — It was first observed in the Crusades and was described 
most fully by Vasco de Gama; in his voyage around the Cape in 1498, 
33 per cent, of his sailors were stricken with scurvy. It has developed 
among prisoners, Canadian lumbermen, Pennsylvania miners and among 
workers on the Chicago Drainage Canal, where in 1893-95 the author 
saw 100 cases. Insufficient, possibly spoiled food causes the majority 
of cases, sometimes in conjunction with lack of fresh meat, impure water, 
damp quarters and overexertion; a lack of fresh meat, vegetables (potas- 
sium salts, malic and citric acids) and fats predispose to scorbutus, though 
no single group is solely responsible. The Drainage Canal cases were 
Poles who lived on coffee, bread and preserved and fresh meats. In 
1849 there were 260,444 cases in Russia and 60,598 deaths; it is still 
endemic there. 

Symptoms. — Scorbutus begins insidiously and progresses slowly; its 
earliest symptom is- (1) anemia (cachexia scorbutica). The skin is scaly, 
pale, lustreless and perhaps pigmented. The mucous membranes are 
livid. The blood coagulation is slow, the red cells and hemoglobin are 
proportionately reduced and leukocytosis is absent, except with inter- 
current inflammation or severe hemorrhage. Emaciation, mental depres- 
sion, muscular weakness, anorexia, hypochlorhydria, intestinal fermenta- 
tion, constipation, palpitation, weak and irregular heart action, a sys- 
tolic functional murmur and edema about the ankles accompany the 
anemia. Splenic enlargement, albuminuria, peptonuria and oliguria 
are common. 

2. Gingivitis begins with turgescence of the gums, which is due to a 
serohemorrhagic infiltration, noticed first about the canine teeth; the 
gums are spongy, painful, particularly on eating, bleed readily and may 
become so swollen as to hide the teeth. There is less gingivitis when there 
are no teeth or roots. The breath is fetid. In severe cases the gums 
necrose and bleed profusely; deep ulcers, on healing, leave cicatrices; 
the teeth may fall out and the salivary and cervical lymph glands and 
tongue may swell. 



096 DISEASES OF THE BLOOD 

3. Hemorrhages occur (a) in the skin, especially on the extensor surfaces 
of the legs and first about the hair follicles; they are at first small petechia?, 
but later enlarge and stretch the skin. Less frequently the first erup- 
tion may resemble acne, herpes or pemphigus, hemorrhages appearing 
later in these exanthems. The face is usually exempt. As the hemor- 
rhages increase, the legs are diffusely mottled with red, green and black 
and are swollen and tense. Similar stains may run upward in streaks 
along the lymph vessels. Some of these changes are due to (6) muscular 
hemorrhages (scorbutic sclerosis), mostly in the calf and thigh, less in 
the buttocks or abdominal wall. The legs are large, extremely hard, 
blood-stained and later pigmented. As the disease regresses the muscles 
usually recover their function, but in some instances scorbutic ulcers, 
suppuration, muscular cicatrization or shortening of the tendons leave 
permanent deformity and contractures, (c) Mucous membrane hemor- 
rhages are less common than in purpura or hemophilia, though epistaxis 
is fairly frequent. Sometimes hemorrhages occur in the conjunctiva, 
air passages, stomach, bowels, perhaps with intestinal ulceration, (d) 
Of serous membrane hemorrhages, articular hemorrhage (hemarthrosis) 
is the most frequent. Next in order of frequency are those in the pleura, 
pericardium, peritoneum and meninges. They are usually sudden in 
onset, extreme in degree and unfavorable in outcome, (e) Parenchy- 
matous hemorrhages are least common, as in the eye, brain and other 
viscera. Subperiosteal and epiphyseal hemorrhages are rare, except in 
Barlow's disease (v. i.). 

4. Scorbutics are subject to various inflammations, (a) Painful joint 
swellings are the most frequent (in 35 per cent, of the author's cases, 
chiefly in the knees); they may be serous or hemorrhagic or in severe 
cases the cartilages or bones may ulcerate or suppurate; deformity 
and ankylosis are possible sequences, (b) Hemorrhagic pericarditis and 
pleuritis are very dangerous, (c) Paronychia, choroiditis and pan- 
ophthalmitis are occasional incidents. Fever is uncommon. 

Course and Prognosis. — The onset -is insidious, the course chronic and 
convalescence protracted. Most cases recover but death may occur 
from (a) cachexia, the autopsy showing fatty degeneration of the heart, 
liver and bloodvessels; (b) profuse hemorrhages, into the pleura, peri- 
cardium, gastro-intestinal tract or rarely into the brain; (c) infections, 
as dysentery, pleurisy, pneumonia or septicopyemia of the terminal type, 
promoted by reduced physiological resistance. 

Diagnosis. — The diagnosis is made without difficulty by the cachexia, 
gingivitis, tendency to hemorrhage and inflammation, the chronic 
course, and the temporary nature of the condition (as contrasted with 
the permanent tendency to hemorrhage in hemophilia). 

Treatment. — (a) Hygienic; avoidance of cured or smoked foods is both 
prophylactic and curative. In Nansen's polar expedition, which lasted 
three years, not one case of scurvy developed; cooked meats, berries, 
sauerkraut, potatoes, radishes, cress, apples, oranges and lemons were 
used. A monotonous dietary is particularly to be avoided, (b) Anemia 
should be treated by strychnine, iron and arsenic. Yeast 3ij> three 
times daily, is recommended, (c) The gingivitis is treated by local appli- 



INFANTILE SCURVY 697 

cations of silver nitrate (10 per cent.), (d) Symptomatic treatment; hemor- 
rhage is benefited by rest and serum. Stimulation is required in inter- 
current infections. Drastic cathartics are to be avoided. Complicating 
arthritis necessitates rest and cold, rarely aspiration or drainage. 

Infantile Scurvy. — Barlow's Disease. — Moller (1852-62) described the 
affection as acute rhachitis, and Ingerslev, Jalland, Cheadle and Gee, 
but particularly Barlow (1883), described an infantile cachexia with 
hemorrhages. In 1898, 379 cases were collected in the United States. 

Etiology. — Unlike scurvy in adults, the hygienic conditions are good 
in 80 per cent, of cases, and it occurs largely in the better classes, (a) 
The obvious cause is feeding with malted, condensed or cooked milk or 
baby foods; these foods lack some unknown substance essential to health. 
In 713 cases only 2.5 per cent, occurred in infants at the breast (S. Weiss, 
1905). (b) Ninety per cent, of cases occur between the sixth and twelfth 
months (Heubner and Neumann). 

Symptoms. — There may be anemia without hemorrhages, hemorrhages 
without anemia, or typically both together. 

1. Subperiosteal hemorrhage is the leading symptom. The primary 
vague symmetrical swelling over the epiphyses later becomes more obvious, 
though no edema is noted. There is pain and tenderness usually in the 
thighs or legs, which are drawn up, flexed or everted and immobile 
(pseudoparalysis). The anatomical findings are subperiosteal hemor- 
rhages; a colloid and fibrillar alteration in the marrow of the diaphyses; 
arrest of ossification; decrease of the osteoblasts; rarefaction of the bones, 
sometimes leading to fractures (spontaneously or after slight trauma) 
or to epiphyseolysis (usually at either end of the femur or the upper end 
of the tibia) ; the joints are normal. Seventy per cent, of the lesions 
are in the thigh, 24 per cent, in the leg and 6 per cent, in the orbit; 
the arms, ribs, spine, skull, sternum and scapulae are seldom involved. 
Rib involvement results in depression of the sternum. 

2. The cachexia is evidenced by the moderate anemia (sometimes 
attended by slight lymphocytosis), asthenia, anorexia, constipation, 
irregular temperature (in 66 per cent.) and severe sweats. 

3. Gingivitis is noticed when the teeth have already erupted or are 
about to erupt; the gums are normal in but 4 per cent. 

4. Other symptoms embrace hemorrhages in the skin in 50 per cent., 
from the bowels (10 per cent.), nose (9 per cent.), kidneys (9 per cent.) 
and rarely in the conjunctiva?, muscles or meninges. 

Diagnosis. — The etiology, typical subperiosteal hemorrhages, gingi- 
vitis and anemia prevent confusion with genuine paralysis, for the 
immobility is voluntary to escape the pain of movement. Syphilitic 
bone disease (Parrot's disease) is similar as to the crepitus, epiphyseo- 
lysis and pain, but other syphilitic or scorbutic stigmata are decisive. 

Prognosis and Treatment. — Proper treatment secures immediate im- 
provement in the majority of cases. Death is uncommon and occurs in 
the third or fourth month of the disease. The diet consists of raw cow's 
milk, potato puree, beef -juice (not broth or extracts), orange-juice, 
apple sauce, pears, cooked berries and spinach. Treatment by drugs is 
superfluous. 



698 DISEASES OF THE BLOOD 

Hemophilia. — Definition. — A congenital and hereditary affection, char- 
acterized by deficient coagulability of the blood and profuse hemor- 
rhages, which are most difficult to arrest. It was named by Schonlein. 

Etiology. — (a) Heredity is the only clear etiological fact (Fordyce 
1784); as Grandidier (1877) remarked, hemophilia is "the most hereditary 
of all hereditary diseases." Brown traced hemophilia through seven 
generations in 200 years. Sometimes a generation may be exempt. 
(6) Broadly speaking, the males of the "bleeder families" are the "bleeders" 
and the females — the "conductors" — transmit the disease to their male 
offspring without manifesting the disease themselves. In 200 families 
of "bleeders," Grandidier found 609 cases in males (93 per cent.) and 
48 in females (7 per cent.). In the Mampel family, first reported by von 
Chelius in 1827, Lossen (1905) found 212 members, of which 111 were 
males; of these exactly one-third were bleeders and 48.7 per cent, died 
of hemorrhage; none of the females were bleeders and all transmission 
of the disease occurred through the women, (c) The disease occurs in 
Germany, England, France and North America. Consanguinity, family 
gout, rheumatism and tuberculosis are suggested as causes. Bleeders 
are generally healthy individuals with blond, delicate skins and blue 
eyes. The factors involved in clotting are calcium and activation of 
prothrombin in the presence of some unknown substance (thrombo- 
kinase). 

Symptoms. — In 75 per cent, of cases, hemorrhages develop in the first two 
years of life; rarely do they first appear after puberty, in the third decade 
or after the seventieth year; only 46 congenital cases are known. The 
hemorrhages are spontaneous or traumatic; they most often occur as 
capillary oozing from a mucous surface; deep interstitial bleeding is 
most unusual. They are copious and hard to still. Epistaxis is the 
most common (50 per cent.); hemorrhages from the gums (12 per cent.), 
intestine (12 per cent.), lungs, kidneys and stomach (each 6 per cent.) 
and uterus are next in frequency. Arthropathies are the rule. According 
to Konig, the joint findings are (a) an hemarthros, with pain, swelling 
and fluctuation; (b) then panarthritis, whose gross pathology resembles 
tuberculous arthritis, with flexion of the joint; (c) regression, or ankylosis 
and deformity, which rather resembles arthritis deformans. The knees 
and elbows are most often affected. Subcutaneous hemorrhages may 
occur. The first bleeding may occur from the navel or may result from 
vaccination, extraction of teeth, circumcision, from a trifling prick or 
cut, from delivery or from rupture of the hymen on the wedding night. 
In various attacks, one part after another may bleed or the hemophilic 
disposition may be confined to one part, as the kidney (renal hemophilia) 
or nose; in Agnew's celebrated case, the patient bled from cuts on the 
head but never from lesions lower. Hemophilia differs from purpura, 
in that bleeding seldom occurs into a serous membrane (excepting the 
joints) or into the viscera. The amount of blood lost may be enormous 
and in Litten's case amounted to 24 pounds in eleven days. Hemophilics 
tolerate loss of blood better than other individuals, and recover from it 
more readily. The coagulation time of the blood is delayed to sixty, 
even eighty-four minutes; the clot, when formed., is porous, but retracts 



HEMOPHILIA 699 

normally. The white cells are normal or slightly decreased, with relative 
lymphocytosis; the percentage of eosinophiles and mast cells is high. 

Diagnosis. — The diagnosis may be for a time uncertain, when hemor- 
rhage develops after an operation or occurs from one organ only, as the 
kidney. The family history clearly stamps the affection and readily 
differentiates it from scurvy, purpura and hemorrhages in the newborn. 
It is peculiar that patients often deny that they are bleeders. The 16 
cases of multiple hereditary telangiectases with recurring hemorrhages, 
described by Osier, may be hemophilic. 

Prognosis. — The prognosis is grave. Any hemorrhage may prove fatal. 
Sixty per cent, of cases die before the eighth year and only 11 per 
cent, reach the twenty-second year; if middle life is reached the danger 
gradually lessens. It is more favorable in girls, despite the apparent 
menstrual dangers. De Bovis (1905) found 69 excessive hemorrhages 
among 150 deliveries in hemophilic women; he believes pregnancy has 
a rather favorable effect on the disease. De Lee reported premature 
detachment of the placenta in hemoohilia. Frankel and Bohm found 
24 mortalities in 104 hemophilics with genital hemorrhages. The rudi- 
mentary or local forms are more favorable than general hemophilia. 

Treatment. — 1. Prophylaxis. — Grandidier lays down the following 
rules : (a) Women, with a hemophilic family tendency, whether bleeders 
or not, should not marry. (6) Men, if not bleeders themselves, may 
marry, unless their family history indicates that male bleeders have 
begotten hemophilic children. General measures to elevate the physio- 
logical resistance and avoidance of trauma or any but life-saving opera- 
tions, are indicated. Vaccination is rarely contra-indicated. 

2. Control of Actual Hemorrhage.— This is almost impossible. 
Wounds should be cauterized or enlarged, as Fordyce discovered that 
in hemophilics large bleed less than small wounds. Bruising the bleed- 
ing part and dusting with thyroid extract are helpful. The Esmarch 
constrictor controls some hemorrhages of the extremities. Styptics as 
MonselFs solution or tannic preparations are useless. Adrenalin, locally 
and internally, has no apparent effect. Calcium lactate is more bene- 
ficial; gr. xv, t. i. d., should be given intermittently, because protracted 
administration decreases the coagulability of the blood. Gelatin may 
be given by mouth. The work of Wirth and Weil indicates that normal 
serum or antitoxin is of much value. Human serum or the entire 
blood is excellent. Saline cathartics are sometimes efficacious, possibly 
by diverting blood from the seat of hemorrhage. Very acute anemia 
necessitates injection of salines or 5" per cent, grape-sugar solution intra- 
venously or under the skin; when the hemorrhage is over, regeneration 
of the blood is remarkably rapid. Joint involvement is treated by rest, 
immobilization and rarely aspiration. 



SECTION VII. 

DISEASES OF THE DUCTLESS GLANDS. 



Certain organs elaborate secretions, which are voided externally as 
it were, as the stomach, duodenum, liver, kidneys, pancreas, testes, 
ovaries, etc. Each of them also secretes substances which are absorbed 
into the blood, by which they reach other organs, as secretin (duodenum), 
products from the islands of Langerhans (pancreas), etc. — an internal 
secretion. Although all the cells or glands of the body probably produce 
some internal secretion, either in the katabolic process or as stimulant 
to the activity of other cells or organs, yet internal secretion, in its narrow 
acceptation, relates particularly to those ductless glands, whose sole 
secretion is internal, e.g., the thyroid, suprarenals, parathyroids, pituitary 
gland and perhaps still others, as the spleen, thymus or lymph nodes. 
The correlation of the ductless glands is effected by hormones, acting 
through the circulation. In various combinations, these internal secre- 
tions supplement or antagonize each other. The subject, aside from 
certain well-defined clinical syndromes, is still in its infancy. 



DISEASES OF THE SUPRARENAL GLANDS. 

ADDISON'S DISEASE. OTHER AFFECTIONS OF THE SUPRA- 
RENAL GLANDS. 

Definition. — A hypoepinephry characterized pathologically by lesions 
(usually tuberculous) in the adrenal glands or chromaffin system elsewhere, 
and clinically by muscular, vascular and mental adynamia, digestive 
disorders, and pigmentation of the skin. 

Etiology. — Suprarenal disease was first associated pathologically with 
melanoderma by Addison in 1855. By far the most common lesion is 
(a) chronic fibrocaseous tuberculosis of the adrenal glands; tubercles of 
the adrenal glands are usually bilateral, destroy most of their structure 
and frequently involve the semilunar ganglia and solar plexus by the 
attendant formation of connective tissue; there is a primary focus in 
the lungs in over 50 per cent., in the genito-urinary, alimentary or gland- 
ular system; in rare cases only is the adrenal tuberculosis primary. 
(6) Less common are tumors, atrophy, fibrous induration (usually tuber- 
culous), gumma, amyloid degeneration, acute inflammation, hemorrhage, 



702 DISEASES OF T)HE SUPRARENAL GLANDS 

embolism, echinococcus, adenoma or other very rare lesions. Addison's 
melasma suprarenale is a disease in which the chromaffin cells in the 
medulla of the adrenals or the sympathetic ganglia waste (Weisel). 
The adrenal cortex contains epithelial structures, and the medulla consists 
of non-medullated nerve fibers and large mononuclear cells; these latter 
chromaffin cells are also found in the sympathetic ganglia, along the 
aorta in Zuckerkandl's bodies, the carotid glands, and perhaps also in the 
coccygeal gland, etc. Epinephrin is the active glandular substance of the 
chromaffin system; it stimulates the skeletal muscles, controls pigmen- 
tation, maintains vascular tonus and stimulates the vasomotor centres, 
the vagus and respiration; when secreted in excess, as in hyper- 
nephroma, the blood tension may be much elevated (Frankel, Neusser, 
Kolisko) and this may induce cerebral hemorrhage. The cortex is con- 
cerned in sexual activity and hypertrophies in pregnancy ; it is hyper- 
plastic in sexual precocity (hirsutism ; virilism) and hypoplastic in infan- 
tilism. The glands elaborate an internal secretion necessary to life which 
renders less toxic substances produced by other tissues, e. g., the "fatigue 
stuffs" of muscle metabolism. 

In Lewin's statistics from 500 cases the adrenals were diseased in 88 
and sound in 12 per cent.; on the other hand, disease of the adrenals is 
attended by pigmentation of the skin in 72 per cent, and unattended 
by it in 28 per cent.; in adrenal tuberculosis without Addison's disease, 
there is no general disturbance of the chromaffin system and in Addison's 
disease with no adrenal tuberculosis, the chromaffin cells elsewhere are 
affected. 

Most cases occur between the fifteenth and fortieth years, 66 per cent, 
in males and 90 per cent, in the laboring classes. 

Symptoms.— 1. Adynamia. — Marked physical and mental adynamia 
is usually the initial symptom and persists till death. The insidious 
languor, weakness, apathy, lack of initiative and muscular relaxation 
contrast sharply with the healthy appearance of the patient in the early 
stages. These symptoms are toxemic, partly from hypoepinephry and 
partly from the tuberculous lesion. Obstinate early insomnia and head- 
ache and later attacks of vertigo, tinnitus, spots before the eyes and 
syncope are frequent. The intellectual functions are weakened, periodic 
irritability is frequent and the deep reflexes are somewhat reduced. 

2. Digestive Symptoms. — Digestive symptoms * generally appear 
next. The tongue is coated; there are a sense of abdominal fulness, 
eructations and sensitiveness over the abdomen. Paroxysmal pains 
in the epigastrium or back radiate widely, especially into the chest, 
like severe tabetic crises. Vomiting is the most distressing, ominous 
and intractable alimentary symptom; it may occur independently 
of eating. At first intermittent, it later hastens the fatal issue. Early 
constipation gives way to terminal diarrhea. 

3. Pigmentation. — Melanoderma, bronzed skin, melasma suprarenale 
develops after the adynamia and alimentary disturbance. It is found 
in the deep layers of the rete Malpighii, to which it is apparently 
brought from the blood by leukocytes. At first the skin has a dirty, 
yellowish-gray color and small areas appear which gradually fuse and then 



ADDISON'S DISEASE 703 

slowly become darker and more diffuse; extensive pigmentation may 
occur with focal areas of deeper discoloration. Pigmentation develops 
particularly (a) where it is normally deepest, as about the nipples, anus 
and genitalia; (b) where pressure or friction is greatest, as over folds 
of the skin, over the clavicles, spine, ischia, scapulae or waist (from belts 
or corsets); (c) where there is exposure to the sun, as in the face, neck 
or arms; (d) where accidental irritation occurs, as by blistering, eczema 
or parasitic affections. The soles, palms and nail-beds are seldom stained. 
Previous scars may be surrounded by a zone of discoloration. The skin 
is dry, yet sometimes bathed with profuse perspiration and may have a 
fish-like odor. Scattered spots of pigment may atrophy (vitiligo) and 
impart a strange appearance. Drawing a sharp object across the skin 
may elicit a "white line," which runs parallel with the cardiac weakness 
(Sargent). The mucous membrane of the lips, gums and palate shows pig- 
mentation later than the skin. The horizontal ink-like stains on the 
cheek where the teeth touch it are particularly diagnostic. The con- 
junctivas are pearly white, though frequently small aggregations of 
pigment can be seen on careful examination. Staining of the larynx, 
nymphse, vagina, glans penis, serous membranes and internal organs is 
infrequent. 

4. Other Findings: (a) The heart shares in the general adynamia; its 
tones and apex are weak; it frequently shows brown atrophy at autopsy. 
Pain over the heart is reflected from the abdomen; palpitation and 
dyspnea are common, but functional murmurs are rare. The pulse 
is compressible and somewhat accelerated. The blood-pressure is 
generally low. The peripheral vessels and abdominal aorta pulsate 
actively. Atheroma is common, even in young subjects, (b) Anemia was 
considered characteristic by Addison, though Nothnagel demonstrated 
its infrequency; in one instance the writer observed a red-cell count of 
2,000,000. Increase in the red cells (polycythemia rubra) and in the 
hemoglobin results from concentration of the blood, due to vomiting 
and diarrhea. Lymphocytosis is ominous, (c) The lymph nodes, Peyer's 
patches, spleen, thyroid, thymus and pineal glands are often enlarged, 
probably vicariously, (d) Emaciation and cachexia are terminal conditions. 
Edema of the ankles is infrequent even toward the end. Characteristic 
metabolic changes are not found; acetonuria is occasional and terminal 
albuminuria may develop. The temperature is most often normal or 
subnormal and a subjective chilliness is experienced. 

Clinical Course. — The cardinal symptoms progress slowly, with occa- 
sional intermissions, and in nearly all cases death results within two 
years; the terminal symptoms are often violent, viz., delirium, convulsions, 
incoercible vomiting and diarrhea, small pupils, pseudomeningitic or 
peritonitic symptoms and finally collapse and coma. Variations include: 
(a) Acute cases resembling typhoid, or acute poisoning; (6) chronic cases 
lasting ten to thirteen years; (c) sudden death before pigmentation 
develops; (d) the course modified by pulmonary or intestinal tuberculosis. 

Diagnosis. — Diagnosis is based on the prostration, cardiac, psychical 
and physical; digestive disorders, vomiting, diarrhea and neuralgia; 
pigmentation; and the chronic lethal course. 



704 DISEASES OF THE SUPRARENAL GLANDS 

A tuberculin reaction may occur from tuberculosis in other tissues. 
Adrenal tumors may cause metastases in the brain or (like tumors of 
the thyroid, prostate and mammse) in the long bones, skull and spine. 
According to Griinbaum adrenal extract, gr. iij, t. i. d., for three days 
raises the blood-pressure 10 mm. if adrenal insufficiency exists. 

Differentiation. — Pigmentation also occurs in (a) poisoning by 
silver (argyria), in which the reduced metal forms a gray deposit in the 
extracellular tissue of the skin, sweat glands, conjunctivae and nail-beds; 
by arsenic, which seldom stains the mucosae; and in pellagra, which is 
exempt from mucous membrane pigmentation, (b) Chronic icterus, 
cyanosis (sometimes pigmenting the oral mucosa), various physiological 
pigmentations, dirt and parasites, as in tramps (vagabondism), (c) 
Abdominal diseases; dyspepsia, gastric ulcer, tumor (cancer, lymphomata 
and Hodgkin's disease), hypertrophic cirrhosis and hemochromatosis 
(hepatic and pancreatic cirrhosis, diabetes and skin pigmentation, 
diabete bronze), (d) Pelvic conditions; pregnancy, uterine and ovarian 
tumors (after the removal of which pigmentation may regress), (e) 
Phthisis, malaria, melanosarcoma of the skin, or exophthalmic goitre. 
In these conditions, pigmentation of the oral mucosa is rare. 

Treatment. — 1. Supporting. — Absolute rest is imperative because of 
exhaustion and proneness to lethal syncope. Alcoholic stimulation is 
poorly tolerated. Careful feeding is necessary because of the sensitive- 
ness of the stomach and bowels. 

2. Symptomatic. — Narcotics for pain, gastric sedatives for vomiting 
(v. Gastritis), opiates for diarrhea (v. Enteritis) should be adminis- 
tered; strong cathartics are always contra-indicated; one case in the 
Cook County Hospital died suddenly after taking a dram of compound 
jalap powder. 

3. Organotherapy. — Of Adam's 105 cases treated by adrenal extract 
by mouth, one-third were benefited and one-sixth recovered. The med- 
ullary portion of the gland is best. It may increase the vascular and 
muscular vigor or even lessen pigmentation. Some advocate adrenalin 
chloride, 5j of 1 to 1000 hypodermically on alternate days. Some 
advanced cases are unfavorably affected. 

Other affections of the suprarenal glands are of slight clinical interest. 
(a) Developmentally the glands are sometimes absent or hypoplastic, 
chiefly with other defects, as encephalocele. (b) Hypertrophy in one 
gland may compensate for hypoplasia in the other. Supernumerary 
glands are not uncommon, (c) Atrophy is usual in advanced age. (d) 
Degenerations embrace the parenchymatous, fatty, hyaline and amyloid 
types, (e) Circulatory disorders are embolism, thrombosis and hemorrhage 
which latter may occur in trauma in the newborn, tumors, inflammation 
and the hemorrhagic diathesis. (/) Inflammation, acute and chronic, 
is uncommon, (g) Granulomata, chiefly syphilitic and tuberculous, are 
rarely primary, (h) Tumors, e. g., carcinoma and sarcoma, are chiefly 
of anatomical importance. In 23 operations on hypernephroma 
the mortality was 50 per cent., recurrence developed in 21 per cent, 
and 29 per cent, recovered, (i) Echinococcus is extremely infrequent. 



EMBOLISM AND ABSCESS 705 



DISEASES OF THE SPLEEN. 

Structurally and physiologically, the spleen resembles the lymph 
nodes, which vicariously hypertrophy after splenectomy. It is not proved 
indispensable to life nor productive of an internal secretion. During 
fetal and perhaps adult life it is concerned in erythrocytogenesis. In 
health it destroys old red blood cells and in certain diseases its hemolytic 
activity is pronounced. In immunization, phagocytosis and perhaps 
some chemical factors are conspicuous. 

ACUTE SPLENIC TUMOR. 

This occurs (a) in acute infections, due to the local action of micro- 
organisms and their toxins or to toxemic paralysis of the splanchnic 
nerve; it is most common in typhoid, malaria, recurrent fever and septic 
conditions; (6) in acute, usually portal stasis; and (c) in embolism (v. L). 
Symptoms are infrequent; pain usually indicates perisplenitis. On 
objective examination: (a) The spleen may sometimes be seen during 
deep inspiration. (6) Palpation alone is reliable; by the bimanual method 
and with the examiner sitting at the right side of the patient the edge 
of the spleen comes iu contact with the fingers and slips sharply down 
below them; splenic crenations are seldom palpable. A palpable spleen 
indicates enlargement or less often, downward dislocation by pleurisy, 
pneumothorax or thoracic tumor, (c) Percussion, valuable in outlining 
the upper splenic level, is unreliable in determining the lower border. 

CHRONIC SPLENIC TUMOR. 

Chronic enlargement is symptomatic of (a) chronic infections, as 
malaria, tuberculosis and syphilis, (b) continued portal stasis, (c) repeated 
embolism, (d) blood affections, as leukemia, pseudoleukemia or splenic 
anemia, and (e) amyloidosis, neoplasms, cysts, polycythemia, arthritis 
deformans, chronic acetanilide poisoning, etc. 

EMBOLISM AND ABSCESS. 

Embolism of the spleen ranks second in frequency to kidney em- 
bolism because of its wide arteries and slow current. It usually develops 
in the course of acute endocarditis or chronic valvular lesions and seldom 
follows local lesions, as splenic vein thrombosis. The symptoms vary 
as the embolus is simple or infective; sudden chill, fever, pain in the side, 
acute splenic tumor and perisplenitic friction may develop, which with a 
cause or embolic symptoms in other organs, justify a diagnosis of embolism. 
Frequently no distinctive symptoms occur. Treatment is symptomatic. 

Abscess from embolism, trauma or invasion by contiguity, occurred 

in 9 per cent, of 430 cases of pyemia (Paget). It is largest in non-embolic 

cases; embolic abscesses are small and multiple. Symptoms are: (a) 

those of the cause, which may mask the lesion; (6) of embolism; (c) 

45 



706 DISEASES OF THE SPLEEN 

of splenic tumor, perisplenitis, friction or pain; (d) of rupture into the 
pleura, kidney or peritoneum; (e) aspiration determines the diagnosis 
and treatment is surgical evacuation. 

PERISPLENITIS. 

This affection may be primary or secondary, simple or suppurative, 
an isolated lesion or part of a chronic peritonitis (see " Icing Liver," 
Chronic Perihepatitis). It usually accompanies the various splenic 
affections enumerated. Without local peritonitic friction, pain or 
tenderness its diagnosis is impossible. There is no therapy. 

AMYLOID SPLEEN. 

Its etiology is considered under Amyloid Liver and Kidney. Patho- 
logically, its two types are (a) the sago spleen, in which there are 
amyloid deposits in the vessels of the Malpighian tufts, and (6) the more 
important, diffuse amyloid infiltration, diagnosticated by (i) its etiology, 
(ii) large size, hardness, smoothness and thick edge, and (hi) coincident 
amyloidosis of the liver and kidneys. 

RUPTURE OF THE SPLEEN. 

Rupture may be traumatic or spontaneous; the latter variety has 
been observed in embolism, malaria, typhoid, leukemia and pregnancy. 
It is more common in tropical than temperate climates. Aspiration and 
even palpation have occasioned rupture. The treatment is surgical; 
104 splenectomies for rupture are reported, with 29 per cent, mortality 
(Hortz). 

MOVABLE OR FLOATING SPLEEN. 

Lien mobile is due (a) to the same factors observed in enteroptosis, 
with which it may be associated, and (b) enlargement and increased 
weight of the spleen. 

Symptoms. — Symptoms are often absent. Pain or a dragging sen- 
sation is frequent, which is either local or radiates to the thorax, left 
shoulder or legs, similar to that observed in neurotics or women with 
pelvic disease. There may be headache, psychical alteration, dyspepsia, 
menstrual anomalies and paresthesias. Objectively: (a) The most impor- 
tant sign is palpatory detection of the spleen in an abnormal location, most 
often in the left ilio-inguinal region but also below the left costal arch, 
near the navel, in a hernial sac, in the pelvis or above the pubes. Its 
hilum usually points upward. The form, notches and possibly the pulsat- 
ing vessels are those of the spleen. It is usually enlarged, from causal 
hypertrophy or later congestion; torsion of its pedicle may lead to 
atrophy, softening, gangrene or even liberation of the spleen as a free 
body. As a rule it can be replaced and its position changes with posture; 
perisplenitis, causing a friction-rub, may result in firm adhesions to the 
colon, bladder or uterus, thereby causing insuperable diagnostic difficulty; 



GOITRE 707 

in such cases the spleen ceases to "wander." (6) The spleen is absent 
from its normal location, the splenic area being replaced by tympany 
from the colon (which changes to dulness when water is introduced into 
the colon), (c) Pressure symptoms include intestinal, pyloric, vesical and 
rectal compression. 

Diagnosis. — The author knows of three laparotomies performed for 
supposed uterine or renal disease in which abundant adhesions rendered 
differentiation impossible. On the other hand, a hard, immovable 
suprapubic tumor was correctly diagnosticated as leukemic spleen by 
the adenopathy and blood findings. 

Treatment. — (a) Bandages are difficult to apply, though sometimes 
of benefit, (b) The spleen may be replaced by operation and well packed 
around with gauze; the resulting adhesions often retain the viscus. 
(c) Splenopexis (Rydygier) may be performed, the spleen being sewed 
in place or deposited in a peritoneal pocket, (d) Splenectomy may be 
performed as a last resort. 

PRIMARY SPLENOMEGALY. 

Reference has been made to Banti's disease and splenic anemia (pp. 571 
and 690), splenomegaly with acholuric jaundice (p. 590), pernicious 
anemia, hepatic cirrhosis, etc. 

Gaucher's splenomegaly (primary endothelioma), of which. 16 cases 
are reported, is characterized anatomically by peculiar large, round and 
multinucleated cells in the hemopoietic system (marrow, spleen, lymphad- 
enoid structures, liver). Its cause is disputed (malignancy, endogenous, 
splenic toxemia, etc.). Besides the splenic tumor, the clinical symptoms 
are a yellowish-brown discoloration of the skin, conjunctival thickening, 
persistent leukopenia, mild anemia, hemorrhagic tendencies, develop- 
ment early in life, chronic course and familial incidence. As in Banti's 
disease, splenectomy is indicated. 

Tumors and Cysts. — New growths are very infrequent. They are 
more often secondary than primary. They include carcinoma, sarcoma, 
enchondroma, fibroma and lymphangioma. They are rarely differen- 
tiated from splenic anemia and like affections. 

Echinococcus cysts (q. v.) are usually found with concomitant cysts in 
the liver. One dermoid cyst is reported (Andral, 1829). Only 38 non- 
parasitic cysts are found in the literature. 

Granulomata (see Tuberculosis and Syphilis). 



DISEASES OF THE THYROID GLAND. 

GOITRE. 

Definition. — Hypertrophy of the thyroid gland. Sporadic cases are 
common in Europe and America. Goitre occurs endemically in Switzer- 
land and Italy, from the drinking water. It is usually acquired and is 
seldom congenital. 



708 DISEASES OF THE THYROID GLAND 

There are three main forms: (a) The parenchymatous type, with for- 
mation of colloid material in the hyperplastic follicles; (b) the cystic; 
and (c) vascular type, with dilatation of the bloodvessels, which form 
borders closely on those physiological variations observed at puberty, 
in defloration, pregnancy, chlorosis and psychical trauma. 

Symptoms. — 1. The thyroid enlargement may be diffuse, as in the soft, 
symmetrical, vascular form, or partial or nodose, implicating but one 
lobe or the isthmus. In most cases there are only local findings. 

2. Compression symptoms are not common. The carotid artery and 
jugular vein are pushed to one side and the sternomastoids become 
thin. The tracheal lumen may be shaped like a sword scabbard; dyspnea, 
bronchiectasis and dilatation of the right ventricle follow stenosis of the 
air passages. Laryngeal paralysis occurs in over 10 per cent., and 
in 25 per cent, of cases in which there is tracheal stenosis. Goitres may 
grow in a retrosternal or retroclavicular direction (5 to 10 per cent.), 
compressing the vagus, sympathetic nerves and vena cava. A goitre 
may disappear into the chest with each inspiration (goitre en dedans), 
or become incarcerated there. 

3. An aberrant or accessory thyroid may occasionally form a tumor 
anywhere from the tongue to the aorta, from the spine to the anterior 
chest wall, in the retropharyngeal or retro-esophageal tissues (causing 
dysphagia or dysarthria), in the trachea, larynx, root of the tongue, 
pleura or mediastinum; it may compress an entire lung; 75 benign, 
16 malignant and 3 cystic and calcarious growths are recorded in 
retrosternal accessory thyroids; there are in the literature 14 intratracheal 
accessory thyroids. 

4. Sudden death may occur from pressure on the vagus or trachea, 
spasm or edema of the glottis, sudden hyperemia of the gland, hemor- 
rhage dissecting into the chest or status lymphaticus. 

Diagnosis. — Confusion is possible with tumors, as carcinoma, adenoma, 
echinococcus cysts (25 reported cases) and sarcoma (100 reports). 
In 83 per cent, of cases cancer develops from a preexisting goitre; early 
metastases are especially common and characteristic; only 10 per cent, 
recovered among 110 operations (Madelung). In 20 cases recorded, 
metastases throughout the body occurred from benign tumors of the thyroid 
(chondroma or myxoma). Thyroid inflammation (strumitis) is usually 
metastatic or traumatic, rarely primary; it may occur in sound or goitrous 
glands; it is most often due to the streptococcus but may be caused by 
the colon, typhoid, pneumonia or other organisms. 

Treatment. — In regions where goitre is prevalent the drinking water 
should be boiled. Medical treatment is of uncertain value. Iodine may 
be used by injection (Maunoir, 1825). Potassium iodide (Coindet, 
1820) is beneficial in some subacute cases, according to Brims, in 75 
per cent.; Kraus found it particularly beneficial in the vascular type, 
with moderate tachycardia and full arteries. The .r-rays and thyroid 
extract are occasionally beneficial. Surgical treatment is indicated in 
large or growing goitres; in Kocher's 5000 cases, 1 death occurred in 
each 600 operations. 



EXOPHTHALMIC GOITRE 709 



EXOPHTHALMIC GOITRE (HYPERTHYROIDISM). 

Definition. — A malady due to excessive activity of the thyroid gland 
and characterized by exophthalmos, enlarged thyroid, tachycardia and 
tremor. It was first described in England by Parry (1786) and Graves 
(1835) and later in Germany by Basedow (1840). 

Etiology. — 1. The cause is overactivity or perversion of thyroid secretion 
(Mobius) which contrasts sharply with myxedema: 

Exophthalmic Goitre. vs. Myxedema. 

(a) Hypertrophy of gland; excessive inter- Atrophy; deficient (hypothyrea) or absent 

nal secretion (hyperthyrea) . secretion (athyrea). 

(6) Increased nervous excitability. Dulness, apathy, cretinism.. 

(c) Vascular erythrism; flushed, moist, Skin dry, thick and cool, and pulse slow. 

warm skin; rapid pulse. 

(d) Increased diuresis and active metab- Decreased. 

olism. 

(e) Thyroid extract increases symptoms; Thyroid extract improves or cures. 

it may produce goitre, tachycardia, 

tremor, even exophthalmos. 
(/) Surgical (partial) excision relieves, and Some cases result from removal of thyroid. 

often cures. Transplantation of new gland improves 

or cures. 
(g) Exophthalmic goitre (glandular hypertrophy with hyperthyroidism) may occasionally 

become myxedema (hypothyroidism from glandular atrophy). 

2. Other etiological explanations are less plausible, as vasomotor neurosis 
or lesions in the corpus restiforme of the medulla. 

3. Exciting factors are: (a) Sex; 80-95 per cent, are women; fibroids, 
pregnancy and puberty are sometimes promoting factors, (b) Age; 
most cases occur between the twentieth and thirtieth years. Barrett 
(1904) could collect only 42 cases in persons under fifteen years, (c) 
Psychical trauma, as fear, and concussion, anemia, phthisis, neuro- 
pathic family tendencies, other neuroses or psychoses favor its develop- 
ment, (d) After thyroidectomy postoperative hyperthyroidism is not 
rare. 

Symptoms. — 1. Cardinal Symptoms. — (a) Tachycardia is the earliest 
symptom. The pulse ranges from 100 to 120 (140 or even 200); it 
varies from time to time. It is associated with other cardiovascular 
symptoms, as (i) increased cardiac action, manifested by a diffuse 
cardiac impulse, sharp tones sometimes heard at a distance of several 
feet and hypertrophy of the left ventricle eventuating in dilatation; 
(ii) a functional systolic murmur over the apex; (hi) palpitation, usually 
antedating tachycardia; (iv) vascular symptoms; a pulse weaker than 
the apex-beat; active arterial pulsation in the carotids and abdominal 
aorta; capillary pulsation in the fingers, forehead or even in the retina, 
palate, liver and spleen; even the peripheral veins may pulsate; and 
(v) irregular failing heart action occurs late and in severe cases. Hemor- 
rhages are not uncommon. 

(b) Exophthalmos, usually a later symptom than tachycardia, is present 
in 90 per cent, of cases and results from dilatation of the orbital vessels. 
The protrusion of the eyeballs and the staring, fixed expression are very 



710 DISEASES OF THE THYROID GLAND 

characteristic (exophthalmos may also occur in extreme myopia, tumors 
of the orbit, nephritis/ and sympathetic irritation). The condition is 
generally bilateral, though often unequal; the author saw unilateral 
exophthalmos with homolateral goitre. The eyelids are unable to cover 
the eye-ball entirely and a rim of the white sclera shows about the iris. 
The protrusion may even amount to dislocation of the bulb, perhaps 
with corneal ulceration and loss of the eye by panophthalmitis. The 
associated eye-symptoms are : (i) von Graefe's sign, the failure of the upper 
lid to follow the eye-ball when it is rolled downward, is present in at 
least 33 per cent, and is of considerable diagnostic value, though present 
also in Thomsen's disease, (ii) Stellwag's sign, which is rarely absent, is 
widening of the interpalpebral fissure (Dalrymple) with infrequent 
winking (Stellwag) ; it also occurs in mania and in old age. (iii) Mobiles' s 
sign is weakness of the internal recti, when the eyes converge; it 
occurs also in other conditions, as paretic dementia, (iv) Becker's 
sign consists of pulsation of the retinal vessels, (v) In Joffroy's sign 
the patient's forehead remains smooth (instead of becoming wrinkled) 
when he glances upward with the head bent somewhat downward. 
(vi) Gifford's sign is the difficulty in everting the upper lid ; (vii) Jellinek 
and Rosin describe edema and pigmentation of the upper lid. Kocher 
noted a spasm of the lid in eliciting v. Graefe's sign. Eye-muscle 
paralyses and retinal or pupillary changes are infrequent. 

(c) The goitre is rarely an initial symptom and usually develops later 
and remittently. It is present in 100 per cent, (i) It typically is vascular. 
Acute thyroidism may develop in thyroiditis, chronic cystic goitre or 
thyroid malignancy. The goitre is smaller than the ordinary bronchocele ; 
it is diffuse or oftener more developed on the right side (an accentuation 
of physiological proportions), shows a vascular, rough surface and is dry, 
gray and granular on section (instead of the normal amber-red color); 
microscopically the alveoli are not rounded, full of colloid matter or 
lined with cubical epithelium, but are extremely irregular in size and form, 
ramifying and encroached upon by epithelial proliferations and the epithe- 
lium becomes columnar; in extreme cases there is epithelial desquama- 
tion; the scanty colloid matter stains faintly and lymphoid tissue de- 
velops; in the later stages some fibrous tissue may develop, (ii) It is 
usually soft, elastic, variable in size, pulsating on inspection, thrilling 
on palpation and revealing on auscultation a loud, systolic bruit or a 
double murmur, which Guttmann considers pathognomonic. The goitre 
is retrosternal in 4 per cent. 

(d) Tremor is present to some degree in most cases and is conspicuous 
in 50 per cent. It is characteristically fine, regular and rapid, numbering 
8 or 9 vibrations to the second. It affects the wrist more than the fingers ; 
sometimes it affects the trunk. 

2. Accessory Symptoms. — {a) Nervous symptoms. Cerebral symp- 
toms are usual, as headache, impaired memory, insomnia, irritability 
or depression. Mania is sometimes observed in the fatal cases. " Giving 
way of the legs" and slight inspiratory increase in the chest measurement 
(Bryson's sign) are expressions of weakness of the muscles, whose strength 
is reduced to one-third or one-fifth of normal (Midler). The reflexes are 



EXOPHTHALMIC GOITRE 711 

often increased. Rheumatic pains may be noted. Vasomotor symptoms 
are common, as reddening of the face, subjective warmth, dry mouth, 
sweats of a peculiar, penetrating odor, or intermittent swelling of the 
joints, (b) Respiratory symptoms include dyspnea and dry cough, 
perhaps simulating phthisis, (c) Digestive symptoms: Severe nervous 
vomiting, abdominal crises and diarrhea may simulate organic disease; 
their persistence is ominous, (d) Cutaneous symptoms: Pigmentation 
may be extreme. Vasomotor edema, urticaria, itching and falling of 
the hair may also occur. A peculiar fulness above the clavicles may 
develop, sometimes with pain in the neck. The electrical resistance of 
the skin is decreased, perhaps to one-fifth of the normal; it is probably 
occasioned by profuse sweating and has no pathognomonic importance. 
(e) Constitutional symptoms: Emaciation and anemia are common, 
especially in blondes. Metabolism is increased, evidenced by the nitrog- 
enous excretion, increased diuresis and elevation of temperature; 
these symptoms may be intermittent. Thompson describes fever and 
symptoms resembling ulcerative endocarditis. Amenorrhea, albumin- 
uria, glycosuria, persistence of the thymus gland (in 80 per cent.) and 
the occasional hyperplasia of the spleen are difficult to explain. The 
lymphocytes and eosinophiles are increased, leukopenia is frequent and 
coagulation is slowed. 

Diagnosis. — The diagnosis is unequivocal when the cardinal symptoms 
are present, reinforced by the secondary symptoms. Atypical forms 
(formes frustes) may cause confusion. The affection is often incorrectly 
diagnosticated in young girls at puberty, in whom thyroid turgescence, 
moderate tachycardia and vascular excitability occur without particular 
significance. Incipient tuberculosis, carcinosis and neurasthenia may be 
simulated. 

Course and Prognosis. — (a) The onset is usually insidious and the 
course chronic and remittent. Chronic cases sometimes begin rather 
acutely. Acute cases are unusual but usually fatal; they occur chiefly 
in men ; Lloyd records a case which was fatal in three days. The author 
has seen 3 cases in which death occurred in two weeks. (b) Death 
occurs in 12 per cent, of cases, commonly due to cardiac failure, (c) The 
outlook is best in the less typical (rudimentary) forms, (d) Complete 
recovery is rare, though 20 to 50 per cent, of cases improve, (e) Unfavor- 
able prognostics are its occurrence in the very young and in men, 
emaciation, extreme tachycardia, persistent vomiting or diarrhea, fever, 
lymphatism and intercurrent myxedema. 

Treatment. — 1. Genekal. — Rest and a quiet life at a moderate ele- 
vation or at the sea-side are very beneficial. Travel, sojourn at resorts, 
gymnastics and excitement are injurious. A simple diet and interdiction 
of alcohol, coffee, tea and tobacco are essential. 

2. Drugs. — Drugs are disappointing; digitalis, strophanthus and spar- 
tein fail to slow the heart. Belladonna, in large physiological doses, is 
recommended by Gowers; the annoying palpitation and abdominal throb- 
bing are most relieved by it. Ergotin, quinine, salicylates, arsenic and 
strychnine are of uncertain value, but the latter seems rather more 
beneficial; iron is useful only in chlorotic girls but in men it aggravates 



712 DISEASES OF THE THYROID GLAND 

digestive and vasomotor disturbances. Constant application of an ice- 
bag to the heart relieves palpitation and somewhat slows the heart rate. 

3. Electricity. — Galvanization is recommended by Erb, who uses 
the anode over the cervical spine and the kathode over various periph- 
eral areas. X-rays are beneficial but render operation difficult by the 
adhesions produced. 

4. Organotherapy. — Thyroid extract and iodides aggravate the symp- 
toms. Thymus extract is uncertain. Adrenalin clysters may check 
diarrhea. Baumann demonstrated that the thyroid gland contained an 
iodine body which Ross proved was the main functional constituent 
of the organ. The active element neutralizes toxins (failing in which 
myxedema results), and if not itself neutralized, Basedow's disease 
results; to neutralize hyperthyroidism serum of thyroidectomized animals 
was suggested. 

5. Thyroidectomy. — In Kocher's 371 operations, only 3.5 per cent, 
died; 2 cases died in the last 153 operations; 83 per cent, were cured. 
Kocher considers (a) the blood-pressure, size of the heart and tachycardia ; 
(b) he hesitates to operate if there is great nervousness, intoxication 
or absence of lymphocytosis, and (c) if the gland is very large, pulsating 
or vascular. Sudden operative death has been ascribed to the narcosis, 
flooding of the blood with thyroid products or enlarged thymus (which 
Capelle found in four-fifths of 60 autopsies) . The mortality is much lower 
when Graves's disease develops from an old goitre (secondary form). The 
Mayos prefer local anesthesia. Kocher prefers trying the a>rays first 
and then ligating the thyroid arteries (after which tetany may occur) 
and later performing partial thyroidectomy; the danger of a "heart" 
death is avoided by early operation. The mortality of operation, for any 
indication, in an exophthalmic subject, is increased 15 per cent. 

MYXEDEMA. 

Definition. — A chronic disease, characterized by (a) loss of thyroid 
function (athyrea), (b) myxedema (an edematous change in the sub- 
cutaneous tissue), (c) cachexia or (d) cretinism (mental failure). It was 
described by Gull (1873), Ord (1877), Charcot, Bourneville and d'Olier. 

Etiology. — The thyroid may be aplastic, hypoplastic, cirrhotic from 
an infective sclerosing thyroiditis (syphilis, tuberculosis, rheumatism 
or erysipelas), hypertrophied (goitre) or removed by operation, but in all 
cases the thyroid function (internal secretion or antitoxic action) is 
suspended or lost. The symptoms vary as to cause and combination, 
whence (i) cretinism, (ii) adult myxedema and (iii) operative myxedema 
will be considered separately. 

CRETINISM. 

Cretinism may be congenital, in which instance life is not long pro- 
tracted ; it usually develops near the time of weaning (infantile form) ; it 
may develop between the fourth year and puberty (juvenile form). 
The endemic form occurs in regions where goitre is prevalent, in Switzer- 



MYXEDEMA OF ADULTS 713 

land, Italy, France, Great Britain, Spain and Sweden; when both 
parents are goitrous, the child is invariably a cretin, is myxedematous 
and may also have goitre. The sporadic form may develop from thyroid 
aplasia, sclerosing thyroiditis or from goitre. In 1905, 100 cases were 
collected in America (Howard). 

Symptoms. — In the last part of the first or in the second year of life, 
retardation of mental and physical development is apparent. The head 
is disproportionately large, the fontanelles persist, the forehead is nar- 
row and the base of the skull is shortened. The face is turgid, pale and 
imbecile, the lids are swollen, as are the nose, the protruding tongue and 
pouting lips. Dentition is retarded and caries is frequent. The skin 
loses its tone and is dry, and the hair is thin. The neck is short, which 
condition is accentuated by supraclavicular deposits of fat. The abdo- 
men is large and pendulous; umbilical hernia is very frequent. The 
body is dwarfed and the extremities are short, stumpy and weak or 
helpless. Metabolism is slow, the gaseous interchange being reduced 
to 60 to 50 per cent, of the normal. 

Diagnosis. — (a) The mental alteration is marked, though mild com- 
pared with the grimaces, grinding of the teeth and compulsory move- 
ments caused by gross lesions of the brain, (b) In hyperplasia of the bone 
cartilages (chondrodystrophia fwtalis) there are great enlargement of the 
head and joints, dwarfing of the body and shortness of the extremities 
(micromelia), but no essential mental change; court fools were probably 
of this type, (c) Infantilism (v. %.). 



MYXEDEMA OF ADULTS. 

Symptoms. — Myxedema spontaneum adultorum, or cachexie pachy- 
dermique (Charcot) is characterized by (1) thyroid atrophy, (2) myxedema 
(pachydermia), (3) intellectual and physical weakness and (4) certain 
accessory symptoms. It is most frequent in England and France, Most 
cases occur between thirty and fifty years of age. 

1. Thyroid Atrophy. — This is less a clinical than a histological con- 
dition, as evidenced by the lack of function sometimes observed in gross 
enlargement of the gland (one-seventh of the cases). Eighty-six per cent, 
occur in women and it is possibly related to the uterine functions or to 
the physiological congestive, thyroid enlargement observed in women. 
It may be hereditary or familial, perhaps associated with exophthalmic 
goitre. 

2. Myxedema. — Mucin fibrils and nuclei — like granulation tissue — 
have been found in the skin and subcutaneous tissues. These structures 
are inelastic, semigelatinous and semiedematous, but do not pit upon 
pressure; the skin is pale, waxy, dry, rough, firm and its electrical 
resistance is increased; the hair and teeth may fall out and the nails 
thicken and break. The loss of the outer half of the eyebrow is described 
by French writers. The facies is somnolent, coarse and swollen, and the 
features are individually changed, rather resembling those of a cretin; 
the cheeks are patchy red, pendulous and tremble like jelly and the 



714 DISEASES OF THE THYROID GLAND 

tongue is big. The supraclavicular tissue is enlarged in lumps and rolls, 
though this is also observed in healthy persons (Verneuil's pseudolipo- 
mata). S. Kuh observed a painful swelling over the clavicle alone, which 
rather resembled keloid. The hands and feet are infiltrated. The 
swellings may change rapidly. The oral- mucous membrane is dry and 
thick, sometimes also the pharynx, larynx and even the rectum. 

3. Mental Weakness. — Intellectual and physical weakness is appar- 
ent. Charcot compares the somnolence to hibernation. Headache is 
common. The patient is apathetic, irritable, weak in memory and slow 
in thought, speech and movement; sometimes delirium and mania pre- 
cede the ultimate dementia. The- gait is clumsy ("hippopotamus gait") 
and muscular fatigue follows moderate exertion. 

4. Other Symptoms. — The accessory symptoms are variable, as 
arteriosclerosis, palpitation; small, sluggish pupils, tremor, vertigo, 
nigkt terrors, sensitiveness to cold; indigestion and constipation; anemia, 
leukopenia, lymphocytosis and rapid coagulation; amenorrhea; scanty 
urine with little urea and low specific gravity, sometimes albuminuria 
and less often glycosuria; hemorrhages, especially from the uterus; 
and subnormal temperature. The thymus is usually enlarged, sometimes 
the hypophysis and adrenals. 

Course. — The course is chronically progressive and covers ten to twenty 
years. Remissions may occur in warm weather, by a change to a milder 
climate or during pregnancy. In the last stage, the myxedema often dis- 
appears. Transient cases of acute myxedema have been observed. Osier 
reported an acute case with melena, mania, glycosuria, tachycardia and 
death in six months. Sudden death is occasional, but most patients die 
of intercurrent tuberculosis or acute infections. 



CACHEXIA THYREOPRIVA OR OPERATIVE MYXEDEMA. 

Horsley reported myxedema, apathy and coma in monkeys after 
complete thyroidectomy; when kept warm the monkeys did not mani- 
fest myxedema, but a species of cretinism. Cachexia follows extirpation 
in man and herbivora; convulsions develop in carnivora, since the 
antitoxic elements of the thyroid are not present to neutralize the nuclein 
of ingested meat. The toxemia strumipriva is accompanied by anemia, 
leukocytosis and degeneration in the bloodvessels. Kocher and Reverdin 
observed cachexia strumipriva in 70 per cent, of cases, more often after 
the complete than after the partial operation, and von Eiselsberg reported 
it in about 23 per cent, of complete excisions. Accessory thyroids (v. 
Goitre) may avert this operative complication. The author knows of 
two instances in which removal of an accessory lingual thyroid (under 
a mistaken diagnosis) caused myxedema. Schiff, von Eiselsberg, and 
Bircher cured operative myxedema by transplantation of a thyroid. 
Unfortunately, the function of the transplanted gland is seldom main- 
tained. 

Treatment of Myxedema, Cretinism and Cachexia Thyreopriva. — 
For these allied conditions we possess in thyroid extract (Glanduke 



TETANY 715 

thyroidese siccse) one of the few actual specifics of medicine; and most 
cases can be cured — in a sense we seldom employ this term. Murray 
first used thyroid extract hypodermically and his first case is alive, 
after twenty-five years; the equally successful administration by mouth 
was advocated by Horwitz, Mackenzie and E. L. Fox. The powdered 
extract should be prepared from the glands of young sheep, for the thy- 
roid atrophies in older animals. Beginning with gr. ij, t. i. d., the dose 
may be increased to gr. v. In a short time the evidences of increased 
metabolism appear, as loss of weight, increased diuresis, increased urea 
and elevation of bodily temperature; normal growth is stimulated, 
myxedema and cretinism disappear, the pulse becomes full and lively, 
the skin moistens and regains its lustre and in every regard the results 
are magical. In some instances toxic effects (hyperthyroidism) are 
apparent, as tachycardia, nervousness, delirium, dyspnea, palpitation, 
flushing, sweating, tremor, less often tonic spasms, severe pains and 
rarely exophthalmos, softening of the bones, or even death; these symp- 
toms are seemingly more frequent in myocarditic and arteriosclerotic 
subjects; arsenic lessens the liability of hyperthyroidism, which after 
all is an infrequent result. Larger doses may be given in winter than in 
summer. At first large doses are indicated and later, after relief is ob- 
tained, smaller doses should be given, averaging gr. j or whatever size 
experience in the individual case may determine. Relapses are common 
after withdrawal of the extract and in most cases it becomes rather a 
food than medication. Change of climate, warm baths and milk or a 
salt-free diet are of decided benefit. 



DISEASES OF THE PARATHYROID GLANDS. 

TETANY. 

Definition. — Tetany, first described by Steinheim (1830) and Dance 
(1831) and named by Corvisart (1852) consists chiefly of (a) peculiar 
tonic, intermittent, bilateral, painful spasms, mostly in the extremities, 
without involvement of the sensorium and (b) increased mechanical and 
electrical excitability of the nerves. The only known diseases of the 
parathyroids are hemorrhage, tuberculosis and surgical ablation. The 
parathyroid hormone normally restrains the excitability of the ganglion 
cells, possibly by promoting calcium assimilation; it antagonizes the 
thyroid gland. 

Etiology. — (a) Tetany occurs endemically, especially in Vienna, Heidel- 
berg, Berlin and Syria, and during March and April. It is rare in America 
(115 cases, Howard), England and Italy; though once frequent (1830- 
1860), it is now uncommon in Paris. In the Vienna outbreaks 46 per 
cent, of cases occurred in shoemakers and 24 per cent, in tailors; 83 
per cent, occur between sixteen and twenty-five years of age. It may 
develop in an entire family, (b) Digestive affections may produce it, as 



716 DISEASES OF THE PARATHYROID GLANDS 

dilatation (Kussmaul, 1871), ulcer or cancer of the stomach or duodenum, 
often with pyloric obstruction; auto-intoxication plus parathyroid 
insufficiency affects the nerve cells. Only 80 cases of gastric tetany are 
on record, (c) Rickets is causal in 90 to 96 per cent. (Cassel) of the 
infantile types; Heubner classifies them as spasmophilia, tetany, laryngo- 
spasm and infantile convulsions, (d) Tetania parathyreopriva is a type 
which follows thyroid operations. Gley (1831) was the first to connect 
tetany with extirpation of the parathyroid glands, first specifically described 
by Sandstrom (1880). Vassali and Generali maintained that absence or 
ablation of the parathyroid glands causes tetany (without cachexia). 
Thyroidectomy should be carefully done in order to spare the para- 
thyroids located alongside the lateral lobes, (e) Tetany occurs also in the 
acute infections, sepsis, nephritis, intoxications with ergot, morphine or 
lead. There are recorded only 32 cases of the puerperal form. Of the 
6 cases which the author has seen in this country 2 occurred with florid, 
secondary syphilis, 1 after an adenoid operation and 3 with gartrectasis. 
It may develop with other nervous diseases. In a few cases there has 
been cloudiness with swelling of the anterior horns. 

Symptoms. — 1. Muscular Contracture. — The earliest and chief 
symptom is the muscular contracture, which usually commences in the 
hand, with stiffness, numbness and pain, and culminates in a tonic, 
symmetrical, painful contracture. The muscles of the hand are hard; 
the attitude is that of the accoucheur's hand, the hand in writing or that 
observed in paralysis agitans; it is produced by contraction of the 
ulnar flexors; less often it resembles the clenched hand of old hemi- 
plegic contracture, and the nails even enter the palm; rarely the fingers 
are tonically spread apart. Except in light forms, the spasm cannot 
be overcome by force. The foot is affected less often than the hand and 
the spasm draws the foot into the equinovarus position, with the toes 
flexed and the sole hollow. The spasm is usually limited to these parts, 
lasts from minutes to hours or even days, disappears and then recurs. 
In rarer and more severe cases the parts above the elbows and knees 
may participate, with adduction of the arms and thighs, cramping of 
the face (risus sardonicus and trismus), neck, chest, tongue, diaphragm 
and ocular muscles, with diplopia, spasticity of the sphincters, dysuria, etc. 

Laryngismus stridulus (Clark, 1815) is common in infantile rickets, 
in which clonic contractures also occur. Pineles describes laryngospasm 
following parathyroid extirpation. 

2. Trousseau's Sign. — This consists in producing the spasm by 
pressure over the nerves, for example, just above the elbow or over the 
peroneal nerve, for a few seconds or minutes. It is pathognomonic. 
Schlesinger's sign; pressure on the sciatic nerve or flexion of the thigh 
with extension of the knee elicits a talipes equinovarus. 

3. Erb's Sign. — There is increased electrical irritability of the motor 
nerves to the galvanic current with early anodal closing and cathodal 
opening tetanus. Anodal opening tetanus is found in this disease alone. 
There is also increased electrical irritability of the sensory nerves (Hoff- 
mann) and of the nerves of special sense (Chvostek, Jr.), to faradic and 
galvanic currents. 



TETANY 717 

4. Chvostek's Sign. — Increased mechanical irritability of the motor 
nerves is observed on tapping or pressing on the facial, median, ulnar 
or other nerves, which produces contraction of the muscles supplied by 
them. It is quite constant but may be absent in children and is not 
pathognomonic, having been found in normal persons, bulbar paralysis, 
neuroses and facial paralysis. The muscles themselves are not over- 
excitable. 

5. Other Symptoms. — The sensorium is usually clear, except in rare 
cases with pyloric stenosis. The special senses and reflexes are normal; 
optic neuritis is extremely rare. Headache and malaise are frequent. 
In contrast to the pain and paresthesia, objective sensory findings are 
absent. In rare cases epileptiform seizures are seen. The temperature 
is elevated in 15 per cent, of cases. In rare cases, there may be dis- 
turbances of the intermediary metabolism of albumin; hypothyroidism, 
trophic, vasomotor and secretory disturbances may occur, as edema, 
polyuria, glycosuria or falling out of the hair (visceral tetany). 

Diagnosis. — The diagnosis in typical cases is most easy from the 
cardinal signs — the peculiar spasms, Trousseau's, Erb's and Chvostek's 
signs. In epilepsy these signs are absent and the aura, the cry, falling, 
tonic and clonic convulsions, biting of tongue and involuntary urina- 
tion are characteristic. Hysteria mimics everything, but the cardinal 
symptoms, except the spasms, cannot be reproduced; certain reported 
epidemics of tetany, as at Gentilly, were clearly hysterical. The other 
cardinal signs easily separate tetany from the occupation neuroses and 
acroparesthesia (v. i.) ; meningitis and brain tumor are distinguished on 
careful examination. 

Prognosis. — Death may occur from dilated stomach or laryngospasm. 
Frankl-Hochwart concludes that the prognosis is worse than is usually 
stated; 20 per cent, of his cases died, 20 remained well and the balance 
had recurrences and serious disabilities. 

Treatment. — The treatment varies with the cause, (a) Rest and quiet 
are indicated on general principles, although tetany is little influenced 
by excitement. Massage, strychnine and electricity should be avoided. 
Change of occupation and location is advisable in the endemic form. 
(6) In the digestive form, washing out the stomach and bowels may induce 
severe spasms. These cases are obstinate and the spontaneous mortality 
in gastric tetany is 75 per cent.; with operation this figure is reduced 
(see page 507). (c) In the rhachitic form, carbohydrates, phosphorus and 
substitution of human for cow's milk are efficient. Inhalations of chloro- 
form in some cases irritate the sensitive larynx, (d) In tetania parathy- 
reopriva the mortality is 80 per cent.; parathyroid grafting or feeding 
is helpful, (e) Cases following acute infections usually run a spontaneously 
short course; those in pregnancy rarely indicate abortion; in nursing 
women, weaning gives prompt relief; for intoxications there are obvious 
indications. Drugs are of little value except calcium salts, gr. xv; chloral 
influences the motor nerves, but is inferior to the bromides, as is also 
morphine. 



718 DISEASES OF THE THYMUS GLAND 



DISEASES OF THE THYMUS GLAND. 

The thymic functions are unknown. It is thought that the thymus is 
concerned in neutralizing infection, and in certain vegetative functions, as 
the growth of bone. There is an intimate, though obscure, relation 
between the thymus, thyroid, pituitary body, parathyroids, testes, 
ovaries, brain and bone-marrow. The thymus wastes as the testicles 
and ovaries develop. Thymic extract causes a fall in blood-pressure, 
cardiac acceleration and, in large doses, fatal collapse. Some class it as 
a ductless gland. The gland is epithelial in origin, but becomes lymphoid 
in structure. Its secretion in the first two years of life is milky and 
contains iodine, cells and a molecular substance. It weighs 12 gm. at 
birth; after puberty it wastes. 

(a) Hemorrhages into the thymus may be found in congenital syphilis 
and asphyxia of the newborn, (b) Thymic cysts are in 50 per cent, 
merely accentuation of the normal findings, in which the lymphoid ele- 
ments overgrow into the convolutions of the gland, (c) Abscess of the 
thymus, described by Dubois (1850), is often mistaken for softened 
gummata, cysts and postmortem softening, (d) The most frequent 
tumors are sarcoma and lymphosarcoma. Less frequent are dermoids 
and granulomata. (e) Persistence of the gland after puberty is described; 
the term is ill-chosen, as the gland normally persists into adult life. (/) 
Some cases of "persistent thymus" are hypertrophy or hyperplasia, which 
is the most common thymic lesion. Microscopically, we find lymphoid 
hyperplasia, Hassal's concentric epithelial corpuscles, eosinophiles and 
even myelocytes, (i) Physical signs. Dulness of more than 1 cm. to 
each side of the sternum is pathological; it is greater to the left and 
shifts on retraction of the head. The gland may be palpated in the 
jugulum or seen by the fluoroscope like a cap on the heart. The gland 
may weigh 150 gm. (ii) Plater (1614) associated enlargement of the 
thymus with sudden death. Grawitz and Jacobi described thymic hyper- 
plasia which caused sudden dyspnea, usually in infants, followed by early 
death ; the gland presses on the vagus, cava or trachea or causes laryngo- 
spasm. These cases are thought to be lymphatism (v. i.). (iii) In thymic 
asthma (Kopp, 1830), also known as Millar's asthma, the stridor, caused 
by thymic compression of the trachea, is pronounced, progressive and 
usually fatal from asphyxia. The enlarged gland may actually flatten 
the trachea (Summa and Benecke), as the distance between the sternum 
and spine is but little more than an inch and compression in this region 
is critical. It may be seen by bronchoscopy. In 48 operations, about 
two-thirds recovered (Veau and Olivier), (iv) Hyperplasia is frequently 
found in Graves's disease, status lymphaticus, myxedema, syphilis, 
acromegaly, epilepsy, myasthenia gravis and atrophy of the splenic, 
lymphatic or myeloid structures. Besides operation, the .r-rays are 
excellent. 



DISEASES OF THE HYPOPHYSIS 719 

LYMPHATISM (STATUS LYMPHATICUS). 

The constitutio lymphatica or status thymicus is a condition in which 
there is hyperplasia of the various lymphoid and kindred tissues and a 
tendency to sudden death. 

The affection is rare and occurs most often in women and children. 
Felix Plates (1614) observed it as a familial affection. 

Symptoms. — I. There is lymphoid hyperplasia. The lymph glands of 
the chest and abdomen are more often involved than the external glands. 
The tonsils, nasopharyngeal, lingual and intestinal lymphadenoid tissues 
are frequently hyperplastic. Moderate splenic enlargement is usual, the 
thymus is swollen and the bone-marrow often reddish. Leukopenia, 
lymphocytosis and eosinophilia may be found. 

II. Associated findings may include thyroid enlargement, tetany and 
laryngismus. Siess and Stoerk give the following symptomatology: (1) 
Atypical arrangement of the hair; (2) abnormal length of the extremities; 
(3) scaphoid scapulse; (4) a wide pelvis in males, narrow in women; (5) 
adiposity of the reverse type, in the lower half of the body in males, 
upper half in females; (6) poor development of the breasts; (7) general 
glandular hyperplasia; (8) small but elongated heart associated with a 
strong apex-beat and an accentuated aortic second sound; (9) low 
blood-pressure; (10) psychoneurotic manifestations; (11) vagotonia; (12) 
infantile type of epiglottis. 

III. Sudden death is often the first evidence of the condition and may 
occur without seemingly adequate cause. It has occurred during or 
after anesthesia, especially with chloroform. In one case a patient with 
enlarged glands died suddenly after receiving but 20 drops of chloroform. 
Operations with local anesthesia have also been fatal. Administration 
of antitoxin has caused death, as in the well-known case in Professor 
Langerhans's family. It may occur while bathing or after falling in the 
water. Sudden deaths during convalescence from acute infections or 
some collapses during hydrotherapeutic treatment may be attributed to 
the lymphatic constitution (Escherich). Children with eczema may die 
suddenly; lymphatism causes 75 per cent, of these deaths. It is said to 
be due to cardiac excitability (Kundrat), to lessened physiological 
resistance with a tendency to cardiac paralysis (Paltauf), respiratory 
paralysis (Meltzer) or lymphotoxism (Blumer). 

The x-rays may induce regression in the hyperplastic tissues. 



DISEASES OF THE HYPOPHYSIS. 

The pituitary body consists of two lobes; the anterior, the larger, is of 
epithelial buccal origin and probably discharges its hormone into the 
blood, influencing growth and sexual development; the smaller posterior 
lobe, partly of epithelial and partly of nervous origin, seemingly empties 
its secretion into the cerebrospinal fluid, increasing blood-pressure 



720 DISEASES OF THE HYPOPHYSIS 

(pituitarin) and influencing diuresis and carbohydrate and fat metab- 
olism. 

Hyperpituitarism, analogous to Graves's disease — as in hypophyseal 
tumors or hyperplasia — is an overfunctioning, perhaps due to chromo- 
phile activity. In early life, before the epiphyses ossify, gigantism results; 
if later, acromegaly. Emaciation, vascular degeneration, calcium reten- 
tion, thyroid activity (stimulated by the anterior lobe) or adrenal stimu- 
lation (from posterior lobe) and lowering of the assimilation limit of 
carbohydrates may be observed . 

Hypopituitarism or deficient internal secretion is analogous to myx- 
edema ; when it operates in life, it induces dwarfism or infantilism, obesity, 
hypoplastic sexual organs and secondary sexual characters (Frohlich's 
type), diabetes insipidus and great tolerance of carbohydrates; deficient 
secretion in later life induces reversive sexual infantilism; often there 
are dry skin, subnormal temperature and pulse, and drowsiness. 

Byspituitarism combines the above types, to some degree, just as 
symptoms of Graves's disease and myxedema may occur simultaneously 
or successively. 

ACROMEGALY. 

Acromegaly (large extremities) described by Marie (1886), is a dys- 
trophy marked clinically by overgrowth of the bones, tissues of the 
face, hands and feet and by other symptoms of hyperpituitarism. 

Etiology. — In 1902, Woods-Hutchinson collected 262 cases; in 77 autop- 
sies the hypophysis was obviously diseased in 73. The process may be 
hyperplasia or adenoma, less commonly sarcoma, colloid degeneration, 
fibrosis, softening or hemorrhage. Benda holds that acromegaly is due 
to excessive activity of the chromophile cells in the anterior lobe. Ac- 
cording to Sternberg, the sexes are about equally affected, and in 50 per 
cent, the affection begins between twenty and thirty, in 75 per cent, 
between twenty and forty and in 14 per cent, under twenty years of age. 

Symptoms. — 1. Acromegaly. — Enlargement of the extremities is 
usually the first clear symptom, but is preceded by paresthesia and 
pains in the extremities, often extreme and due to expansion, (a)' A 
remarkable change occurs in the face; the superciliary ridges protrude, 
the maxillae enlarge and the nose, ears, lips, tongue and chin attain mas- 
sive proportions. The general contour of the face is hexagonal. The 
teeth separate and the tongue sometimes protrudes beyond them. The 
eyes by contrast appear small. Pathologically, the change in the bone 
is simple hypertrophy, with increase in the vascular furrows, widening 
of some foramina (with narrowing of others), some roughening 
and localized protuberances which are not osteophytes; the skull is 
thicker and larger, especially the sphenoid, superciliary ridges, mastoid 
and occipital protuberances; the orbit may be narrowed by ethmoid 
bulging and the sinuses and sella turcica are increased as shown by the 
.T-rays. (b) The hands and feet are greatly but symmetrically hyper- 
trophied. The fingers and toes show either the long or the thick type; 
they are square at their ends — the "spade-like fingers." The palms and 
soles become flattened. The .T-rays show simple hypertrophy of the peri- 



ACROMEGALY 721 

osteal, subperiosteal and soft tissues; in some cases the soft parts are 
more hyperplastic than the bones. A common statement in the history 
is that the patient "must each year buy larger-sized hats, gloves or shoes." 
The nails are thin and small. The antithesis of acromegaly is micro- 
melia. (c) The changes in the trunk are less conspicuous. The sternum 
is increased anteroposteriorly and the ribs and clavicles are thickened. 
,The anteroposterior diameter of the thorax is increased, the head is 
held backward and the dorsal kyphosis is rather characteristic. The 
muscular weakness and lean arms and legs contrast sharply with the first 
impression of strength imparted by the massive face and extremities. 
The breathing is largely abdominal, (d) The skin is hyperplastic and also 
the mucous membrane of the nose, tongue, pharynx and larynx. The 
enlarged larynx may explain the deep, rough, monotonous voice. Hyper- 
trichosis is common. 

2. Nervous Manifestations. — (a) Symptoms of brain tumor (hypo- 
physis) are common, as headache, vertigo, mental alteration, vomiting, 
periodic loss of consciousness and eye symptoms in 52.5 per cent., hemi- 
anopsia, optic atrophy (40 per cent.), paralysis, anosmia, auditory disturb- 
ance and exophthalmos, (b) Changes in character, anxiety, apathy and 
insomnia which deepens into terminal somnolence, are common; severe 
pains, paresthesia, acroparesthesia and subjective warmth are frequent. 

3. Constitutional Symptoms. — (a) Glycosuria occurs in 40 per cent. 
Sometimes polyuria occurs without glycosuria, (b) Profuse sweats are 
common, even with glycosuria; the skin is sometimes pigmented; obesity 
is common, (c) Sexual disturbance is the rule, as amenorrhea often 
preceded by dysmenorrhea; in men impotence is not unusual; the 
-external genitalia are often hypertrophied, the internal infantile, (d) 
The heart is often dilated and hypertrophied from the concomitant arterio- 
sclerosis, deformed chest and rarely from actual overgrowth (cardio- 
niegaly). The vessels are wide and thick. Splanchnomegaly may be 
observed (intestines, tonsils, spleen, thymus and thyroid). In most cases 
the lymph nodes, particularly the cervical, are palpably enlarged. 

Course and Prognosis. — (a) Acromegalic subjects seek advice for the 
enlargement of the extremities or tonsils, sweats, pain, eye symptoms 
or polyuria; (b) remissions are common, the constitutional symptoms 
and, to a slight extent, the enlargements subside; on the other hand, a 
fitful advance may be noted, (c) The average course is chronic, covering- 
ten to twenty years, though relatively benign cases occur, lasting thirty 
or even fifty years, and acute malignant cases are known, which are due 
to malignant adenomata, (d) Death is inevitable; it may result sud- 
denly or from gradual marasmus, diabetic coma, intercurrent infection, 
cardiac insufficiency or pyelonephritis. 

Diagnosis. — Charcot held that physicians in general see and diagnos- 
ticate only what they have seen and learned to diagnosticate; the 
diagnosis is made at a glance by one who has seen a single case; undue 
regard to a single symptom, as the skin changes, amenorrhea or glyco- 
suria, may cause error. 

Differentiation. — 1. In the cranium progenium, the hyperplastic 
lower jaw protrudes and its teeth are directed forward; the upper jaw 
46 



722 DISEASES OF THE HYPOPHYSIS 

is hypoplastic; it may occur in acromegaly, cretinism, healthy individ- 
uals, degeneracy and idiocy. 

2. Gigantism occurs in over 20 per cent, of acromegaly, particularly 
when acromegaly develops early in life. Forty per cent, of giants are 
acromegalic (Sternberg). Gigantism implies symmetry of overgrowth; 
there are normal "giants" and giants with acromegaly, leontiasis (v. i.), 
facial hemihypertrophy, etc. 

3. Diffuse hyperostosis (Starr, Putnam, Prince) occurs in the young, 
involves all the skull bones, but seldom the extremities or spine; exoph- 
thalmos, blindness, deafness, bilateral facial palsy, dysphagia, dyspnea 
and other basilar symptoms are noted, which culminate fatally in stupor, 
idiocy, epileptiform convulsions and paralysis of the extremities. A 
subtype (leontiasis ossea, Dana) occurs in the form of tumor-like 
protuberances on the skull and other bones. Prince (1902) collected 20 
cases from the literature. He maintains that it is a form of osteitis 
deformans. 

4. Osteitis deformans (Paget 's disease) is a combined rarefying and 
hypertrophic osteitis. It begins slowly in subjects over forty years old, 
with pains and deformity of the thighs, legs and spine; the legs bow 
widely outward and somewhat forward, the cervical and upper dorsal 
spine becomes kyphotic, the thorax narrows transversely and widens 
anteroposteriorly, the abdomen is diamond-shaped and crossed by a sul- 
cus and the head hangs forward. The soft parts do not hypertrophy as 
in acromegaly, the face is rarely involved, the head is larger above than 
below and the arms are little altered. Clopton (1906) found 75 cases on 
record. 

5. Hypertrophic osteo-arthropathy, known since the time of Hippoc- 
rates, w 7 as especially described by Bamberger and Marie, in 1889. The 
ends of the fingers and perhaps the toes become clubbed or "drumstick" 
in appearance. While the nails are thin and small in acromegaly, in 
hypertrophic osteo-arthropathy they are large, thick, wide and curved 
downward. The alteration typically involves the terminal phalanges, 
but also in severe cases the ends of the ulna, radius, tibia and fibula. 
The pathology is a toxemic, chronic periostitis, with hypertrophy and 
osteophytic grow r th. The most common cause is chronic lung disease 
(chronic phthisis, bronchiectasis, emphysema or fibrosis), whence Marie's 
name of osteo-arthropathie hypertrophiante pneumonique; it may develop 
in congenital heart disease, aneurysm or, less frequently, in hepatic 
cirrhosis, gastric dilatation, syphilis, cystitis or various other infections. 

Treatment. — The treatment of acromegaly is symptomatic. Extract 
of the hypophysis has been given and in a few cases with temporary 
success. Operation seldom helps. 

INFANTILISM. 

The persistence beyond puberty of the physical and mental characters 
of childhood. 

I. The Frohlich Type, dystrophia adiposogenital, is hypopituitarism 
— obesity, persistence of, or reversion to. the secondary sexual characters 



INFANTILISM 723 

of childhood, hypotrichosis, poor mammary or testicular development, 
gracile figure, lack of the masculine voice and hypoplasia of the sexual 
organs. 

II. The Brissaud type, referable to hypopituitarism (or hypothyroidism, 
Brissaud), presents a "round face, lips projecting and plump, small nose, 
smooth face, clear skin, fine hair, eyebrows and eyelashes scant, eyes 
prominent, large, round cheeks, infantile face and head, skeleton under- 
developed, neck short and chubby, body long and cylindrical, abdomen 
prominent, limbs, round and large, a layer of fat over the whole body, 
infantile pelvis, lumbar lordosis, rudimentary sexual organs, no hair 
except on head, high-pitched voice, thyroid small, mind slow, retarda- 
tion of ossification, and absence or retardation of second dentition." 

III. The Lorain type is as follows: "Small stature, delicately formed, 
slender skeleton, skin soft and pale, large shoulders, lower extremities 
long and slender, trunk relatively small, infantile sternum and pelvis, 
epiphyses normally united, no fat increase, abdomen normal, finely 
chiselled face, voice high, neck long, genital atrophy, absence of or 
slight secondary sexual characteristics." 

IV. Herter's Intestinal Infantilism. — The child stops growing as it stops 
gaining in weight; the mental development is fair. Marked abdo- 
minal distention is common, often with dilatation of the abdominal 
veins. There is a moderate anemia, a very characteristic fatigue, 
looseness of the bowels with occasional attacks of diarrhea, often 
with fatty stools, an excessive appetite^ and thirst, an increased 
secretion of urine, and cold hands and feet. There is an absence of the 
ordinary intestinal flora of the intestines of young children. The pre- 
vailing organisms are the Bacillus bifidus, Bacillus acidophilus and 
Bacillus infantilis. There is a rise in the ethereal sulphates, indican, 
phenol and aromatic oxy acids. 

V. Other types include malnutrition, myxedema, lues, congenital heart 
lesions, etc. Gilford describes micromegaly, ateliosis (continuous youth 
and premature old age), or progeria. A pancreatic form, due to deficient 
pancreatic secretion, is associated with recurring severe diarrhea in 
children. 



SECTION VIII. 

CONSTITUTIONAL DISEASES. 



DIABETES MELLITUS. 

Definition. — A disease of metabolism characterized (a) by a permanent 
lessened capacity of the organs fixing, storing and consuming grape-sugar; 
(b) by excess of sugar in the blood {hyperglycemia) , resulting in (c) grape- 
sugar in the urine {glycosuria); {d) acid-intoxication; and (e) causal 
changes in the pancreas. 

Willis (1674) differentiated between diabetes mellitus and diabetes 
insipidus and Dobson (1776), of Liverpool, fully described the symptoms; 
Aretseus (150 a.d.) used the term diabetes. 

The liver, the reservoir for carbohydrates, contains up to 14 per cent, 
glycogen. It collects carbohydrates from the portal vein, stores them 
as glycogen and again imparts them to the blood as grape-sugar, for use 
in the tissues. The muscles also manufacture glycogen from the grape- 
sugar of the blood. Glycogen may also be produced from the albumins 
and possibly from fats. When there is a temporary carbohydrate short- 
age, the reserve store of glycogen is drawn upon. Fat is converted in the 
liver into sugar when neither the carbohydrates nor the albumins suffice 
to maintain the normal proportion of sugar in the blood. The fate of 
carbohydrates when ingested in excess is : {a) glycogen storage (up to 
400 gm.); (b) conversion into fat; (c) glycosuria from hyperglycemia, 
when sugar in the blood exceeds 0.2 per cent.; this "alimentary glyco- 
suria" is physiological and occurs when the blood-sugar exceeds the 
assimilation limit. Alimentary glycosuria is tested by giving 100 gm. 
of grape-sugar, after a light breakfast of bread and coffee. If more than 
1 per cent, of sugar appears in the urine or if 2 or 3 per cent, of the entire 
amount administered is found, it indicates diabetes rather than glycosuria. 
Most absorbed sugar goes to the liver, but some absorbed by the lym- 
phatics appears in the urine, whence its presence is not necessarily a sign 
of diabetes; in liver cirrhosis, sugar may reach the blood by the col- 
lateral circulation. Traces of sugar (0.01 to 0.02 per cent.) are normally 
present in the urine, but are not detected by the usual tests. 

Etiology. — 1. The pancreas {q. v.) has long been considered an etiolog- 
ical factor. Opie (1900) discovered atrophic changes in the cells of the 
islands of Langerhans which produce an internal secretion, regulating or 
inhibiting the conversion of glycogen into sugar. Weichelbaum found 
" Langerhans's insufficiency' ' in all of 183 cases, as hydropic changes in 



726 CONSTITUTIONAL DISEASES 

younger subjects or as sclerotic, atrophic or hyaline changes, in arterio- 
sclerotic or obese cases. This internal secretion from Langerhans's islands 
is wholly distinct from the external secretion of the pancreatic juice voided 
into the intestine, (a) Total pancreatic extirpation in animals and man 
produces glycosuria; (b) after partial extirpation and suture of the 
remaining portion to the abdominal wall, diabetes fails to appear, but 
develops if this portion is later removed; (c) when a tenth part is left, 
glycosuria occurs only after the ingestion of carbohydrates; (d) sub- 
sequent destruction of the remaining portion of the gland produces a 
severe form; (e) when more than one-tenth of the functionating gland is 
left behind no diabetes ordinarily results; (/) diabetes does not occur 
in simple ligature of the pancreatic duct, excluding its juice from the 
intestine, nor when the fluid escapes through a cutaneous fistula, whence 
the argument for an internal secretion (Minkowski and v. Mehring); 
(g) Cohnheim suggests that a pro-enzyme secreted by the pancreas, joins 
another ferment secreted by the muscles and that the united ferments 
break down the sugar molecules to produce heat and energy. 

2. Other Ductless Glands. — The adrenals stimulate the conversion of 
glycogen into sugar, mobilizing the sugar, and antagonizing the pancreatic 
action; adrenalin injected intramuscularly causes transient glycosuria, 
acting on the peripheral sympathetic. Adrenalectomy is followed by 
hypoglycemia ; in Addison's disease the tolerance for sugar is high and 
it is impossible to produce adrenalin glycosuria. The hypophysis is 
antagonistic to the pancreas and is associated with adrenal hyper- 
function and thyroid hypof unction ; in acromegaly glycosuria is common; 
in dystrophia adiposogenitalis high carbohydrate tolerance is noted. 
The parathyroids inhibit thyroid action; after parathyroidectomy sugar 
tolerance is reduced and adrenalin glycosuria readily effected. The thyroid 
antagonizes pancreatic activity, but stimulates adrenal activity. After 
thyroidectomy and in myxedema, there is hyperf unction of the pancreas; 
sugar tolerance increases and adrenalin causes no glycosuria. Thyroid 
feeding and Basedow's disease produce glycosuria. 

3. Neurogenous diabetes occurs through the sympathetic and chromaf- 
fin systems, controlling the various ductless glands. Claude Bernard's 
well-known puncture of the fourth ventricle (piqure glycosuria, 1844), 
may possibly lessen via the sympathetic the power of the liver to hold 
glycogen. Apoplexy, tabes, brain tumors, multiple sclerosis, meningitis 
syphilis, softening of the brain, diseases of the cord, vagus and sym- 
pathetic system may induce glycosuria. Hoffmann distinguishes between 
(a) neurogenous diabetes, which occurs chiefly in men, with no tendency to 
furuncles, carbuncles or cataract, with no connection with gout, and is 
temporary; and (6) diabetes of the obese, which occurs in either sex, often 
produces carbuncles, is often connected with gout and is very chronic. 

4. Obesity embraces cases with ordinary diabetes, obesity without 
glycosuria (masked diabetes) and obesity with consecutive glycosuria. 

5. Gout, arteriosclerosis, liver lesions (cirrhosis) and possibly acute 
infections have apparent relations with diabetes. Renal diabetes (glyco- 
suria without excessive sugar in the blood) may develop in nephritis, 
renal hemorrhage, chyluria, etc. Lactosuria may occur in late pregnancy, 



DIABE1TES MELLITUS 727 

the puerperium and nurslings; von Noorden's hypothesis is that in the 
" puerperal state the capacity of the tissues for breaking up milk-sugar 
is diminished, an instance of adaptation to an end in that the cells of the 
mother refuse a material which is preeminently suited to the nutritive 
wants of the nursling." 

6. Predisposing factors are (a) sex; men (3:2) are especially subject 
to diabetes; (b) age; its frequency is as follows: In persons from thirty 
to forty years, 18 per cent.; forty to fifty years, 25 per cent.; fifty to 
sixty years, 30 per cent.; in Stern's collection of 117 infantile cases 1 
was apparently congenital, (c) Heredity: A family history of obesity, 
consanguinity, neuropathic taint or gout is especially significant; cases 
are reported in which the grandfather was diabetic, the son gouty and 
the grandson diabetic (alternating diabetes), (d) Race: Diabetes is 
comparatively rare in the colored race and is especially common in Jews. 
(e) Occupation: Diabetes is more often seen in private than in hospital 
practice. Wealth and culture increase tenfold the predisposition to 
diabetes. It is frequently found in scientists, lawyers, musicians, poets, 
teachers, statesmen, merchants, speculators and in those leading a 
luxurious or self-indulgent existence with sedentary habits; it also results 
from overwork, excitement, overeating and overdrinking. 

Symptoms. — I. Hyperglycemia. — The blood-sugar rises to 0.1 to 1.6 
per cent., either because the diabetic cannot store or oxydize sugar or 
because sugar is formed in excess. 

II. The Urine. — Glycosuria is the leading symptom of diabetes. 
A daily excretion of 5 to 12 grams is not uncommon; the maximum 
amount recorded is 1500 gm.; the largest quantity of sugar is voided 
late in the morning or after 6 p.m. A percentage of from 1 to 4 is 
common, 8 or 9 per cent, is rare and the maximum is 20 per cent, 
(personal observation). The diabetic's capacity to consume sugar is 
considered under Therapy. Muscular exercise usually decreases it. It 
is often increased by psychic disturbances and may be suspended during 
an acute intercurrent infection, especially typhoid; chronic diseases 
with fever, especially pulmonary tuberculosis, have less influence. It may 
be reduced or absent in the final stages of diabetes, diabetic coma and 
when granular nephritis develops. Gouty diabetics as a rule pass no 
sugar during an attack of gout (diabetes alternans). 

Tests for Sugar. — (a) For Fehling's test, two solutions are kept sepa- 
rate; one contains copper sulphate and the other sodium and potassium 
tartrate and sodium hydrate. Equal parts of these solutions are heated, 
but not boiled, and the urine is added drop by drop. The volume of 
urine should never exceed that of the solution. Reduction of the blue 
copper solution to the yellowish-red suboxide of copper indicates sugar. 
Chloral, phenacetin, chloroform, formalin, morphine, uroleukinic and 
homogentisinic acids (the probable causes of alkaptonuria), glycuronic 
acid, cascara, rhubarb and salicylates may also reduce Fehling's solution, 
particularly after boiling. In doubtful cases (6) the fermentation test 
may be used; yeast is shaken thoroughly with a quantity of urine, the 
air allowed to bubble up and the mixture placed in a saccharometer — 
a tube closed at the top and graduated for estimation of percentages. 



728 CONSTITUTIONAL DISEASES 

The sugar, fermenting, is measured by the amount of carbon dioxide 
formed. A control test should be made, (c) The polarization test shows 
dextrorotary reaction, (d) The very delicate phenylhydrazin test may 
be used, (e) In Robert's test, the sugar percentage equals the difference 
between the specific gravity before and after fermentation, multiplied 
by 0.23. 

Quantity and Specific Gravity. — The urine is acid even after fermenta- 
tion (lactic acid) and has a sweet taste. The quantity of urine secreted 
during the night is less than that secreted in the daytime, whereas 
in other polyurias frequently f to f of the urine is secreted during the 
night. A secretion of ten quarts is not rare and 17 and 28 quarts are re- 
corded. Higher figures suggest simulation, patients having been known 
to add sugar to the urine. In part, polyuria results from the inability of 
the kidneys to concentrate the urine. Pollakiuria (frequency of urination) 
is common. The urine is pale; if dark and if uratic deposits are present, 
the prognosis is good. Foam often remains long on its surface and the 
sediment is scant or absent. Prout dated the onset of diabetes when 
the urine ceased having a turbid, uratic deposit. 

Amount in 
litres or quarts. Specific gravity. Sugar. 

1.5 to 2.5 1.025 to 1.030 2 to 3 per cent, 

2 . 5 to 4 1 . 030 to 1 . 036 . . . . . 3 to 5 per cent. 

4 to 6 1 . 032 to 1 . 046 4 to 7 per cent. 

6 to 10 1.036 to 1.040 6 to 9 per cent. 

The average specific gravity is 1.030 to 1.040, it is rarely more than 
1.050, and the highest record is 1.074; very high specific gravity suggests 
fraud; the lowest records are 1.003 and 1.002. If under a meat diet the 
urine becomes entirely or nearly free from sugar, the quantity approaches 
normal; the specific gravity remains high because the urine is rich in 
meat end-products. There is no absolute parallelism between the per- 
centage of sugar and the specific gravity. In some cases, though there 
is a large percentage of sugar, only a pint or a pint and a half of urine is 
excreted, described by Peter Frank a century ago as "diabetes decipiens." 
Crystals of sugar may be seen on the shoes, clothing or in the vessel. 

Nitrogenous Constituents. — Diabetics usually excrete 15 to 20 gm. 
or more of nitrogen daily (the normal being 10 to 15 gm.); the urea 
may reach even 60 to 150 gm., (metabolism being increased 15 per cent, 
in severe types); larger figures are reached in no other disease; the con- 
dition is pathological when the amount of nitrogen in the urine exceeds 
that in the food. 

Ammonium, normally 0.5 or 1 gm. per diem, may increase to 3, 6 or 
even 12 gm., and may constitute 10 to 20 per cent, of the total nitrogen 
output (instead of the normal 3 to 5 per cent.); over 5 gm. indicate a 
severe type, probably with death within a year, especially in subjects 
over fifty years of age; the highest figures are seen exclusively in diabetic 
coma. The organism excretes increased ammonia to neutralize acidosis. 
Creatinin may reach 1 or 2 gm. per diem. The uric acid is nearly normal. 

Acetonuria, or ketonuria, indicates the presence in the blood of j3-oxy- 
butyric and diacetic acids. This acidosis results from either (i) an 



PLATE XIX 




'Sfjflli 



Crystals of Phenyl-glueosazone. (Musser.) 
(Oc. 4, Obj. D.) Drawn by J. D. Z. Chase. 



DIABETES MELLITUS 729 

entirely abnormal type of metabolism or (ii) intermediate substances, 
which the diseased organism cannot split up into normal end-products 
(water and C0 2 ), thus robbing the body of native alkali and decreasing 
the power of the blood to take up C0 2 . These acid sustances are derived 
from the fatty acids and possibly from protein. (3-oxybutyric acid is 
absent in diabetics in good physical condition and not infrequently also 
in those who are suffering from marked loss of albumin. The urine 
and breath may be odorless or may smell like chloroform, fruit or wine. 
The daily excretion varies from a few grams to 50 to even 100 to 180 gm. 
Its abnormal excretion once begun, is uninterrupted and constantly 
tends to increase. It is of the gravest prognostic significance because in 
most cases, at the end of days, weeks or months, fatal diabetic coma 
develops. An excretion of more than 30 gm. indicates imminent coma. 
/3-oxybutyric acid is thought by some to be the parent substance of ace- 
tone and diacetic acid. Acetone and diacetone are present in the urine 
in diabetes, fevers, cancer, inanition or auto-intoxications and indicate 
malnutrition. When the amount of acetone progressively rises from 
1 gm. upward, the outlook is unfavorable, its normal daily output being 
0.01 to 0.03 gm. Acidosis may be measured by the amount of ammonium 
excreted or, more roughly, by the amount of sodium bicarbonate neces- 
sary to render the urine alkaline. 1 

Albuminuria is found in 35 per cent, of cases; it is slight and is due 
(a) to cystitis, pyelitis, intercurrent diseases as gangrene or infection, 
pulmonary tuberculosis or without relation to diabetes, as in the arterio- 
sclerotic and gouty types of diabetes, liver cirrhosis, etc. ; (b) to circu- 
latory disturbances, and (c) in uncomplicated diabetes it may be due to 
the action of the sugar, /3-oxybutyric and other acids and toxins on the 
kidneys; albuminuria is a frequent forerunner of diabetic coma (de- 
creased renal permeability with retention in the blood of toxins). 
Diabetes may develop into chronic interstitial nephritis and the sugar 
then disappears. 

Sodium chloride, sulphuric and phosphoric acids and the ethereal 
phosphates are abundant, caused by the amount of food ingested. Much 
lime is excreted, which suggests osseous waste. 

Pneumaturia. — The butyric acid bacillus, the Bacillus coli, yeast 
fungus and other bacteria may cause fermentation in the bladder, pro- 
ducing gas. Lipuria has been observed. 

III. Direct Consequences of the Glycosuria and Polyuria. — 
(a) The exaggerated thirst (polydipsia) is secondary to the polyuria, (b) 
Nutrition: For each gram of sugar in the urine four calories are lost to 
the tissues, and for each gram of /3-oxybutyric acid, five calories. There- 
fore the nutritive requirements are great, the appetite is excessive (poly- 
phagia) and in severe cases emaciation and fatigue are pronounced. 
Increase in weight may follow reduction in the sugar. The temperature 
in uncomplicated cases is subnormal from inanition. 

1 L. Blum finds that from 5 to 10 grams of sod. bicarbonate are sufficient to render the 
normal urine alkaline, while with mild acidosis 20 grams are necessary. With an acidosis 
of moderate intensity from 20 to 30 grams are required, in severe cases of acidosis 50, and 
in diabetic coma 150 grams or more are necessary to make the urine alkaline. 



730 CONSTITUTIONAL DISEASES 

IV. Complications. — Complications and other symptoms result from 
various causes : (a) excess sugar in the blood, (b) malnutrition and lowered 
physiological resistance; both conditions predispose to (c) infection, 
particularly by the Bacillus tuberculosis, (d) acidosis and other ill-under- 
stood degenerations and toxemias. 

1. Nervous. — (a) Intellectual depression, headache and neurasthenic 
symptoms are common; psychoses are infrequent. In rare instances focal 
symptoms develop without anatomical findings, (b) Diabetic coma occurs 
in 20 per cent, and causes half the deaths in diabetes ; it is most frequent 
in youth and in acute and severe types ; Naunyn holds that it is favored 
by a strict antidiabetic diet. All coma in diabetes is not diabetic; patients 
may succumb (i) to cerebral apoplexy, embolism, thrombosis, sepsis or 
uremia; (ii) to heart failure, which may cause sudden death, or coma with 
death after a short time or (iii) diabetic coma proper, due to acidosis and 
closely resembling experimental acid poisoning. Most writers believe 
that /3-oxybutyric acid is causal, though in three of the author's cases it 
was not present in the urine. Coma is imminent when the daily output 
of ammonium exceeds 3 gm. It may occur suddenly without obvious 
cause or may follow exertion, excesses, excitement or gastro-intestinal 
disorders. In some cases there are prodromal headache, stupor, restless 
anxiety or symptoms resembling acute alcoholism. The pupils are 
dilated, the reflexes abolished, the small pulse averages 110 and the tem- 
perature is usually subnormal. Convulsions are most uncommon. The 
breath has the wine-like acetone odor. The breathing is characteristic; 
inspiration is deep, long-drawn and energetic and expiration is short 
and slightly sighing; in this, KussmauVs dyspnea (1876), the inspiratory 
energy contrasts strongly with the general bodily weakness; respiration 
is generally somewhat accelerated; there is no stridor nor, at the onset, 
cyanosis. The albuminous urine contains innumerable short, broad, 
granular casts (Kulz) ; a few drops of ferric chloride give the Burgundy 
wine color; sugar is present, though it may disappear as the coma 
develops. Partial consciousness may return, but, with few exceptions, 
death occurs within a few hours to two days, with subnormal temperature, 
slowed respiration and cardiac weakness. The autopsy reveals no con- 
stant brain changes, (c) Toxemic degeneration in the posterior columns 
of the cord may develop, (d) Neuralgia is common and may indicate 
incipient neuritis or may appear and disappear varying with the amount 
of sugar in the blood and urine. It is often an early symptom; it is 
more often bilateral, most frequently affects the sciatic nerves and is a 
most obstinately recurrent symptom. Neuritis occurs in severe forms of 
diabetes and in its later stages. Neuritis may involve the cranial nerves, 
mostly the abducens, or with greater frequency the spinal nerves; the 
lower are affected more often than the upper extremities and, like diabetic 
neuralgia, bilateral involvement of the crural or sciatic nerves is the most 
common type. Its symptoms are those of neuritis or polyneuritis, as 
paralysis, obstinate pain, painful paresthesia in the legs, muscular 
cramps, abolished patellar reflexes, reaction of degeneration and trophic 
disturbances, as falling of the hair and nails, glossy skin, herpes or per- 
forating ulcer of the foot (mal perforant). In severe cases tabes is simu- 



DIABETES MELLITUS 731 

lated, pseudotabes diabetica, described by Fischer (1886) (see Multiple 
Neuritis), (e) Special senses. Retinal disease (Jager, 1856) occurs under 
four forms: (i) albuminuric retinitis; (ii) retinitis centralis punctata with 
characteristic shining bilateral spots, with hemorrhagic points; (iii) 
the ordinary hemorrhagic type (see Plate IV, Fig. 1); (iv) lipemia retin- 
alis, in which the vessels appear white and red. . It occurs in 19 per 
cent. Neuroretinitis and retrobulbar neuritis with consecutive atrophy 
are progressive and occur more frequently in severe cases. Twenty per 
cent, of diabetics with retinitis die within one year and 60 per cent, live 
over two years (Nettleship) . 

Amblyopia and amaurosis often first induce the patient to seek medi- 
cal advice. Paralysis of the ocular muscles occurs in 7 per cent, of cases; 
accommodation paralysis is the most frequent type, and then that of the 
external rectus; the most probable cause is neuritis. Cataract occurs 
in 4 per cent. Aural complications include external furuncles and otitis 
media, with a tendency to hemorrhage and mastoiditis. 

2. Circulatory. — (a) The blood may become concentrated, for much 
water is required to eliminate the sugar; the blood-sugar is increased. 
Fat in the blood (lipemia) is a frequent finding; what appears to be fat 
is sometimes albumin or cholesterin in combination with fatty acids; 
Fischer in 1 case found 18 per cent, of fat. In lipemia, acidosis is always 
present, although acidosis may develop without lipemia. Bremer's test 
is based on changes in the hemoglobin; thick smears of blood are made 
on a slide, heated and treated with 1 per cent. Congo red solution for two 
minutes. Diabetic blood will not stain. Williamson's test is based on the 
fact that diabetic blood decolorizes a weak alkaline solution of methyl blue. 
Acidosis (v. s.). (b) The arteries are frequently sclerosed and cause car- 
diac hypertrophy or dilatation, angina pectoris, cardiac asthma, hemi- 
plegia, albuminuria, senile gangrene and intermittent claudication, (c) 
The heart may be altered variously (v. s.). Hypertrophy occurs in about 
10 per cent, and is less ominous than atrophy, which occurs in uncom- 
plicated diabetes of the young. Heart failure may occur after moderate 
exercise or may develop precipitately, ending in coma or asphyxia and 
classified as an acidosis sign by Erdmann. Von Noorden observed 5 
sudden deaths in 140 fatal cases. The pulse is accelerated and its tension 
reduced. Dropsy is uncommon. 

3. Respiratory. — (a) Tuberculosis is most frequent in the poor classes 
and in the young, but much less so in older, obese and gouty subjects; 
25 per cent, of diabetics contract tuberculosis. Hemoptysis is very rare; 
the sputum is abundant; in the secondary necrosis, to which all diabetics 
are prone, the marked clinical and pathological lung findings may sharply 
contrast with the few tubercle bacilli in the sputum. The course is rapidly 
fatal, (b) Gangrene is much less common than tuberculosis; it is char- 
acterized by fever, pulmonary hemorrhage, purulent sputum and fetor 
which is less conspicuous than in other forms of pulmonary gangrene. 
(c) Intercurrent pneumonia is usually fatal. 

4. Digestive. — (a) The mouth is dry and acid from decomposition of 
sugar; the saliva is scanty; stomatitis and gingivitis are common and 
the growth of aphthae is promoted by the acid reaction of the mouth, 



732 CONSTITUTIONAL DISEASES 

though preventable by cleanliness. The teeth may decay from alveolar 
periostitis, or drop out from trophoneurotic changes, (b) The stomach is 
affected with remarkable infrequency, considering the oral findings and 
the polyphagia. Anorexia is uncommon, though the patient may refuse 
fatty and nitrogenous foods. The stomach is usually dilated, (c) The 
bowels are generally costive. Gastro-intestinal catarrh sometimes seems 
to precipitate coma, but it may be merely an associated symptom. 
Severe abdominal crises may simulate tabes or surgical conditions (cord 
degeneration), (d) The liver is usually enlarged and sometimes tender; 
it is rose-colored, transparent, homogeneous; fatty changes in Kupffer's 
stellate cells and peculiar refractile bands along the capillaries are con- 
stant (Rossle). Gall-stones are concomitants in 10 per cent, of cases, but 
they have no intrinsic relationship to diabetes. Hanot and Chauffard 
described a pigmentary cirrhosis in diabetes (diabete bronze) which prob- 
ably develops in the following sequence: (i) hemolysis, (ii) pigment 
deposit in the liver, pancreas and skin from the altered blood (hemo- 
chromatosis), (hi) chronic interstitial inflammation, chronic hepatic 
cirrhosis and (iv) chronic pancreatitis, causing diabetes (see pages 572 
and 603). 

5. Genito-urinary . — (a) Albuminuria may be present (see Urine). 
The kidneys are hypertrophied and hyperemic; various degenerations 
may be noted, including Ehrlich's glycogenic degeneration. Interstitial 
nephritis may follow and replace diabetes, chiefly in gouty and corpulent 
individuals, (b) Cystitis is common; the urine may ferment in the 
bladder, just as it decomposes in the urinal; this may lead to pyelone- 
phritis or pneumaturia (v. s.). Cystitis may cause temporary disappear- 
ance of the glycosuria, (c) In the female, menstruation may be dis- 
turbed or suspended. The sexual inclination is usually lessened in severe 
cases, but may be increased from genital pruritus (v. i.). Conception 
may occur even in advanced cases, but in 33 per cent, there is spontan- 
eous abortion or premature delivery. In severe diabetes interruption of 
pregnancy is indicated. In Offergeld's series, the maternal mortality 
was 30 per cent, from coma (collapse, infection) and, in all, 50 per cent, 
within two and one-half years, and the child's mortality was 66 per cent, 
either in utero or within ten days. Fungous development about the 
labia and vagina is promoted by lessened general resistance and local 
contact with the saccharine urine, particularly in careless subjects; 
pruritus pudendorum, vulvitis, vaginitis, urethritis, furunculosis and even 
gangrene may develop, (d) In the male, impotence results from spinal 
degeneration. Phimosis, balanitis, erosions near the urethra, urethritis, 
itching at the meatus causing tenesmus, curious nodes on the corpora 
cavernosa, furuncles and necrosis may first engage the physician's atten- 
tion. Genital symptoms in men are less conspicuous than in women. 

6. Cutaneous. — The skin is dry and harsh when there is much polyuria 
and emaciation. . Itching is caused by toxemia irritating the cutaneous 
nerves, as in uremic and cholemic pruritus. Skin eruptions include 
pityriasis, erythema, eczema, bullae, acne, purpura and herpes. Infec- 
tion is favored by reduced physiological resistance and hyperglycemia; 
furunculosis (15 per cent.), due largely to the staphylococcus, may 



DIABETES MELLITUS 733 

initiate lymphangitis, phlegmon or gangrene; erysipelas is promoted 
by reduced resistance. Gangrene is most frequent in late or middle life, 
and in mild cases; it usually begins on the toes and extends upward, as 
dry or moist gangrene; it results from obliterating endarteritis or the 
ordinary plaque-like atheroma. Unfortunately gangrene is usually pro- 
gressive. Wounds in diabetics heal better than in pre-antiseptic times, 
but delayed healing, infection and gangrene are still frequent. Enlarge- 
ment of the lymphatic glands is seldom absent in severe forms with 
emaciation. 

Course and Prognosis. — The onset may be acute and the course short, 
covering weeks, or protracted and remittent, covering twenty years or 
more; 80 per cent, lose their tolerance of carbohydrates within ten 
years. Complications modify the duration and outcome. In von Noor- 
den's summary of the prognostic signs, favorable signs are: (a) onset 
late in life; (b) long duration, with no grave complications or emacia- 
tion; (c) traumatic or (d) syphilitic origin; (e) the occurrence of mild 
forms of diabetes in the family of the patient; (/) precedent and co- 
existent obesity; (g) coexistent uric acid diathesis; (h) marked oscilla- 
tions and increasing tolerance of carbohydrates; (i) circumstances which 
permit of dietetic and hygienic prescriptions. Unfavorable prognostics 
are: (a) onset in early life; (b) great loss of strength, despite a brief dura- 
tion of the diabetes; (c) a history of severe forms in the family; (d) early 
appearance of grave complications; (e) a high degree of glycosuria, with 
complete intolerance of carbohydrates; (/) excretion of (3-oxybutyric 
acid; coma; (g) circumstances frustrating dietetic treatment or avoid- 
ance of bodily and mental overwork. 

Diagnosis. — Only when the urine in every case is examined as a routine 
procedure, can the lighter cases, amenable to treatment, be discovered. 
In many cases the thirst, polyuria, emaciation, itching and the complica- 
tions per se are suggestive. Pentosuria; 19 familial or hereditary cases are 
recorded. Pentose reduces Fehling's solution, even after fermentation 
of the urine. 

Treatment. — 1. Diet. — Regulation of diet, dating from Rollo (1797), 
is the most essential point. The carbohydrates normally supply nearly 
half the bodily requirements for food and. energy. The diabetic loses a 
large part by their escape through the kidneys, which entails a waste 
of digestive energy, irritation of the tissues by the unused sugar and a 
growing decrease of the tolerance of the tissues for it. A man weighing 
70 kilograms (150 lbs.) requires a diet representing 2500 calories, i. e., 
roughly, 35 calories for each kilogram. The dietary must therefore regard 
not merely the symptom, glycosuria, but the maintenance of body weight 
and energy. The therapeutic aim is to limit the carbohydrates and 
replace them with albumin and fat, increase the tolerance for carbo- 
hydrates and supply sufficient calories. 

General Outlines of Dietary. — Explicit written directions should be 
given each patient. All diabetics may eat the following foods: meat: beef, 
veal, mutton, game, tongue, lung, heart, brain, marrow, sweetbreads, 
fatty liver, peptones, gelatin and meat jellies; fish: caviar, cod-liver oil, 
clams, oysters, lobsters and crabs; eggs (10 to 20 per cent, of fat) ; animal 



734 CONSTITUTIONAL DISEASES 

and vegetable fats, bacon, suet, olive oil, cocoa butter; butter con- 
tains 85 per cent, fat, and should be used on meats, eggs or spinach or 
melted in milk; rich cream; all cheeses (3 to 30 per cent, fat), especially 
Swiss varieties; vegetables: cress, tomatoes, cabbage, cauliflower, sprouts, 
artichokes, mushrooms, truffles, olives, onions, garlic, celery leaves, 
lettuce, cucumbers and radishes; of fruits, only whortle-berries, young 
raspberries and green gooseberries should be eaten, though fruit-sugar 
(levulose) is better tolerated than starch or cane-sugar. Desserts (suffles) 
of eggs, gelatin and lemon; tea, coffee, Rademann's diabetic cocoa and 
von Hoevel's saccharine chocolate may be taken. 

Of the calories necessary in health, 1800 are supplied by carbo- 
hydrates; these must be replaced by protein and fat; protein cannot be 
greatly increased, at the most 500 gm. of cooked meat (700 gm. raw 
meat) = one pound (lean meat = 500, and fat meat = 1000 calories) . Fat 
must make up the balance. 

To some cases we allow after determining the limit of tolerance, 
beans and peas; turnips, carrots, celery bulbs, wax beans; radishes; 
walnuts, hazel-nuts, almonds (no chestnuts); apples, pears, apricots, 
peaches, berries; cooked apples, plums, pears, peaches, cherries and 
milk; some diabetics tolerate levulose, cane-sugar or honey, in small 
amounts and intermittently. (See "Food Values, pages 53 and 54). 

Gradual withdrawal of carbohydrates is tolerated better than abrupt 
restriction. Glutin flours differ but little from ordinary flours in their 
percentage of starch. Aleuronat or soy bean flour contains 7 per cent, 
of starch. Fat is best absorbed when some carbohydrates are given 
with it. If some starch can be given Mosse prefers potatoes, which are 
more easily assimilated and contain but 20 per cent, of starch (bread 
contains 55 per cent.). Saccharin should be used in place of sugar, 
gr. iss daily; it is 280 times as sweet and is antifermentative, but an 
excess may occasion dyspepsia. Naunyn advised an occasional fast-day, 
and Austin Flint kept his cases in bed and without food from Saturday 
night until Monday morning. As the disease is eventually progressive, 
a schematic diet should not be insisted upon; reasonable restriction, with 
occasional dietetic treats is less often violated by the diabetic, who is 
always hungry for bread and potatoes. The patient's weight, color and 
strength are of more significance than the urine, remembering that there 
is little or no carbohydrate metabolism, increased protein and perverted 
fat metabolism. Alcohol aids in the absorption of fat, prevents tissue 
waste and contributes energy and heat; not over 30-70 gm. should be 
given; it is contra-indicated in obvious hepatic disease and sweet or 
white wines and beer are injurious. 

Treatment of individual forms is conducted by determining the limit of 
tolerance; the percentage of sugar on a general diet is found, then the 
amount on a sugar-free diet and finally the amount of carbohydrate which 
can be given without glycosuria ensuing, (a) Mild forms of glycosuria; 
in elderly persons it is not necessary to determine with great accuracy 
the sugar tolerance (about 100 gm. bread). The patient may eat bread, 
potatoes and vegetables, for the quantity of sugar in the urine is usually 
insignificant (1 or 2 per cent.). The older the patient and the more 



DIABETES MELLITUS 735 

corpulent, the more caution necessary in reducing the body weight; fatty 
foods should be increased — butter used freely on bread, potatoes, vege- 
tables and meat; and bacon, eggs, fatty cheese, light wine, coffee, tea and 
carbonated water are also given. In young persons, carbohydrates should 
be given with great caution, as carelessness in diet is more frequent and 
the glycosuria more often progressive. The patient may not tolerate, 
e. g., 90 gm. bread yet pass no sugar on 80 gm. bread plus 20 gm., potato, 
300 gm. milk and 20 gm. oatmeal. The limits of tolerance for carbo- 
hydrates should be closely watched. All carbohydrates must be for- 
bidden excepting bread and potatoes, in addition to which the patient 
should have butter, 16 pats (each 9 gm. = 80 calories) with bread, cheese 
and potatoes (480 calories); 2 eggs (150 calories); olive oil 6 table- 
spoonfuls (750 calories) with salad, cucumbers, etc. (90 calories); 
30 gm. of fatty cheese (115 calories); 1 quart of milk (590 calories); 
and one ounce of alcohol; and meats (v. s.). (b) Moderately severe forms 
embrace cases in which the excretion of sugar is reduced to 1 or 2 
per cent, only by total abstinence from carbohydrates. The rise or fall 
of the tolerance limit should be watched every month, and every few 
months all carbohydrates must be withdrawn for three weeks. The 
diet must contain much fat; butter, 3 ounces (gm. 110 = 800 calories), 
must be weighed out every morning and eaten on bread, vegetables, meat, 
fish, etc., either in solid form or melted. Olive oil should be taken on 
salad (lettuce, chicory, cress, cucumbers, tomatoes, red cabbage), and 
as mayonnaise dressing for salad, cold meat, fish, lobster, etc. Bacon, 
5 eggs and one ounce of brandy (280 calories) should be given. In addi- 
tion the patient receives meats and some articles mentioned in the 
conditional list, (c) In severe forms, despite a continued rigid diet, sugar 
and acetone are constantly excreted. These cases usually occur with 
emaciation, complications and a fatal issue after a few months or a year. 
Careful dietetic treatment may retard the progress of the disease, prevent 
complications and delay the fatal issue (v. i. Acidosis). 

2. General Treatment. — (a) Exercise lessens glycosuria and is 
permissible in mild cases, guarded in severe cases and interdicted in 
acidosis; fatal syncope and diabetic coma may follow exhausting exertion. 

(b) The mouth and skin require special attention. Cleanliness averts 
in large part gingivitis, furunculosis and genital complications. Frequent 
warm (not cold) baths and change of underwear, gentle brushing of the 
teeth and soothing salves for eczema, and similar eruptions are imperative. 

(c) Diabetics for the most part should be kept at home and at work, for 
they often become restless and desire to travel. A prolonged stay in a 
quiet place is better. Sea bathing and exposure to cold and dampness 
increase glycosuria, (d) Suggestive treatment and optimism are needed with 
depressed subjects, (e) Mineral springs are suitable only for mild cases; 
Carlsbad and other spas are contra-indicated in severe, youthful, very 
aged, reduced and nephritic cases. (/) The mode of life should be quiet 
and worry avoided. 

3. Treatment of Acidosis. — If the patient has been on a mixed diet, 
the carbohydrates are gradually reduced; if he has been carefully dieted, 
the protein is reduced, and vegetables, carbohydrates, oatmeal and 



736 CONSTITUTIONAL DISEASES 

alkalies are indicated. Often glycosuria and ketonuria are refractory, 
till protein is reduced to 200-150 gm.; vegetable is better than animal 
protein. The fatty acids of metabolism are burned in the fire of car- 
bohydrates; alcohol is thus valuable and also oatmeal, which is poor 
in protein and stimulates sugar combustion, especially when preceded or 
followed for a couple of days by a green vegetable diet or actual starving. 
Oatmeal, 250 gm., boiled in Oiij of water and strained while hot is mixed 
with butter 250 gm. and 8 eggs; 200 gm. are given every three hours, 
as gruel or fried, with which coffee, tea or brandy is allowed. It may 
induce diarrhea, but increases sugar tolerance. Its favorable action is 
lacking when given steadily with meat, or in mild cases or after several 
trials. Levulose may operate equally well. Sod. bicarb, and citrate 
neutralize ketones and facilitate their renal elimination; a teaspoonful 
is given every three hours by mouth if swallowing is possible, 4 table- 
spoonfuls in water (Oij) by rectum (drop method) or in impending coma, 
a 5 per cent, solution intravenously, after phlebotomy if there is hyper- 
tension; subcutaneous injection may cause sloughing. Coma (acidosis, 
protein poisoning, dehydration) indicates large quantities of water. Like 
salt, the alkalies may be retained, causing increase in weight or even 
pulmonary edema. Levulose (10 per cent.) may be given by mouth, 
subcutaneously, intravenously or by rectum, lessening acidosis and not 
augmenting glycosuria. 

4. Tkeatment of Types. — (a) Minimal or transitory glycosuria should 
be regarded as diabetes and dietetic carelessness avoided, not giving over 
150 gm. of bread daily, (b) Neurogenous diabetes ; nervous conditions are 
more potent than diet, excitement increasing and rest decreasing the 
sugar, which often amounts to 6 per cent, with 1500 c.c. urine; strict 
diet is poorly stood; bromides, opium or acetanilide may be indicated 
but opium alone exerts an appreciable influence upon the glycosuria 
(Dobson 1776); it affects the severe more than the light type, i. e., 
it decreases the transformation of albumins into sugar, but does 
not control the transformation of starch into sugar; the average 
dose may be gradually increased without the patient exhibiting toxic 
symptoms or suffering from its reduction afterward. Codeine, gr. j-x, 
is less effective than opium; it may be combined with sodium bromide 
5 ss. Neuralgia (q. v.) and neuritis should be treated dietetically and by 
salicylates, (c) Renal diabetes is rare; hyperglycemia is absent and 
diet is without influence, the patient even standing 100 gm. glucose. 
(d) Tuberculosis is serious and allows of only moderate dietetic restriction ; 
if incipient, the diet may be rigid, (e) Gangrene should be treated 
expectantly until there is a possible halt in the process and definite 
demarcation ; positive rules of treatment are laid down with difficulty. If 
there is no acidosis, diet is usually efficacious; if acidosis, surgery is indi- 
cated (after oatmeal, alcohol, alkalies and much water) ; advanced diabetics 
stand operative shock and anesthesia poorly and most die from rapid 
syncope or dyspneic coma. Other operations may be performed, when 
indicated as absolutely , necessary life-saving procedures and only, if 
possible, after strict dieting. Boils and furuncles are excised, not 
incised. (/) In arteriosclerotics and lithemics, protein should not 



DIABETES INSIPIDUS 737 

exceed 100 gm. Sudden carbohydrate reduction should be avoided in 
obesity. Uremia and decompensation contra-indicate strict diets and 
constipation, drastic purges. 

DIABETES INSIPIDUS. 

Definition. — A chronic malady characterized by large amounts of urine 
of low specific gravity. Willis (1674) differentiated between diabetes 
mellitus and insipidus (without taste, i. e., non-saccharine); 55 cases 
occurred in 113,600 in the Berlin Charite. 

Etiology. — Two groups of cases are observed : (a) the idiopathic (nervous 
or vasomotor) and (6) the symptomatic, which occur in (i) brain disease, 
especially basal syphilis and less often traumatism, basilar meningitis, 
apoplexy, lesions of the hypophysis, medulla, fourth ventricle, middle 
cerebellar lobe or corp. trapezoides, etc. (ii) It may result from ab- 
dominal diseases, aneurysms, tumors, kidneys (losing their power to 
concentrate the urine) or tuberculous peritonitis, (iii) Malnutrition 
with tuberculous, diabetic, syphilitic or gouty ancestry, acute infec- 
tions and alcoholism are numbered among its possible causes. Weil 
collected 36 cases among individuals of four generations, all of whom 
enjoyed good health. Rare congenital cases are recorded. Most cases 
occur in males; 10 per cent, are under five years old, 14 per cent, under 
ten and 45 per cent, were between ten and twenty-five years of age. 

Symptoms. — The onset is usually gradual, though abrupt symptoms 
have followed fright, (a) The urine is greatly increased, 20 to 40 pints 
daily, even 90 pints and more at night than by day; less urine is excreted 
than water ingested. It is passed rapidly (tachyuria). Its specific 
gravity ranges between 1000.5 and 1005. It is pale and sometimes the 
urea, chlorides and phosphates are increased, being washed out from 
the tissue. Albumin, sugar and inosite are very uncommon, (b) Poly- 
dipsia is secondary, though perhaps the earliest symptom noticed. In 
one case, a physician with brain syphilis, 2 gallons of water were drunk 
each night between 10 p.m. and 7 a.m. (c) The skin is dry; carbuncles 
are rare. The saliva is decreased. Phenomenal polyphagia marks some 
cases. Headache, irritability, increased knee-jerks, impotence and 
severe lumbar pain radiating into the legs, are quite frequent. Nutrition 
is often good in the idiopathic cases and no unusual metabolic findings 
are noted; in the symptomatic variety the nutrition depends on the causal 
disease; in children growth may be retarded. The temperature is low 
and chilling occurs readily. Aside from causal lesions, there is no constant 
autopsy finding except hypertrophy of the kidneys from increased 
activity, and sometimes dilatation of the bladder and renal pelvis. 

Diagnosis. — Differentiation is required from (a) diabetes mellitus, with 
which it has no common symptoms except polyuria and polydipsia; 
there is no glycosuria, acidosis, gangrene, carbuncles or neuritis; (b) 
from interstitial nephritis, in which the specific gravity is higher, the 
urine is less abundant, is albuminous and contains casts, and which is 
associated with cardiovascular, retinal and uremic manifestations; (c) 
from primary polydipsia, which is exceedingly rare; and (d) from transi- 
47 



738 CONSTITUTIONAL DISEASES 

tory polyuria, distinguished by its course or etiology, as recent fever, 
hysteria, etc. 

Prognosis. — The prognosis is more favorable in idiopathic forms. 
Less than one-half of the patients recover, though death results less 
frequently from the disease itself (save cerebral or abdominal tumors) 
than from intercurrent infections, notably pulmonary tuberculosis. 

Treatment. — Aside from antisyphilitic therapy, drugs are of little 
use. Iodides improve some non-syphilitic cases. Salt or water restriction 
may work benefit. Opium may be useful and large doses are of ten well 
tolerated. Ergot (fluidextract lUxx, t. i. d.), sodium bromide (3ss, 
t. i. d.) and acetanilide (gr. v-x, t. i. d.) are recommended. Talquist 
advocates a vegetable diet. 

GOUT. 

Definition. — An obscure metabolic disease, characterized by acute 
periodic or chronic inflammation of the joints with uratic deposits. 

Mentioned by Hippocrates, gout was clearly described by Sydenham 
(1683), who suffered from the affection for forty years. Forbes (1792) 
and Wallaston (1797) recognized its uratic nature. 

Etiology. — 1. The actual cause is unknown. Garrod (1848) held that 
uric acid accumulated periodically in the blood before the gouty seizure. 
His, Vogel and Magnus Levy maintain that in gouty subjects it is 
increased all the time, and that the urine contains less uric acid before 
and more during and after the seizure. Pf eiffer holds that it is really less 
a question of its amount than of its insolubility or form. The endogenous 
uric acid (which constitutes 90 per cent, of the purin bodies) is derived 
from the nucleins of the body tissues and the exogenous uric acid from 
the food nucleins. The subject is still much involved but it appears 
that the uric acid elimination (perhaps from reduced renal action) is at 
fault rather than any increased formation or suboxidation of the acid. 

2. Predisposing factors, (a) Heredity is a factor in 60 per cent.; trans- 
mission is more common by the father than mother and to the younger 
rather than the older children, (b) Mode of life; lack of exercise, over- 
eating, meat diet and alcoholism are potent factors. The old verse 
read that "Wine was the father, Eating the mother, and Venus the 
midwife" of gout. Though gout often affects the well-to-do (arthritis 
divitum) and arthritis deformans the poor (arthritis pauperum), gout 
is not uncommon among the lower classes. Heavy ales and beers are 
more injurious than whisky and light wine. Gout may occur in temperate 
individuals. Obesity, diabetes, arteriosclerosis and calculous tendencies 
are concomitant rather than causal conditions, (c) Lead poisoning is 
observed in 15 per cent, of cases, particularly in England; saturnine 
nephritis may explain it. (d) Men are particularly prone to gout (1 to 
13 or 25). (e) Age: Gout begins between thirty and forty years in 38 
per cent., thirty and fifty in 60 per cent., and before the seventeenth 
year, less than 1 per cent.; Gairdner observed 1 case in a nursling. 
(/) England leads in frequency of its occurrence. In the LTnited States 
it is rare, though Futcher shows that the cases in Baltimore and London 
hospitals stood as 2 to 3. Few cases seek hospital treatment. 



GOUT 739 

Symptoms. — These may be considered under two captions, (1) acute, 
and (2) irregular, chronic and visceral gout. 

1. Acute (regular, sthenic or) typical gout usually appears without 
prodromes, though sometimes an attack is heralded by digestive disorder 
(pyrosis, gastralgia), cerebral congestion, vertigo, tinnitus, irritability, 
paresthesia, cramps or pain in the muscles or dark lateritious urine. 
The paroxysm is remarkably characteristic, (a) Local findings: The 
patient is awakened one to three hours after midnight by an agonizing 
pain in the metatarsophalangeal joint of the large toe (podagra), described 
as crushing by a vise or burning by a hot iron. Localization in the toe 
(95 per cent., Garrod) is practically diagnostic of gout; the skin becomes 
red, tense, slightly edematous and exquisitely sensitive; the shorter the 
attack the severer are the symptoms. Serum exudes into the joint. 
The pain abates toward morning, but the inflammation increases. Each 
early morning sees a repetition of the pain for three to five or less often 
six to seven days; the paroxysmal pain and the local findings then 
gradually subside; in two-thirds of the cases, the skin desquamates 
over the joint. Later attacks involve the thumb, knee and other 
joints, less commonly than in chronic gout (v. %.). The pathological 
changes probably develop in this sequence: (i) local stasis (inflammation), 
(ii) uratic deposit; (iii) necrosis; the ordinary urates (biurate of sodium 
in conjunction with sodium phosphate) do not cause such local reaction, 
but the biurate alone, even in most dilute solutions (0.004), produces 
inflammation; residual swellings (acute gouty tophi) consist of this 
biurate precipitated by the carbonates of the blood and tissues. Con- 
valescence is complete in ten days, often with greatly improved spirits 
and health. During the seizure (b) constitutional symptoms are present, 
as the temperature, 100.5° or 101°; the pulse is slow and hard, sometimes 
arrhythmic and seldom exceeds 100. The heart may palpitate. Slight 
leukocytosis, nausea, vomiting, epigastric cramping and eructations are 
not uncommon. The urine is dark, decreased, acid and higher in specific 
gravity; Bain and Futcher find the uric and phosphoric acids, both 
derived from disintegration of nuclein, fall below normal in the quiescent 
period and increase during the attack. 

Subsequent acute seizures are likely to occur, notably in the spring and 
fall, precipitated by excesses in alcohol or eating, trauma, exertion or 
excitement; in one case it would occur within fifteen minutes from 
a glass of champagne. 

Retrocedent or suppressed gout was once thought to develop when an 
acute paroxysm abated "too rapidly"; many of its symptoms are 
doubtless coincident arteriosclerosis or uremia (v. i.). 

2. Chronic, irregular, atypical gout generally follows acute attacks 
which increase in frequency, decrease in acuity and show slight tendency 
toward resolution. Sometimes tophi appear to begin as chronic gout, 
particularly in the aged, cachectic or women of a gouty family, all of 
whom lack reactive power (asthenic gout), (a) Local findings: There 
are less pain, fever and redness but greater and more permanent swelling 
than in the acute form, until the condition eventually becomes chronic; 
the "attacks" may be rudimentary and remissions alternate with exacer- 



740 CONSTITUTIONAL DISEASES 

bations. The lower extremities and hands are most often affected; it 
may develop in the thumb (chiagra), knee (gonagra), elbow (pechiagra) 
and spine (rhachisagra) , but the shoulder is very seldom and the hip 
almost never invaded. In some cases its moving from joint to joint 
(urarthritis multiplex seu vaga) may cause confusion with acute rheuma- 
tism. Uratic deposits {tophi arthritici) form in the cartilage and later 
in the capsule and ligaments, and the swelling never recedes essentially. 
These prominences and the attendant fibrosis lead to deformation, sub- 
luxation, fluctuation, crackling, anyklosis and contractures. The proximal 
joints of the fingers may point to the radial and the others to the ulnar 
side. Tophi may rupture, evacuating yellowish-white urates, though in- 
completely, as they are partly diffused through the tissues; these gouty 
ulcers heal tardily, if at all, for their basis is fibrous and indolent. Tophi 
occur also on the ear (25 per cent.), bursse, tendons, aponeuroses (which 
may explain some cases of Dupuytren's palmar contracture), and even 
in the skin, eyelids, nose, larynx, penis or scrotum, (b) Visceral gout 
includes a curious mixture of real gouty complications and incongruous 
doubtful symptoms (arthritisme, herpetisme and the "uric acid diathesis"). 

Complications. — Renal, the most important visceral complications, 
sometimes dominate the clinical picture. In 1440 cases, Garrod observed 
albuminuria in 26.5 per cent., more often in advanced than in early 
cases. It may follow the metabolic changes, or may possibly constitute 
a primary gout. At first albuminuria may be considered toxic, congestive 
or arteriosclerotic, but later the renal, cardiovascular and retinal findings 
of interstitial nephritis develop with all its accidents; uratic deposits 
occur in the intertubular tissue and in 15 per cent, in the secreting 
tissue of the cortex and medulla, or as calculi in the renal pelvis; hema- 
turia, oxaluria and pyelitis may occur. 

Arteriosclerosis of the ordinary type is promoted by metabolic changes, 
alcoholism, plumbism and nephritis; with nephritis, it causes most 
of the so-called visceral symptoms, as the cerebrospinal (headache, 
vertigo, congestion, epileptiform and apoplectiform attacks, encephalo- 
malacia), the circulatory (hypertrophy, myocarditis, angina, valvular 
lesions, phlebosclerosis) , the respiratory (stasis, bronchitis, asthma) and 
retinitis. 

Eczema (18 per cent.), scleritis and episcleritis (with circumscribed 
points of inflammation and sometimes semimicroscopic tophi), neuralgia 
or less often, lumbago, sciatica and brachial neuritis, burning, psoriasis- 
like patches on the tongue, digestive symptoms (v. Prodromes) and 
burning in the eye-balls are probably often gouty. On the other hand, 
many so-called visceral gouty manifestations are neurotic, paroxysmal 
(calculous colic, migraine or asthma) and other conditions common in 
persons not suffering from gout. 

Diagnosis. — (a) Acute gout is most typical in its etiology, history, 
acuity and localization. In a few cases (urarthritis multiplex), a diag- 
nosis of acute rheumatism may be made; fibrous rheumatic nodes may 
be confused with tophi, but if the possibility of gout is recognized there 
is usually no error, (b) Chronic gout is suggested by a history of acute 
attacks, involvement of the distal joints of the hands and feet, unequal 



GOUT 741 

distention and thickening of the soft parts and often by its association 
with early arteriosclerosis, contracted kidney, obesity, renal calculus 
and diabetes. The z-rays sometimes show the tophi as light spots and 
the joints smooth. Visceral gout is an entity only when it develops in 
a patient undoubtedly gouty. 

Prognosis. — Gouty patients may live to an old age, but with a tendency 
to chronic gout, of which the issues are (a) uremia, (b) arteriosclerosis, 
as coronary disease or apoplexy or (c) terminal pericarditis, pneumonia 
or pleurisy, induced by the (d) gouty marasmus. In general the out- 
look is better in frank than in irregular gout and better in cases which 
develop after forty years of age. 

Treatment. — 1. Acute Paroxysm. — (a) Absolute rest is indicated. 
(b) For pain, the use of colchicum is empirical (Storck, 1763) but it relieves 
pain and inflammation and acts as a cholagogue (5iss of the vinum 
colchici radicis [not seminis] daily). It requires care in nephritic and 
marantic subjects. It should be stopped when pain is alleviated and 
diarrhea intervenes. Full therapeutic doses produce a slow pulse, 
vomiting, pain and purging; inversely to its action on the bowels, there 
are diaphoresis and diuresis. It is eliminated by the kidneys, bowels 
and skin. After toxic doses, retching, serous and finally hemorrhagic 
purging, great pain, prostration, paralysis of the sensory nerves, motor 
cord and respiratory centre (the usual cause of death) develop. 

If colchicum produces no effect, sodium salicylate (5j~ij daily) 
usually relieves the pain and swelling and aids in solution of the uric 
acid; its early effect is greatest and it usually fails after the third day. 
Acetphenetidinum (gr. viij-x) and morphine are indicated in severe 
paroxysms. In prolonged attacks, potassium iodide, gr. v (given with 
care in nephritis) and wine of colchicum Tfl,x are useful. Atophan (gr. 
vij, t. i. d., for 4-5 days) increases the uric acid output three- or fourfold, 
more efficiently than salicylates and is less irritant to the stomach when 
combined with alkalies, (c) The diet, according to Pfeiffer, should con- 
sist of foods which "release uric acid in a free form," as meal soups, 
rice and other carbohydrates; meat, eggs, alcohol and lemonade are 
withheld. Plain or acid water, as Seltzer (not alkaline water as Vichy) 
and hydrochloric acid, are given freely, (d) Local measures induce 
necrosis and tophi, especially vesicants, the ice-bag and massage; warm 
applications of 50 per cent, alcohol or lead-water (tinctura opii, liquor 
plumbi subacetatis aa 3ij and water 5 j) may be used. 

2. Between Attacks. — (a) Regulation of diet is the cardinal indica- 
tion. Moderation in the quantity is more important than the quality 
of food. Quantity: a full diet increases the uric acid, taxes resorption 
which is usually impaired and favors acid fermentations which engage 
the diphosphates and carbonates of the food necessary for the formation 
of soluble uric acid salts; three medium-sized meals are allowed. Quality: 
(i) alcohol is absolutely forbidden; (ii) water may be given freely on an 
empty stomach, (iii) Moderate amounts of fat are allowed, (iv) Fruits 
and vegetables increase diuresis and their malates and citrates help to 
dissolve the uric salts, (v) Meats are allowed; urea seems to dissolve 
uric acid which the meat does not increase if given in moderation (meat 



742 CONSTITUTIONAL DISEASES 

1 part, vegetables 3 parts of the diet). Meat is essential in marantic 
cases. There is no difference between the effect of light and dark meats; 
those rich in purin (sweet-breads, liver and kidneys) are avoided; milk 
and eggs are purin-free. (vi) Carbohydrates should be largely decreased, 
though following their ingestion the uric acid (as compared with the urea) 
increases nearly twofold. In severe cases the purin contents of peas, 
beans, corn or oats, contra-indicates them, (b) Exercise is indispensable, 
avoiding fatiguing effort, hurry and worry, (c) Medicinal treatment is 
secondary. Alkalies are useless, though claimed to produce an increased 
output of uric acid; they operate only by preventing decomposition of 
the neutral (bi-) sodium phosphate (the chief uric solvent), e. g., lithium 
carbonate, sodium bicarbonate or mineral waters. Luff advises guaiacum 
resin, gr. v-x, t. i. d. Piperazin, lysidin, urotropin, urosin and sidonal 
are inert. 

3. Chronic Gout. — This is difficult to treat. For general dietetic, 
hygienic and medicinal measures, see above. Colchicum wine, Tfl,x, 
and potassium iodide, gr. v, may relieve arthritis, asthma, neuralgia 
and eczema. Tonics, principally arsenic, are indicated in marantic 
forms. Tophi should not be operated on; local measures are useless, 
save Bier's stasis, gentle massage, dry heat or salicylate salves (ac. 
salicylic. 4, lanolin 40, and oleum terebinthinse 1 part). 

RICKETS. 

Definition. — A metabolic affection of early infancy, characterized 
chiefly by hyperemia and deficient calcification of the growing bones. 
The disease was first well described by Glisson (1650). The name is 
derived from an old English word meaning "twisted," and Glisson 
suggested the Greek "rhachitis" (vertebral inflammation) because the 
spine was often involved, and the term sounded like "rickets." 

Etiology. — All theories advanced, such as abnormal calcium metab- 
olism, infection or reduced activity of the thymus, are insufficient. 

(a) The diet is of prime importance; proprietary foods, condensed 
milk, cow's milk, excess of carbohydrates, prolonged lactation or 
nursing during pregnancy are probable factors. A deficiency in animal 
fats and proteids is causative; after 20 litters of lion cubs had been lost 
from rickets in the London Zoological Gardens, Bland Sutton found 
that a diet of milk, powdered bone, meat and cod-liver oil prevented it. 

(b) Unsanitary surroundings may be causal, as lack of fresh air and 
sunlight, crowded quarters and kindred factors observed largely among 
the poor classes in large cities; among nurslings Kassowitz (Vienna) 
observed it in 89 per cent, and Joucousky (St. Petersburg) in 90 per cent. ; 
in the United States it is most frequent among negroes and Italians. 
Hereditary syphilis is a predisposing factor, (c) Age. In over 600 cases 
Baginsky did not observe it in children under three months of age; his 
figures show 7 per cent, in children between three and six months and 
88 per cent, between three months and two years. The occurrence 
of congenital rickets is usually denied. Rickets which develops later, 
up to puberty, is called rhachitis tarda. 



RICKETS 743 

Symptoms. — An experienced observer may diagnosticate the gradual 
onset from the prodromes, as the irregular or tardy dentition; irritability, 
insomnia and throwing off of the bedclothes; sweating about the head 
and neck; bronchitis; digestive disturbances, anorexia, malnutrition, 
meteorism or diarrhea; immobility, the child crying when moved or 
touched and general hyperesthesia. However, a positive diagnosis is 
not justifiable until the bone symptoms develop. 

1. Bone symptoms are most marked in the skull and thorax, (a) The 
skull shows the earliest changes, generally in the first year of life. The 
face appears small and the head large. Nodes of bone appear on the 
frontal and parietal regions, which with the occipital flattening produce 
the caput quadratum (tete caree). The anterior fontanelle and sutures 
(which normally close at the fifteenth or eighteenth month) remain open, 
even until the fourth year. The occiput softens (craniotabes) in 40 per 
cent., near the lambdoid suture; the occipital protuberance remains 
hard. Craniotabes may less frequently occur in the frontal bones; 
besides the actual bone changes (v. i.), the pressure of the pillow and 
brain further its development. In extreme cases the peri- and endo- 
cranium actually touch, and in moderate degrees the skull feels "parch- 
ment-like." Though it occurs also in syphilis, craniotabes is rather 
characteristic, with the tender quadrate head, head sweating, thin 
occipital hair and blue scalp veins. The frequent systolic murmur heard 
over the greater fontanelle is also heard in other affections or in health 
and is said to occur only in conjunction with a similar bruit in the 
carotids. The upper jaw becomes long and narrow and the lower jaw 
hexagonal, from muscular traction on the soft bones. The eruption of 
the teeth is delayed until the second or even the third year; the second 
teeth are crowded, carious, curved and eroded. (6) In the thorax, the 
rhachitic "rosary" appears toward the end of the first or early in the 
second year; it is so-called from the bead-like succession of enlarged 
chondrocostal joints — enlarged epiphyses. The chest is altered toward 
the end of the second year, due to the softness of its bones, traction 
exerted by the diaphragm, atmospheric pressure and sometimes by 
external influences, as holding of the child with a hand on the chest. 
Louis's angle is often prominent, and the sternum juts forward, causing the 
"chicken breast" (pectus carinatum). There is also a depression outside 
of the costochondral junctions which extends outward and downward, 
and is accentuated by some eversion of the costal arch. The thoracic 
deformity promotes respiratory complications and dyspnea, which in 
turn aggravate it. With this deformity we may group lumbar kyphosis 
which is arcuate and not angular, the thickened or bent clavicles and the 
thickening of the spine or edges of the scapulae, (c) In the extremities, 
the epiphyses, particularly of the ulna, radius, tibia and fibula, are enlarged, 
at the same time as the rosary, craniotabes and wide fontanelle. The 
epiphyses also are tender and painful and may look like "double joints" 
Deformities may develop from muscular traction or the weight of the 
body ; the arms may incline outward and forward or the forearms become 
convex toward their extensor surfaces. The thighs sometimes become 
convex anteriorly and outwardly; the legs bow outward or less often 



744 CONSTITUTIONAL DISEASES 

forward, especially when early walking is encouraged. Spiral deformities 
are less frequent. The gait is waddling. ' Green-stick or actual fractures 
sometimes occur, (d) The flat rhachitic pelvis develops by the weight 
of the body pushing the sacrum into the pelvis and the counter-pressure 
of the thighs narrowing the anterior pelvis, so that the pelvic aperture 
may become heart-shaped, the acetabula lie more anteriorly and the 
iliac crests flare outward, (e) Pathology. Normal bone grows in length 
as follows: there are two zones in the epiphyseal surface facing the shaft; 
(i) the first zone is nearest the shaft, is faintly yellow and measures 2 
mm.; it is the zone of preliminary calcification, into which normally the 
bloodvessels grow and form medullary canals by absorbing small areas 
of bone, and in which osteoblasts appear and calcification develops. 
In rickets the calcification is imperfect and irregular in this zone and 
the bloodvessels grow not merely into these calcified areas but beyond 
them, even into the cartilage area, and absorb what little new bone is 
formed, (ii) The second zone lies outside the one described, is sharply 
demarked from it, is normally bluish, measures 1 or 2 mm. in thickness 
and is known as the hyperplastic zone, in which the cartilage cells divide 
and proliferate. In rickets this zone becomes larger, proliferates 
irregularly and is invaded by bloodvessels and irregular foci of abortive 
calcification; the demarkation between the first and second zones is 
ill-defined. Normal bones grow in thickness by bony increase beneath 
the periosteum. In rickets this layer becomes several millimeters thicker, 
irregular and nodose. Normal bone develops in the skull and face in 
the connective tissue. In rickets the lime salts are either not deposited, 
are insufficiently deposited (craniotabes) or overdeposited as bosses 
(osteosclerosis). The essence of this inflammation or dystropy is undue 
hyperemia and irregular, deficient calcification; which one is primary 
remains a disputed point; the bones may contain but 20 to 30 per cent, 
of the normal amount of lime salts. 

2. General Symptoms. — (a) Muscular weakness is pronounced, as 
evidenced by impaired breathing, the tardy efforts to hold up the head 
and disinclination to walk; in this myopathia rhachitica there is a great 
reduction of the caliber of the muscle fibers, much nuclear multiplica- 
tion and increase of their longitudinal and decrease of their transverse 
striation. (b) Nutrition; there is anemia, sometimes with leukocytosis 
and often with emaciation, (c) Nervous system: Mentality is unim- 
paired; rhachitic patients frequently grind their teeth; spasmodic 
conditions are not infrequent, as generalized convulsions, tetany and 
spasm of the glottis, (d) Temperature always denotes complications, (e) 
Digestive disturbances are common; there may be anorexia, diarrhea, 
more commonly constipation and distention of the abdomen, from enlarge- 
ment of the liver and spleen, and possibly from thoracic changes. The 
amount of chalk in the feces may be increased. The spleen is enlarged in 
70 per cent., and, less often and less markedly, the liver. (/) Rickety 
children catch cold easily and bronchitis frequently leads to atelectasis 
and bronchopneumonia, (g) The heart may be luxated from the altered 
thoracic conformation, which frequently causes hypertrophy of the right 
ventricle, (h) Eczema is common. 



RICKETS 745 

Course, Complications and Prognosis. — (a) The onset is insidious and 
the clinical course covers a year or more. (b) Complications include but 
few of immediate danger, as bronchitis, pneumonia and spasm of the 
glottis. Later complications include the contracted rhachitic pelvis of 
obstetrical importance, kyphosis and pulmonary tuberculosis, which 
is found in 36 per cent, of the fatal cases; its early diagnosis depends 
largely upon auscultation, for percussion is peculiarly deceptive when 
the chest is deformed. (c) The prognosis is, with these exceptions, 
excellent as to life, and with care, as to deformity, for deformities 
may regress. 

Diagnosis. — The diagnosis is based chiefly upon the bone changes. 
Errors are possible from precipitate diagnosis, based on the prodromal 
phenomena, (a) Barlow's disease (q. v.), misnamed acute rickets, has 
no connection with it. (b) Syphilis predisposes to rickets but is other- 
wise distinct and separate; it usually develops at a time (first to sixth 
month) when rickets is most uncommon and is usually stamped by other 
syphilitic stigmata, as cutaneous and mucous syphilides ; when it invades 
the epiphyses, the femur is usually its seat, and between the cartilage 
and bone, the wall-like, very tender, painful and doughy swelling is rather 
fusiform, compared with the rounder rhachitic nodes; epiphyseolysis 
may occur in syphilis, but never in rickets; in doubtful cases an ex 
juvantibus diagnosis and the sero-test may be made, (c) Vertebral tuber- 
culosis is easily distinguished; the rhachitic kyphosis is arcuate, not 
angular. 

Treatment. — 1. Hygiene. — Fresh air and sunlight produce wonderful 
results, particularly in the country, mountains or at the sea-side. 

2. Dietetic. — In nurslings (who seldom develop the disease), a wet- 
nurse may entirely cure the disease. In older children it may be less a 
question of food than of digestion. 

3. Medicinal. — No specific is known, but phosphorus is more impor- 
tant than any other drug. Under its use the child becomes easier and 
brighter; the nervous symptoms abate, as insomnia, convulsions, tetany 
or laryngospasm; the osseous symptoms are improved, bone is deposited 
and dentition occurs, both clinically and in experiments. Phosphorus 
itself is given in doses of gr. 2-q ioo m piU form or as the ol. phospho- 
ratum (1 per cent, solution) Hftj, t. i. d., or better, in 1 per cent, cod-liver 
oil; the oil or emulsion should be freshly prepared, for both deteriorate 
readily on exposure to light. (Its toxic symptoms are fever, thirst, 
anorexia and weakness; vomiting of food, mucus, bile, later blood and 
sometimes phosphorescent material; abdominal pain, diarrhea or con- 
stipation, phosphorescent, clay-colored or bloody feces; jaundice; the 
liver at first may be large, but becomes small; there may be cholemia; 
albumin, bile, casts, leucin and tyrosin in the urine and hemorrhages 
from the uterus, abortion or miscarriage and bleeding from other sur- 
faces.) Cod-liver oil was recommended by Bretonneau in 1827; if it is 
well tolerated by the stomach, the general level of health may be 
elevated by its use; if not, cream and butter should be given. Iron 
is a good tonic. It is proved that a sufficient quantity of calcium 
salts is present in the food. 



746 CONSTITUTIONAL DISEASES 

4. Orthopedic. — During the florid stage the child should be kept 
quiet upon a firm mattress and off his feet. Later, corrective measures 
are indicated for the kyphosis and deformity of the limbs. 

OBESITY. 

Etiology. — Obesity (adiposity, corpulence or polysarcia adiposa) is 
favored (a.) by heredity; it frequently occurs in entire families; con- 
genital cases are known; (b) by mode of life, e. g., lack of exercise, over- 
eating and alcoholic indulgence, (c) The menopause is frequently attended 
by increase in weight, (d) Diseases of the thyroid or hypophysis or 
nervous or osseous system; and gout, diabetes, anemia, valvular dis- 
ease and emphysema, which act rather by preventing adequate exercise 
than by deficient oxygenation. 

Symptoms. — The general habitus requires no description. Fat develops 
in the subcutaneous tissues, in parts where it is normally found, as in 
the omentum and around the kidneys and it may cause fatty infiltration 
and degeneration of all internal organs excepting the brain and spleen; 
even the blood may contain fat (lipemia). 

1. Cardiac. — The heart is embarrassed by increased resistance to 
the capillary flow, fatty infiltration of the myocardium, and fat accu- 
mulation in the chest wall, omentum and mediastinum. The pulse is 
more often frequent than slow. Hypertrophy may occur. Edema is not 
uncommon. 

2. Respiratory. — The breath sounds and heart tones are faint and 
thoracic percussion is difficult because of the subcutaneous fat. Bron- 
chitis is common and probably results from the ready sweats and conse- 
quent chilling. Dyspnea may occur on exertion. 

3. Digestive. — Digestive disturbances may develop. The large liver 
is less frequently fatty than congested and hypertrophic. Constipation 
and hemorrhoids are frequent. 

4. Urinary. — The urine may be scanty in oxaluric, lipuric, lithuric, 
albuminuric or glycosuric subjects. Actual impotence is not uncommon, 
as well as mechanical obstacles to coitus. 

5. Lessened physiological resistance to infections, surgical measures or 
phlebotomy, and (6) such associated affections as diabetes, gout, calculous 
disease and less often contracted kidney, arteriosclerosis and apoplexy 
may be noted. 

Treatment. — Treatment is (a) that of the fundamental condition and 
(6) dietetic. The various "cures" enumerated possess more than his- 
torical interest — (i) Banting's cure. Banting, a merchant, was treated 
so successfully by Wm. Harvery for obesity that he addressed a " Letter 
to the Public on Obesity" (1863). This diet, largely albuminous, consisted 
of fish, meat, eggs, tea without sugar or milk, vegetables, fruit, some red 
wine and toast without butter. It may cause indigestion, nervousness, 
palpitation or gout, (ii) Ebstein, himself a sufferer, proposed (1872) 
a diet with larger proportions of fat; his diet consisted of meat, fish, 
eggs, tea, leguminous vegetables, fruit, fats and butter, but restricted 
the carbohydrates; digestive disorders may also occur under this system. 



ADIPOSIS DOLOROSA OR DERCUM'S DISEASE 747 

(iii) Oertel allowed more carbohydrates, limited the fats and fluids and 
insisted upon sweats and graduated exercises. From the following it 
will be seen that all these methods are " starvation cures" The 
average man requires 118 gm. of nitrogen, 56 gm. of fat and 500 gm. 
of carbohydrates, equaling 3054 calories. 

The diet of Banting contains 172 gm. of nitrogen, 8 gm. of fat, and 
81 gm. of carbohydrates, equaling 1112 calories. 

The diet of Ebstein contains 102 gm. of nitrogen, 85 gm. of fat, and 
47 gm. of carbohydrates, equaling 1401 calories. 

The diet of Oertel contains 183 gm. of nitrogen, 38 gm. of fat, and 143 
gm. of carbohydrates, equaling 1690 calories. In any reduction-cure 
the patient may suffer from breaking-down of the body proteids, which 
causes the weakness. In all cases the total amount of nitrogen in the 
urine, which constitutes 90 per cent, of the nitrogen excreted, should be 
watched; if more is excreted than ingested the nitrogenous food should 
be increased to obviate muscular and cardiac weakness. The diet then 
should consist of moderation in all foods, with restriction of the carbo- 
hydrates, whose easy reduction into water and carbonic acid spares the 
tissue waste. Alcohol should be forbidden. Beer contains not only 3 to 
5 per cent, of alcohol, but double this percentage of soluble starch and 
dextrin. The fluid ingested should be reduced to 2 or 3 pints daily. A 
milk or vegetable diet is sometimes successful. 

(c) Active and graduated exercise is indispensable, except in marked 
cardiac disease (v. Fatty Heart, Myocarditis and Dilatation). 

{d) The patient should sleep not more than seven hours and should 
bathe daily to avoid skin complications and to promote perspiration. 
Thyroid extract is not to be taken, unless thyroid insufficiency is sus- 
pected, for it breaks down the albumins rather than the fats. 

ADIPOSIS DOLOROSA OR DERCUM'S DISEASE. 

This dystrophy was described by Dercum (1888), as a "disorder 
characterized by unequal symmetrical deposits of fatty masses in various 
parts of the body, preceded or attended by pain." There were only 50 
reported cases up to 1909, most of which were females. It develops in 
middle life, chiefly after the fortieth year. 

Pathology. — In the 8 autopsies the thyroid gland was affected in 7 and 
the hypophysis in 5. In the cases of Dercum and Burr an interstitial 
neuritis was found, which is likewise noted in the fatty tumors removed 
during life; symmetrical lipomatosis has been observed in multiple 
neuritis. 

Symptoms. — Two cardinal clinical features are observed, as the term 
adiposis dolorosa indicates: (1) The obesity is either diffuse or is local- 
ized fatty tumors or both in combination; lipomata, from the size of a 
pea to large dimensions, occur on the trunk and proximal parts of the 
extremities, but never on the face, forearms, hands, legs or feet. Indeed 
the thinness of the wrists and legs contrasts sharply with the massive 
body, thighs and upper arms. The pendulous abdominal fat may hang 
down like an apron. In one of the author's cases the localized abdominal 






748 CONSTITUTIONAL DISEASES 

fat resembled a circular life-buoy, sagging down over the thighs. In 
another it almost resembled myxedema, save for its circumscribed dis- 
tribution and facial exemption. (2) The pains may be neuralgic or 
paresthetic. 

Subcutaneous hemorrhages, hematemesis, epistaxis and metrorrhagia 
are not uncommon. The patients are often nervous, perhaps hysterical 
and lack initiative. In the later stages epilepsy has developed and 
death from asthenia, psychoses, nephritis or intercurrent affections is 
recorded. A number of cases improved under thyroid extract. 



SECTION IX. 

DISEASES OF THE NERVOUS SYSTEM. 



DISEASES OF THE BRAIN. 

CEREBRAL LOCALIZATION. 

Autopsy findings in carefully studied cases, animal experimentation 
and constantly increasing surgical intervention have developed the 
nature of lesions and important results regarding their localization. The 
doctrine of Flourens that all parts of the brain were equally important 
met its first contradiction in Broca's discovery (1861) that motor aphasia 
was due to disease of the third left frontal convolution. In 1870 Fritsch 
and Hitzig discovered that stimulation of certain areas, now known as 
the motor cortex, resulted in contraction of definite muscles of the oppo- 
site side of the body. Since then Bevor, Horsley, Meynert, Jackson, 
Flechsig, Ferrier, Munk, Glotz, Nothnagel, Charcot, Wernicke and 
others contributed to the development of brain localization. 

I. The Motor Cortex. — This embraces chiefly the central convolutions 
on either side of the fissure of Rolando (the ascending frontal and ascend- 
ing parietal lobes and anterior two-thirds of the superior parietal lobe), 
the foot of the three frontal convolutions and on the inner surface 
of the hemisphere, the paracentral lobule. In this area lie the large 
pyramidal cells which Betz discovered were the origin of the motor or 
pyramidal tracts. The centres run somewhat into adjacent areas, espe- 
cially those with physiological associations. The leg centre occupies the 
upper quarter of the ascending frontal and ascending parietal convolu- 
tions and part of the superior parietal lobe (all adjacent to the longitudinal 
fissure) and passes over to the inner aspect of the hemisphere to the 
paracentral lobule, which is the centre for the thigh, pelvis and gluteal 
muscles (Fig. 50). A lesion in the falx cerebri or dura near the longi- 
tudinal fissure may, in rare cases, involve both leg centres and produce 
cerebral paraplegia, although most paraplegias are spinal in origin. The 
arm centre is the largest, covers the middle two quarters of the central 
convolutions, lies below and somewhat overlaps the leg centre. In Fig. 
51 it is seen that there are certain general as well as separate centres 
for the thumb and fingers. The head centre is below the arm, covering 
the lowest quarter of the central convolutions (the entire operculum), 
the upper part of the Sylvian fissure, the posterior part of the lowest 
frontal convolution and possibly the first and second frontal gyri. The 



750 



DISEASES OF THE BRAIN 



face centre lies directly beneath the arm centre, and is mostly located 
on the anterior ascending convolution, the upper facial component lying 
higher than the lower facial centres. The eye centre of the facial is 
bilateral, probably consisting of several foci. The mouth has several 
centres. The motor speech area is principally in the lower left frontal 
gyrus and is probably the chief centre for chewing. The trunk centre 
lies in the posterior part of the first frontal convolution and also on its 
median aspect, just anterior to the paracentral lobule; there is a trunk 
representation between the leg and arm centres and a neck centre between 
the arm and face. The more complicated the function, the larger is the 
centre (as for the tongue, fingers, mouth) and the more unilateral the 
localization in the brain. Muscles used rhythmically or in pairs are 




Fig. 49. — General distribution of centres in cerebral localization; outer surface of brain. 



supplied from both hemispheres, as the muscles of the forehead and 
respiration or swallowing and to some degree the legs and trunk. Pro- 
trusion of the tongue to one side has a monolateral centre, though its 
protrusion in the median line and its withdrawal depend on both 
hemispheres. 

Total lasting hemiplegia of the opposite side of the body, with sensory 
disturbance, aphasia and intellectual disturbance, results from complete 
destruction of the entire motor cortex of one side. Cortical hemiplegia 
is less common than monoplegia (paralysis of one member) which always 
suggests a cortical lesion., Crural monoplegia is rare and is due largely 
to vascular lesions in the paracentral lobule (anterior cerebral artery). 
Brachial monoplegia may result from vascular lesions, tumors or trauma; 



CEREBRAL LOCALIZATION 



751 



the finest selection, as of the thumb alone, fingers or wrist, is noted. 
Sensory disturbance is common (v. i.). Pure facial monoplegia is 
unknown, although a faciolingual form with motor aphasia is observed. 
Associated monoplegia is more usual, most commonly paralysis or paresis 
(partial paralysis) of the arm and face (brachiofacial monoplegia, although 
strictly not a monoplegia). Next in frequency is the arm-and-leg type 
(brachiocrural) in which two contiguous centres are involved. A leg- 
and-face type never occurs, because their centres lie too far apart. A 
lesion involving one part after another speaks for cortical localization. 
Cortical paralyses are not attended by the reaction of degeneration. In 
cortical lesions with paralysis, twitchings or convulsive movements are 
common, "cortical, partial or Jacksonian epilepsy;" the lesion partly 
destroys the motor cortex (paralysis) and at the same time causes irri- 
tation (convulsions) precisely as contractions are produced in animals 




Fig. 50. — Cerebral localization; inner surface of hemisphere. 



by electrical stimulation of the cortex; they are mainly (a) mechanical, 
as irritation or increased intracranial tension (50 per cent, of cases are 
rapidly growing tumors), or (b) vascular (hemorrhage, embolism or 
inflammation); stationary lesions rarely produce Jacksonian epilepsy 
unless they are located in the cortex. The spasms may involve but one 
part (monospasm), as the arm, exclusively a sign of cortical irritation, 
or they may pass from one centre to others. They always commence 
in one centre and proceed in a fixed order; if the arm region is the seat 
of a tumor the Jacksonian epilepsy flexes the fingers, moves the thumb, 
then the forearm, arm and shoulder and then passes down the cortex 
region, so that it involves the face, mouth and finally the leg (see Fig. 49). 
If the lesion is in the face area, the various facial muscles contract and 
the eye deviates, then the next area above participates, and finally the 
higher leg centre is implicated. That is, the spasm never skips over a 
centre. 



752 



DISEASES OF THE BRAIN 



The spasms are often preceded by a tingling in the part and are mostly 
clonic, or clonic broken by tonic spasms. Consciousness is maintained, 
unless the fits reach the other side, are very frequent or the lesion is 
deep, below the cortex. The opposite side is involved through the 
commisural fibers of the corpus callosum. Jacksonian differs from 
regular epilepsy in that no cry is observed, the commencement is local 
and more gradual and consciousness, if lost, disappears gradually, not 
precipitately. The seizure lasts several seconds to a minute or two and 
is followed by some vertigo, nausea, stupor or disturbance of speech; if 
spasms occur without paralysis, paresis in the involved parts follows, 



HEAD TO OPPOSITE SIDE 



HEAD AND EYES TO 
OPPOSITE SIDES 



TO MID LINE. 
CHEWING 



ASSOCIATED 

MOVEMENTS 

OF EYES 




FINGERS_ALONE 



THUMB_ALONE 



FISSURE OF ROLANDO 
Pf FISSURE OF SYLVIUS 

Fig. 51. — Cerebral localization in detail: F\, Fz, Fs, first, second and third frontal con- 
volutions; A.F., ascending frontal convolution and A. P., ascending parietal convolution; 
S.P., supramarginal and A.R., angular convolution; 0\, O2, O3, first, second and third occipital 
convolutions; Ti, T2, Tz, first, second and third temporal convolutions. The explanation 
of line A', A is given under Internal Capsule. 



due to transient exhaustion of the cortex. Jacksonian epilepsy in its 
lightest forms may be sensory. 

Regarding sensory localization in the cortex, Munk held that the 
sensory and motor areas are the same (v. i.). Vasomotor disturbance 
is common in cortical lesions. 

After total lesions of the central convolutions, the hands improve 
very little in adults; other members improve, to some extent, through 
assumption of function by the sound side of the brain; in young indivi- 
duals the sound pyramidal tracts in the cord may hypertrophy to double 
their size. The motor fibers running from the pyramidal cells of the cortex 
to the anterior horns of the spinal cord, constituting the upper motor 



CEREBRAL LOCALIZATION 753 

neurone, undergo descending degeneration, that is, degeneration in the 
direction of the motor impulse. 

II. The Cortex of the Parietal Lobes.— Our knowledge of function 
is less definite, (a) Lesions of the first lobe (Pi, Fig. 51, the precuneus 
in Fig. 50), supplied by the anterior cerebral artery, cause disturbance 
in motility of the leg, with altered muscle sense, " mind-blindness/ ' 
inability to read (alexia) and perhaps hemianopsia. (6) Disease of the 
supramarginal convolution (S.P., Fig. 51), also involving the motor cortex, 
produces greater disturbance of sensation than when the lesion is con- 
fined to the motor centres; muscular sense is disturbed, usually with some 
motor paralysis or paresis. Muscle sense is disturbed in 23 per cent, of all 
cases of cerebral hemiplegia; in more than 50 per cent., no special sensory 
disturbance is noted. There may be loss of the stereognostic sense, 
whereby the patient fails, when his eyes are closed, to recognize the 
geometric form of solid objects, as a key or ball. Cortical ataxia some- 
times results, on account of disturbance in the association fibers. It 
differs from the tabetic and cerebellar ataxias in that the muscular 
strength is usually diminished and the finer movements impossible. 
Cortical hemianesthesia is not frequent, (c) Ptosis and paralysis of 
the orbicularis palpebrarum are said to result from lesions of the gyrus 
angularis (A.R., Fig. 51) and also inability to read (alexia), optic aphasia 
and "mind-blindness." Wernicke diagnosticated softening in this lobe 
by conjugate deviation of the eyes and head. Disease of the posterior 
inferior part probably causes crossed amblyopia. 

III. The Cortex of the Occipital Lobes. — The visual centre lies in 
the cuneus (Fig. 51) and the first occipital lobe. A lesion produces 
(a) bilateral homonymous hemianopsia (see Affections of the Optic 
Nerve), (b) Hemichromatopsia, an homonymous color-blindness, in 
which the lesion is superficial and anterior; (c) total cortical blindness, 
if the lesion is bilateral or both optic radiations are destroyed, (d) 
"Mind-blindness" results from a lesion in the anterior outer surface of 
the left occipital region, especially the second occipital lobe or of the 
gvrus angularis. The visual memory is lost; things actually seen are 
misinterpreted and the patient confuses persons and things, (e) Alexia, 
inability to read, also called "word-blindness," wherein the patient can 
read but fails to understand the letters or words he reads. His memory 
for words is lost. It is due to destruction of the subcortical association 
fibers in the second occipital lobe and the gyrus angularis; it most 
commonly follows vascular disease. (/) Optic aphasia results from foci 
in the left occipital lobes (and also in the angular and supramarginal 
convolutions) and consists of misinterpretation of visual impressions, 
so that the patient miswrites and misnames objects seen, though able 
to name them when he feels them. 

IV. The Cortex of the Temporal Lobes (T u T 2 , T 3 , Fig. 51).— The 
outer surface of the posterior half of the first (and second) temporal 
convolution is the auditory centre; disease in this cortex produces (a) 
deafness in the opposite ear; atrophy of this lobe is encountered in con- 
genital deafness. Deafness is usually transitory, fibers passing to both 
ears from each centre. If this lobe is destroyed on both sides, total 

48 



754 DISEASES OF THE BRAIN 

deafness results, (b) Conjugate deviation of the eyes is said to be a reflex 
from auditory impressions, (c) Disease of the first temporal lobe pro- 
duces "word-deafness" or " mind-deafness," a loss of the comprehension 
of speech. In the uncinate gyrus (Fig. 50) the special sense of smell 
probably has its centre. The gyrus fornicatus (Fig. 50) is said to be the 
centre for taste and pain. 

V. The Frontal Cortex and Aphasia. — Regarding the frontal lobes 
anterior to their participation in the motor cortex, profound disease may 
exist without clinical symptoms. They have long been thought to be 
the residence of (a) the psychical functions, especially for ethical and 
abstract thought (Meynert and Flechsig). " Defect in character" fol- 
lowed the passage of a large crowbar, 1J inches thick and 3 J feet long, 
through both frontal hemispheres, in Harlow's famous case, (b) Flechsig 
considers the frontal lobe the anterior association centre, the middle one 
being the cortex of the island of Reil and the posterior one the large area 
posterior to the motor cortex, (c) The motor speech area lies in the lower 
frontal convolution. The history of aphasia marks the beginning of 
cerebral localization; Bouillaud, in 1825, referred aphasia to the frontal 
lobes; Dax, in 1836, narrowed the localization to the left frontal region 
and the motor centre was finally confined to the posterior part of the 
lower left frontal convolution in 1861 by Broca, whose name is given to 
this convolution. The sensory element, necessary to all voluntary move- 
ments, was unknown until later, when Meynert and Wernicke (1874) 
discovered the auditory centre in the first temporal convolution; Wer- 
nicke localized "word-deafness" in the same convolution of the left side 
and Naunyn referred disturbance of writing, visual aphasia, etc., to the 
gyrus angularis and adjacent parts of the occipital lobes. 

Motor Aphasia. — The motor speech centre in Broca' s lobe controls the 
motor centres next described and retains the impressions or memories 
necessary to their exercise. The corresponding lobe on the right side is 
the actual centre in left-handed persons and often assumes the functions 
of the left speech centres after disease of the latter, especially in children. 
Articulate speech depends upon the integrity of the lower part of the 
ascending frontal convolution, in which lie the centres for the mouth, 
lips, tongue, jaw and larynx, (a) These constitute the cerebral mechanism 
of speech, whose disturbance is designated motor aphasia. Motor fibers 
run from the cortex through the centrum ovale, internal capsule and 
cms to their nuclei in the pons and medulla, whence the peripheral bulbar 
nerves to the tongue and larynx take their origin, (b) These lower 
tracts constitute the bulbar mechanism of speech, disease in which causes 
abolition of articulation (anarthria) or more often, imperfect articula- 
tion (dysarthria). To speak, the individual must have ideas, conceptions. 
To illustrate, a cortical lesion in Broca's convolution, as small as a hazel- 
nut, may produce motor aphasia, either absolute or partial; the patient 
may pronounce correctly some few words, possibly only under emotion 
or in certain relations, or he may pronounce words wrongly, although 
he recognizes his mistake. He comprehends what is said to him, for 
the lesion involves no special sense element. He can read writing and 
print, especially if educated, because "sight may stimulate images with- 



CEREBRAL LOCALIZATION 755 

out intervention of the motor centre/' but he cannot speak voluntarily 
nor repeat what is said to him ; he cannot read aloud ; as a rule he cannot 
write (agraphia), because impulses cannot pass to the hand centre. He 
may be able to copy. The cortical is the usual form of motor 
aphasia. 

A subcortical lesion in the centrum ovale may sever the fibers between 
Broca's convolution and the motor cortex for the tongue, lips, etc. The 
patient cannot speak, but the speech centre is normal, and he can write. 
This pure motor aphasia is a rare lesion. It involves the commissural 
fibers of the corpus callosum to the right side and produces permanent 
aphasia, because compensation by the right hemisphere is precluded; 
if the lesion is in the internal capsule, aphasia is transient (compensation 
through the corpus callosum). 

Sensory Aphasia. — In speech sensory relations and memories are neces- 
sary — hearing, sight, taste and, in the blind, touch. 

Auditory Aphasia. — Hearing is most important and develops in the 
child long before speech. When a child begins to talk, or when one who 
has lost speech relearns it, the brain cortex, through an association of 
centres, learns to connect certain sounds or words with definite objects; 
through the auditory nerves which run from each side to both auditory 
centres in the first temporal convolution of either side, he hears mechan- 
ically, as we may hear without understanding a foreign language, and 
learns to associate the sounds with objects, conditions or ideas, for which 
an auditory speech centre in the left first temporal convolution (in right- 
handed persons) is developed. Remembering a sound he has heard 
but perhaps has never spoken, the child calls into play Broca's con- 
volution, the cortical centres for the lips, tongue, etc., and speaks. Hear- 
ing is necessary to articulate speech, unless, as in deaf-mutes, education 
replaces, by sight and touch, the associations usually acquired by hearing. 
Destruction of the auditory speech centre profoundly disturbs speech. 
The patient then hears by the auditory nerves and centres or reads by 
the visual apparatus, but does not understand what he hears or reads, 
sensory {auditory) aphasia or tvord-deafness; recovery is more common 
than in motor aphasia. The subject in speaking transposes words (para- 
phasia) but does not realize his mistakes, an important distinction from 
motor aphasia. Often he later becomes speechless. He cannot repeat 
words, write from dictation, or revive words. Writing is impossible, 
but copying of words is sometimes maintained. 

Subcortical auditory aphasia or pure word-deafness (the rarer subcor- 
tical form), results from disease between the auditory speech centres and 
the two centres for hearing. Auditory impressions cannot reach the 
auditory speech centres of the patient, who cannot understand what 
is said, cannot repeat or write from dictation, but can read, speak and 
write, as the auditory speech centre is normal. 

"Amnestic'" aphasia may be a simple difficulty in recalling certain 
words in speaking or writing, or it may be very pronounced (word-deaf- 
ness). It is also poorlv called conduction aphasia (Wernicke) and is 
due to interruption, probably in the island of Reil, of the fibers between 
the motor and sensory speech centres. 



756 DISEASES OF THE BRAIN 

Visual Aphasia. — Sight is very important in sensory speech. The 
child who has learned and is able to speak words, reads by associating 
the sounds heard and spoken, with words, letters or symbols seen by him. 
While in most individuals mental processes are carried on by the memory 
of words, in rare instances visual memory may be more important. 
Destruction of the angular and supramarginal convolutions by causing 
a loss of the visual memories produces alexia, word-blindness, an inability 
to read. In some cases the patient can read, but without understanding. 
He usually cannot write (agraphia) and cannot copy, but can speak fairly 
well and understand what is spoken. If the optic centre in the occipital 
lobes is intact he cannot name objects after seeing them, since the visual 
memory centre is destroyed, but may recognize a watch by hearing it 
tick or by feeling it. Lesions just below the visual memory centre, 
involving the afferent fibers, produce pure subcortical word-blindness, or 
alexia, with hemianopsia and preservation of voluntary speech and 
writing. Word-deafness and word-blindness often coexist; 41 instances 
of congenital word-blindness were collected by McCready. 

Pure are less common than complicated forms. The anatomical lesions 
are largely the result of softening, the entire sphere of speech being sup- 
plied by the artery of the fossa of Sylvius. Motor aphasia is likely to 
occur, with disease of the motor cortex or cerebral pyramidal tracts, and 
the sensory form with disease of the optic fibers. Apoplexy, trauma and 
in children tuberculosis of the brain or meninges are also causative. 
Lasting aphasia in children is usually due to mental causes, since the 
right frontal area usually takes up the function of Broca's convolution. 
Congenital aphasia may follow bilateral meningeal hemorrhage. Aphasia 
also occurs in idiocy, melancholia, migraine, convulsions and from 
functional causes in children, as from fever, fright, worms, etc. In 
adults the outlook is less favorable; reeducation may yield fair results. 

VI. Centrum Ovale. — Focal symptoms may be entirely absent, if a 
lesion occur between the associative, commissural, motor or sensory 
fibers (corona radiata). A lesion must be (a) very near the cortex to 
produce Jacksonian or general convulsions. A monoplegia, hemianopsia 
and subcortical aphasia may occur in this location. A lesion in the 
island of Reil may produce conduction aphasia. Psychic symptoms may 
result from interruption of the association fibers which run from one 
part to another of the same hemisphere or commissural fibers running 
from one hemisphere to the other, as through the corpus callosum. 
(6) Internal capsule symptoms result from lesions low in the centrum 
ovale. 

VII. The Internal Capsule. — It is compacted and consists of nearly all 
the motor, sensory and special sense fibers between the brain and the 
lower parts. The capsule is divided into an anterior limb, the knee and 
a posterior limb. 

Anterior Limb. — It contains fibers from the frontal cortex to the optic 
thalamus and fibers which, in lower horizontal sections, run into the knee 
and are found in the basal median bundle of the crus, whence they run 
to the pons nuclei for the eye, head, neck and probably larynx, tongue 
and mouth. Lesions here are very rare. 



CEREBRAL LOCALIZATION 757 

Knee. — The knee (see Fig. 52) contains from before backward fibers 
for opening of the eyes, associated movements of the eyes and head, 
the tongue and mouth and phonation fibers for speech, probably including 
those of the larynx. 

Posterior Limb. — The posterior limb contains motor fibers in its anterior 
and middle thirds (v. Fig. 52); in its posterior third (Charcot's "sensory 
crossway"), those for sensation and the special senses. The number 
of fibers to a muscle depends less on its size than on its fineness of move- 
ment; e. g., the fingers receive a large number. If a ruler be placed 
anterior to the line {A' , A) in Fig. 51 and slowly moved to the right, pre- 
serving its parallelism, the cortical motor areas touched will approxi- 
mately correspond with their order in the internal capsule. The most 
common sequence of lesions of the internal capsule is cerebral hemiplegia 
of the opposite side of the body. Though hemiplegia may result from 
lesions elsewhere, in the vast majority of cases, hemiplegia is the result 
of disease of the internal capsule. If the latter is destroyed, total hemi- 



Fig. 52. — Localization in internal capsule. 

plegia results, paralysis of the arm, leg and lower part of the face (the 
upper part of which and the head escape because they have a bilateral 
supply from both hemispheres). The hypoglossus is but moderately 
involved and aphasia is usually temporary. There is also associated 
hemianesthesia, hemianopsia and unilateral disturbance of smell, taste 
and hearing, by lesion of the fibers ascending from the tegmentum; with 
hemiplegia are observed contractures, descending degeneration, decrease 
or absence of the skin reflexes, especially the cremasteric, and increase 
of the tendon reflexes. Monoplegia is rare, because the tracts are so 
compact; a linear lesion may involve the outer part of the capsule's 
knee, affecting the face and leaving the arm free. Hemianesthesia (skin 



758 DISEASES OF THE BRAIN 

sensation and muscle sense) rarely exists without some paresis of the 
leg. Some tingling or, in incomolete lesions, some pain may result, for 
some sensory fibers course with the motor fibers. Hemitremor, -athetosis 
and -chorea result from lesions of the sensory area, usually associated 
with disease in or just below the optic thalamus. Disease back of the 
general sensory tracts may injure the optic radiation (running between 
the occipital sight centre and the lateral geniculate body) or interrupt 
the auditory and other special sense fibers. Psychical disturbance, 
aphasia, alexia, agraphia and involvement of any cranial nerve are not 
symptomatic of disease of the internal capsule. 

VIII. The Corpus Striatum. — This is composed of the caudate and 
lenticular nuclei. The lenticular nucleus is extensively connected with 
the superior peduncle of the cerebellum and the tegmentum of the cms. 
The caudate nucleus is connected with the internal capsule and the crus; 
these fibers seem to end in the pons and cerebellum. Nothnagel held 
that hemiplegia is permanent only when the internal capsule is injured, 
but Landouzy reports a case of contralateral hemiathetosis from isolated 
disease of the lenticular nucleus. 

IX. The Optic Thalamus. — This is surrounded by gray matter, con- 
tinuous with that surrounding the third ventricle and central canal of 
the cord and is connected by fibers with all parts of the cerebral cortex, 
the tegmentum and superior cerebellar peduncle. Nothnagel (1879) 
first described its topical symptomatology. The following findings are 
observed, alone or in combination: (a) Contralateral hemianopsia may 
develop from a lesion in the posterior part of the thalamus, the pulvinar 
or a lesion which also invades the lateral geniculate bodies. These 
areas are connected by the optic radiation with the optic centre. This 
hemianopsia is distinguished from that caused by a cortical lesion by the 
hemianopsic pupillary reaction and the absence of the marginal field of 
vision, (b) Disturbance of the mimetic movements of expression may 
develop (Nothnagel, Bechterew). The optic thalamus is the reflex 
centre of the involuntary movements of expression, as weeping or laugh- 
ing. A patient with hemiplegia from destruction of the left internal 
capsule cannot voluntarily move the lower right part of the face, but 
the paralyzed portion of the face moves when the patient laughs, for the 
centre is in the posterior part of the thalamus. On the other hand, in 
isolated thalamic disease, the opposite side — indeed both sides of the 
face — can be voluntarily moved, since the facial nerve runs in the internal 
capsule, but the patient cannot laugh or weep, (c) Sensory disturbances 
may occur, such as hemianesthesia, hemichorea, hemitremor, hemi- 
hyperalgesia or hemiataxia (involvement of the internal capsule?). There 
may be vasomotor changes, atrophy and disturbance in the evacuation 
of the bladder and rectum (v. Thalamic Syndrome, page 794). 

X. The Corpora Quadrigemina. — There is variance of opinion regard- 
ing the function of these masses of gray matter whose fibers lie over the 
aqueduct of Sylvius and the tegmentum. 

Disease of the anterior corpora quadrigemina produces (a) moderate 
involvement of sight, of greater localizing significance if there is no optic 
neuritis. These bodies are connected with the external geniculate bodies 



CEREBRAL LOCALIZATION 



759 



and, by way of the internal capsule, with the optic radiation, (b) In 
acute lesions, narrowing of the pupil is suggestive. In old lesions, one 
or both pupils are wide and without reaction to light or accommoda- 
tion, (c) The eye muscles may be partially paralyzed (ptosis and upward 
movements) but are not pathognomonic, because the lesion is so near 
the nucleus of the third nerve. Disease of the posterior corpora quaclri- 
gemina may result in (a) ataxia; some refer it to cerebellar disease, to 
connections with the cerebellum through the nucleus ruber or to disease 
in the fillet of the tegmentum; (b) trochlearis paralysis, in which the 
eyes cannot be turned inward or outward; and sometimes abducens 
paralysis; (c) difficult mastication from involvement of the descending 
branch of the quintus; (d) contralateral disturbance of hearing, since 




Fig. 53. — Lesion in crus (shown by dotted lines), producing a superior alternating or 
crossed hemiplegia; the lesion involves the pyramidal tract (P.R.), the cranial nerves (tongue 
and face, C.R.) and the oculomotor nerve (IIIf) which is paralyzed on the same side as the 
lesion, while P.R. and C.R. are paralyzed on the opposite side. A.S., aqueduct of Sylvius; 
III, nucleus of third nerve; C.G.I., corp. geniculatum int.; F\, upper part and F2, lower 
part of fillet; N.R., nucleus ruber; S.N., substantia nigra. 



the post. corp. quadrigemina are connected with the fillet of the tegmen- 
tum and, by means of the "sensory crossway" of the internal capsule, 
with the hearing centre. 

XI. The Crus (Cerebral Peduncle). — The motor fibers to the cranial 
nerves decussate higher than the pyramidal tracts which decussate in 
the medulla; the fibers to the third nerve largely cross in the upper 
crus. Crossed paralysis (hemiplegia alternans oculomotoria superior) 
is common in crus lesions; it consists of a hemiplegia of the side of the 
body opposite to the lesion and a paralysis of the third nerve on the same 
side as the lesion, known as Weber's paralysis, though first described by 
Gendrin (Fig. 53); the oculomotor paralysis is peripheral, with strabis- 
mus, ptosis, inability to look up or down and a wide, reactionless pupil. 
This crossed or alternating hemiplegia is called superior because inferior 



760 DISEASES OP THE BRAIN 

alternating hemiplegia may occur in lesions of the pons. We distinguish 
whether the hemiplegia and paralysis of the third nerve occurred together 
(indicating a crus lesion) or whether the third nerve paralysis followed 
the hemiplegia (indicating a lesion near the internal capsule pressing 
secondarily on the oculomotorius) . 

A lesion in the tegmentum may cause (a) sensory disturbance, as hemi- 
anesthesia (skin sensation and muscle sense); such a lesion is in the 
fillet; hypesthesia (reduced sensation) is more common. (b) The 
special senses are sometimes involved, hemianopsia, or poor hearing in 
the opposite ear. (c) Ataxia, alone or with other symptoms, differs 
from the cerebellar type in that it is manifest only on motion. Involve- 
ment of the red nucleus produces cerebellar ataxia, (d) Oculomotor 
paresis on the side of lesion is characteristic when combined with crossed 
hemiataxia, hemiplegia or hemianesthesia. Fig. 53 shows how a teg- 
mental focus can rarely miss the diffuse nuclei of the third nerve. If the 
lesion is in the lower part of the .crus, the oculomotor paralysis is usually 
complete, but if in the tegmentum it is always partial, electing the pupil, 
the lid or the superior or internal rectus. 

XII. The Pons. — A small lesion, as a thin tumor, may give no local- 
izing symptoms. Lesions (commonly tumors, hemorrhage, softening or 
abscess) usually produce a typical picture: . From a lesion of the upper 
pons, i. e., above the facial nucleus, a hemiplegia results like that pro- 
duced by lesions of the internal capsule. (See Fig. 54, focus A.) The 
facial paralysis is supranuclear, partial and with no reaction of degenera- 
tion. In a focus in the lower pons (focus B, Fig. 54), where the facial 
fibers have already crossed, the tongue, arm and leg are hemiplegic 
on the side opposite to the focus and the facial paralysis is on the side 
of the lesion, hemiplegia alternans facialis, first described by Millard 
and Gubler. The facial paralysis is peripheral and nuclear, involves all 
branches and gives the reaction of degeneration. Other alternating 
paralyses are also observed, as hemiplegia with crossed paralysis of the 
third, fourth, fifth and sixth nerves, both nuclear and peripheral. Hemi- 
plegia may occur with conjugate paralysis of the lateral eye muscles, as 
the external rectus (abducens nerve) of one side, and the internal rectus 
(third nerve) of the other, due to a lesion just in front of the abducens 
centre, involving its fibers, or sometimes also including its nucleus. In 
the conjugate paralysis, the antagonist muscles pull the eyes to the other 
side and the eyes look away from the side of the lesion toward the paralyzed 
side. In this form even the paralyzed internal rectus will functionate 
and converge when one eye is tested at a time. Involvement of the 
motor branch of the fifth nerve produces difficult mastication. While 
alternating paralysis is the usual pons lesion, sometimes double hemiplegia 
occurs, or again, involvement of the third to seventh cranial nerves with- 
out hemiplegia. The auditory nerve is rarely involved, save in acute or 
very extensive lesions affecting the lateral lemniscus. Dysarthria and 
dysphagia, due to disease of the cortical motor paths of the hypoglossus 
and vagus, are less common in lesions of the pons than are affections of 
their nuclei in diseases of the medulla oblongata. Ataxia may result 
from involvement of the fillet. An alternating sensory paralysis may 



CEREBRAL LOCALIZATION 



761 



occur, as (a) hemianesthesia involving the muscle sense and cutaneous 
sensation of the extremities opposite the lesion, caused by disease of the 
tegmentum, and (b) an anesthesia of the fifth nerve on the side of the 
lesion. Irritative symptoms sometimes develop, as pain, paresthesia, 
painful convulsions of both arms or both legs, tonic and clonic spasms 
in the opposite arm and leg, contractures, paroxysms of coughing and 
trismus. The patient may "look toward the lesion" when the eye mus- 
cles are irritated (conjugate deviation). A tendency to fall toward the 
side on which the lesion is located is indicative of disease of the middle 
peduncle of the cerebellum. Aphonia, dysarthria and dysphagia are 
symptomatic of localization in the medulla (q. v.), especially when the 



PYRAMIDAL 
TRACT 




DECUSSATION OF PYRAMIDS 




B 

Fig. 54. — A illustrates a lesion in the upper pons, producing the usual hemiplegia (face, 
arm and leg paralyzed on the opposite side) . B illustrates a lesion in the lower pons, produc- 
ing alternating paralysis; all branches of the face (peripheral paralysis) and tongue on the 
side of lesion are paralyzed with paralysis of the contralateral arm and leg. 



hypoglossus is paralyzed, shows the reaction of degeneration and produces 
atrophy of the tongue. Glycosuria, albuminuria, disturbed respiration 
or heart action (vagus) and vomiting are other bulbar symptoms. Disease 
may cause paralysis of both arms and legs or rarely of one arm and the 
opposite leg (hemiplegia cruciata). 

XIII. The Cerebellum. — Physiology. — Physiologists admit the possi- 
bility of some psychical function. Its sensory relations are important, 
because of its reception of numerous fibers from the spinal cord, including 
the direct cerebellar tract and the posterior median column of Goll, of 
which it is an "end organ" (Luciani). It harmonizes the movements of 
the body, maintains equilibrium, conserves muscular strength and inhibits 



762 DISEASES OF THE BRAIN 

the contralateral cerebral motor cortex, i. e., it coordinates (a) the sensory 
impressions ascending from the spinal cord with (b) those gained by 
hearing (the auditory nerve having connections with the middle cerebellar 
lobe) and (c) probably with those impressions resulting from the eye 
movements. 

General Pathology. — Disease of a lateral lobe affects the same side of 
the body, but lesions of the middle (vermiform) lobe influence both sides. 
Krauss found, in 100 cases of cerebellar disease, tumors in 80 per cent., 
abscess in 10, cysts in 7 per cent, and softening, hemorrhage and agenesis, 
sclerosis and gliomatosis in the balance. Acute disease of the cerebellum 
produces symptoms more frequently than does chronic disease, in which 
latter the cerebellum or the cerebrum has opportunity for accommodative 
compensation; rapidly growing tumors, abscess and acute vascular disease 
often produce the following symptoms: 

Topical Symptoms. — 1. Cerebellar ataxia is almost always present and 
occurs when the patient stands; the body sways (static ataxia), as though 
the subject were trying to balance himself. Ataxia also occurs when the 
patient moves (dynamic ataxia) and concerns especially the trunk and 
legs. It is due to disease of the middle lobe or vermis and the consequent 
withdrawal from the cerebrum of the cerebellar coordination. The gait 
is that of an inebriate (demarche d'ivresse); the individual stumbles a 
zig-zag course sometimes toward the side of the lesion. The arm and 
hand movements are usually normal. In ataxia resulting from other 
cerebral localization (cortex, internal capsule and tegmentum) the 
incoordination affects the finer movements, is associated with disturbed 
muscle and stereognostic sense and very often with paresis. Bouillaud 
first described cerebellar ataxia and differentiated it from the tabetic 
type; cerebellar ataxia disappears when the patient is lying down and 
closing the eyes does not increase it (indeed it may often disappear). 
The affected limbs can be held steadily. 

2. Vertigo is very frequent and usually occurs rather when the patient 
sits than when he lies down; objects turn around him or he feels himself 
being turned. The vertigo is constant or paroxysmal and is due to lesion 
of the vestibular nerve which connects the semilunar canals with the 
cerebellum by the corpus restiforme. 

Secondary Symptoms.— The following are less significant than ataxia and 
vertigo : (a) Choked disk is rarely absent in cerebellar tumors and amau- 
rosis results from hydrocephalus internus with pressure on the chiasm. 
(b) "Forced" postures and movements are due to disease of the middle 
peduncle (cms cerebelli ad pontem). Constrained postures of the head 
and trunk are observed; one eye looks upward and inward, while the 
other is directed downward and outward. Forced movements consist 
of turning to one side, movement in a circle and a tendency to fall toward 
the side of lesion and sometimes backward, (c) Muscular weakness is 
frequent in animals and occasional in man, as hemiparesis on the side 
of lesion. The patient may not be able to rotate the trunk, straighten 
the body after bending or ,get up after falling, (d) The patellar reflexes 
are usually normal or increased, (e) Vomiting and pain in the head or 
neck are of some localizing value. (/) Occasionally the following develop: 



CIRCULATORY DISEASES OF THE BRAIN 763 

nystagmus, rhythmical contractions of the head, convulsions, paralysis 
of the cerebral nerves from pressure on the midbrain, disturbed hearing, 
intention tremor, muscular rigidity, irritability and weak memory. 

CIRCULATORY DISEASES OF THE BRAIN. 

I. Anemia of the Brain. — This term has been much abused. 
Etiology. — (a) General systemic anemia may result from cachexia and 

hemorrhages of medical, surgical or obstetrical nature, (b) Decreased 
blood supply, due to cardiac insufficiency, valvular stenosis, vessel stenosis, 
evacuation of an enormously distended bladder and tapping of pleurisy 
or ascites leading to paresis of the thoracic or abdominal vessels may be 
causal, (c) Capillary compression by hydrocephalus or tumors may 
produce anemia, (d) Local causes in the vessels will be considered under 
softening. Convulsions by pressure on one carotid are indicative of 
cerebral atheroma. 

Pathology. — The brain is pale, firm and dry and puncta vasculosa fewer. 
The fluid in the ventricles is often increased. 

Symptoms. — Local anemia of the brain leads to imperfect function, 
then loss of function and finally to necrosis, as in embolism or thrombosis 
(q. v.). In sudden general anemia after hemorrhage or fainting, the sub- 
ject becomes drowsy, syncope occurs and subsequent amaurosis, or ring- 
ing in the ears is frequent. The pupils at first contract from irritation 
of the third nerve and later dilate from its paralysis, a sign of danger. 
The skin is pale and clammy, the muscles lax and nausea frequent. 
Epileptiform convulsions often occur when much blood is lost. Anemia 
of the medulla causes the slow, sighing respiration and yawning. Death 
after syncope was called nervous apoplexy by the old writers. In grad- 
ually developing anemia symptoms develop, as described under Pernicious 
Anemia. Palpitation and thoracic oppression are common symptoms. 
The pulse varies in rate and rhythm. 

Marshall Hall described hydrencephaloid, a variety of cerebral anemia, 
seen in children suffering with acute diarrhea, and characterized by 
contracted and later dilated pupils, depressed, fontanelles, sunken face, 
pallor, early irritation followed by stupor or even coma. It may resemble 
meningitis from the strabismus. 

Treatment. — Treatment, diagnosis and prognosis are chiefly those of the 
cause. The anemia is treated by putting the patient in the recumbent 
posture and employing opiates, stimulation, coffee by rectum and 
enemata or subcutaneous infusions of salt solution. Firm bandaging of 
the extremities, sometimes called autotransfusion, is valuable. Nitro- 
glycerin is valuable in cases due to vasomotor spasm. 

II. Hyperemia of the Brain. — Andral (1836) described eight varieties, 
and when Trousseau, in 1861, referred some varieties to epilepsy and 
Meniere's disease, he drew down upon him the wrath of the entire 
Academy. The hyperemia in nephritis is usually uremic and the arterial 
fluxion once attributed to erysipelas is toxemic. When the vessels dilate 
from paralysis of the sympathetic system the rapidity of the capillary 
flow decreases, whence there is no hyperemia, but a lessened capillary 



764 DISEASES OF THE BRAIN 

flow, adiamorrhysis. When the vessels contract from sympathetic irri- 
tation, the brain is not anemic, but the capillary flow is accelerated, 
hyper diamorrhy sis . 

Etiology. — Active congestion results from cardiac overaction; overfilling 
of the brain vessels, as in stenosis of the isthmus of the aorta; contraction 
of the arterioles in other parts; dilatation of the brain vessels by alcohol, 
nitroglycerin, coffee, thyroidism, excessive brain work, neurotic states 
and insolation. In plethoric men with florid faces, thick necks and short 
thoraces, active congestion may cause fugitive brain symptoms. 

Passive congestion results from general venous stasis, as in valvular 
heart lesions, or local venous stasis, as sinus thrombosis. 

Pathology. — The brain may appear anemic after death by strangula- 
tion and may become congested after death because of its posture alone. 
The sinuses and veins are turgid and the color of the brain is darker. 
Microscopic examination shows distention of the capillaries or rupture 
into the perivascular lymphatic sheaths or brain. 

Symptoms. — In active congestion, chronic cause fewer symptoms than 
acute factors. Whether toxemic symptoms of the acute infections are 
due to hyperemia is an open question. Paroxysmal throbbing of the 
vessels, flushing, headache, delirium, sometimes nausea and fever are 
relieved by nosebleed and venesection. Irritability, spots before the 
eyes and ringing in the ears are said to occur. In progressive paralysis 
the transient pyrexia, heat in the head or coma is referred to congestion 
of the brain. 

Passive congestion, if gradual in onset, may be well tolerated or may 
produce stupor, dulness or delirium. If intermittent, as from coughing, 
there are a fulness in the head, headache and sometimes convulsions. 

Diagnosis. — Focal symptoms, as hemiplegia, indicate organic disease. 
Flushing, heat and pressure in the head, are most often neurasthenic 
or hypochondriacal. Marie and Leube never made the diagnosis of 
brain hyperemia. 

Treatment. — Active congestion is treated by elevation of the head, 
venesection in plethoric adults or in children by leeches over the mastoid 
bone, the veins of which connect with those of the brain; by free purga- 
tion, by 2 drops of croton oil, followed by concentrated salines, to draw 
the blood to the large abdominal vessels; by hot baths, to draw the blood 
to the periphery; bromides and vasoconstrictors, especially digitalis. 
Alcohol and opiates should be avoided; ice may be applied to the head 
and carotids; a fluid diet should be given. 

III. Edema of the Brain. — Etiology. — Edema of the brain results 
from the same causes as general edema: circidatory disturbances, as 
venous congestion in cardiac disease and the marantic group, including 
cachexia and nephritis. Collateral and inflammatory edema may develop 
around brain tumor, abscess or hemorrhage. Brain edema may develop 
in the death agony or when the brain shrinks, hydrops ex vacuo. 

Pathology. — The brain is pale, moist and glistening on section, the 
so-called "wet-brain." Tlje affection may be general or local; the ven- 
tricular and subarachnoid fluid is increased. The volume of the brain 
may be increased in the generalized form. 



CEREBRAL HEMORRHAGE 765 

Symptoms. — A diagnosis cannot be made between edema and decreased 
capillary velocity. When the edema is localized, transient focal symp- 
toms may develop, as unilateral convulsions or hemiplegia, or even crossed 
paralysis, observed personally in nephritis. Traube held that brain 
edema causes uremia, a view opposed by Cohnheim. Variability in the 
symptomatology of organic brain disease may be due to associated edema. 

IV. Cerebral Hemorrhage. — This most common and important of all 
brain lesions involves an enormous part of brain pathology. Apoplexy 
strictly refers to a "stroke," which is symptomatic of various other 
lesions, yet it is used to designate spontaneous hemorrhage into the 
brain (Rochoux). 

Etiology. — (a) Miliary aneurysms are the direct cause of cerebral 
hemorrhage. Their pathogenesis relates to (b) arteriosclerosis (alcoholism, 
plumbism, hard work, contracted kidney, overeating), but some main- 
tain that atheroma does not per se predispose to hemorrhage. Eighty 
per cent, of hemorrhages occur after the fortieth year of life, and in men. 
It may occur in early life from glioma, whooping-cough or trauma. Her- 
edity relates rather to renal and arterial lesions than to an actual heredity. 
Hemorrhage is most common among civilized races and in temperate 
zones, because of the strenuous habit? of life. The importance of the 
apoplectic habitus (plethora, ruddy face, short, thick neck, wide shoulders 
and chest, round, small body and large muscles) has been much empha- 
sized; Gowers finds most cases in thin individuals. Contracted kidney, 
found in 33 per cent, of cerebral hemorrhage, is a prominent cause 
of atheroma and miliary aneurysm, (c) Increased arterial tension is 
less important than its relation to arteriosclerosis and miliary aneurysms, 
which occur where the blood-pressure is greatest, as where the vessels 
branch. Rupture is seen in cardiac hypertrophy from stenosis at the 
isthmus of the aorta. Syphilis more frequently produces softening than 
hemorrhage; it is a causal factor of aneurysms of the large cerebral vessels. 
Violent exertion, alcoholic excesses, excitement, coitus, overeating, 
vomiting, coughing or convulsions may rupture an already-diseased 
vessel or a miliary aneurysm; a healthy vessel almost never bursts. 
Embolism from heart disease may produce the "embolic aneurysm. " 
Sometimes trauma is a factor, usually, however, with the causes above 
mentioned, (d) Permeability of the bloodvessels causes a few cases, by 
hemorrhage by diapedesis, as in nephritis, purpura, anemias and 
infections. 

Pathology. — Hemorrhage most often occurs in the branches of the 
arteria fossae Sylvii; the lenticulostriate artery of Duret, Charcot's artery 
of hemorrhage, is the seat of hemorrhage in 75 per cent, of cases. This 
small vessel is likely to rupture because it is so near to the large internal 
carotid and its course is very direct; it has no special external support; 
and there is no collateral circulation, hence no relief to pressure, render- 
ing the vessel tortuous. Rupture occurs very often in the long direction 
of the fibers of the internal capsule, where also the veins stagnate very 
easily. Miliary aneurysms were described by Brunner (1700) and 
Morgagni (1761), but Charcot and Bouchard (1866) emphasized their 
relation to brain hemorrhage. They are fusiform, more rarely sacciform, 



76(3 



DISEASES OF THE BRAIN 



enlargements of the arterioles, usually multiple, like a bunch of grapes, 
and measuring T ^~o to 2V of an inch; they are false aneurysms; they may 
be seen with the naked eye, by careful washing or macerating in water, 
or on a slide under a low power. They are found where hemorrhages are 
most common, i. e., the central ganglia and where the blood-pressure is 
highest. Charcot and Bouchard described periarteritis but Eichler and 
Zeigler held that intimal changes were primary; Roth finds atrophy of 
the muscular coat the accepted theory. Large aneurysms will be 
considered separately. 

Localization. — Hemorrhage is most common in the caudate and len- 
ticular nuclei, internal capsule and adjacent centrum ovale, extending 
to, but rarely beginning in, the optic thalamus. Hemorrhage in the white 
matter has usually an elongated form. It is much less common in the 

cortex, pons, crus, cerebellum or medulla. 
It occurs mostly in the substance of the 
brain, but may rupture on the surface or 
into the ventricles, causing sudden death, 
the usual autopsy finding. Hemorrhage 
is usually single. The multiple form is 
observed in anemia. When the skull is 
removed, the dura is tense, the convolu- 
tions flattened and pale, the falx pushed 
toward the other side and the fissures 
indistinct. Fluctuation may be felt in 
rare cases; on section the focus is seen, 
usually the size of a hazel-nut or walnut; 
it sometimes involves the entire hemi- 
sphere or may be no larger than a pea. 
The brain around the focus is softened 
from pressure, edematous and in the 
focus, torn and pulpy. The dark clot be- 
comes chocolate-colored, then yellowish- 
red and finally yellowish-white. The wall 
of the focus is irregular in the gray nuclei 
and regular in the white matter and 
threads of bloodvessels run through it. 
Leukocytes laden with fat drops, hematoidin and disorganized tissue are 
found. As the blood absorbs, the cavity becomes encapsulated by inflam- 
mation and contains a serous, milky fluid (the apoplectic cyst of Virchow). 
An apoplectic scar is much less common. Traumatic hemorrhage may occur 
infrequently near the point of injury or conire coup on the opposite side; 
the late traumatic hemorrhage of Bollinger takes place after a week or 
more, near the fourth ventricle and aqueduct of Sylvius, and probably 
in areas of traumatic softening. Brain hemorrhage may sever the internal 
capsule. 

Secondary degeneration occurs in the pyramidal tracts, chiefly from 
a lesion of the internal capsule; sound and diseased fibers intermingle; 
it descends through the crus, pons, medulla and cord (the direct anterior 
pyramidal tract and part of the crossed lateral tract). These areas 




Fig. 55. — Showing course of individ 
ual fibers of motor tracts. 



CEREBRAL HEMORRHAGE 



767 



become progressively smaller and cease just above the conus medullaris. 
In children a cerebral lesion may cause degeneration in the anterior horns 
of the cord and their fibers. An ascending degeneration occurs only 
when the large pyramidal tracts of the cortex are diseased, except in the 
young, in whom degeneration of all neurones is prone to follow the 
destruction of one neurone. (See figures under Localization in the 




Fig. 56. — Horizontal section through the right hemisphere: 1, cortex; 2, white substance; 
3, internal capsule; 4, optic thalamus; 5, lenticular nucleus; 6a, anterior horn; and 66, 
posterior horn of the lateral ventricle. (After Dejerine.) 



Spinal Cord.) Other degenerations : (a) The optic radiation degenerates 
when a lesion occurs in the cortex of the cuneus and also degenerative 
changes in the external geniculate body and pulvinar. After years it 
may reach the optic nerve, (b) Hemorrhage in the second and third 
frontal lobes leads to degeneration in the anterior limb of the capsule, 
median basal fibers of the crus and the fibers connecting the optic thala- 



768 DISEASES OF THE BRAIN 

mus with the cortex, (c) Lesions in the temporal lobes cause degenera- 
tion in the lateral part of the crus. (d) Degeneration in the median 
lemniscus follows diseases of the cortex, the subthalamic region and the 
upper part of the pons; it crosses to the opposite nuclei of the medulla 
and after years destroys the ganglion cells in the posterior columns of 
the cord. 

Symptoms. — Miliary aneurysms produce no symptoms until they 
rupture and premonitory symptoms are due to atheroma and are not 
pathognomonic. They may be general (v. i., softening); cardiorenal, 
as hypertrophied heart or hypertension; or rarely focal, as alexia, facial 
paresis, preparalytic chorea, etc. Prodromal symptoms are seldom due 
to an initial small hemorrhage or to hemorrhage developing very slowly. 

1. The Insult and its Primary Symptoms. — The "stroke" is usually 
sudden; its most common general symptom is coma, which may be absent 
in small lesions and its most common focal symptom is hemiplegia. It 
may develop during effort or excitement, or more often without cause, 
as during sleep. In ingravescent apoplexy the onset is gradual, with 
delirium, convulsions and finally coma; it is due to hemorrhage external 
to the lenticular nucleus, which later involves the internal capsule. 
Death may, in very rare instances, occur in five minutes from rupture 
into the ventricles or direct pressure on the medulla (fulminating 
apoplexy) . 

The insult is due chiefly to anemia of the cortex and to some extent 
to direct brain trauma, pressure on other vessels, serous infiltration 
and alterations in the cerebrospinal fluid in which lumbar puncture 
sometimes shows blood. Its cardinal typical symptoms are coma, which 
is greater the nearer the lesion is to the optic thalamus and third ven- 
tricle; flushed face, sometimes pallor or cyanosis; a tense, regular and 
slov) pulse; long, deep, stertorous breathing (due in part to palate par- 
alysis) ; the cheeks puff out, but are drawn in on inspiration, as a result of 
paralysis of the buccinator muscle; inspiration is sometimes irregular; 
yawning is frequent; the temperature usually suffers an initial fall, but 
rises when reaction sets in, though lesions in the pons, medulla or central 
ganglia may cause an initial rise. The pupils are usually wide, from 
paralysis of the third nuclei or sympathetic stimulation; they are some- 
times unequal and in deep coma reactionless. They may be narrow from 
irritation of the oculomotor nucleus in lesions of the pons, or when the 
ventricles are involved. The head and eyes look toward the side of the 
brain lesion ("conjugate deviation"), a flaccid hemiplegia occurs, in which 
the limbs fall limp when they are lifted; the reflexes are gone and there 
are involuntary evacuations of urine and feces. An increase of the urine 
with a low specific gravity (1.004) and transitory albuminuria and glyco- 
suria are due to a large lesion exerting indirect pressure on the medulla 
or to a lesion in the medulla itself. 

2. The permanent damage can be estimated only when the reaction 
is passed. The direct focal symptoms are those of the hemorrhage itself 
and the subsequent cyst or scar; they are permanent if essential struct- 
ures are involved, as the internal capsule. Indirect focal symptoms are 
those of other structures disturbed by pressure, edema or inflammatory 



CEREBRAL HEMORRHAGE 769 

reaction (the pulse and respiratory symptoms, conjugate deviation, 
albuminuria and temperature). Time is required to separate these two 
classes of symptoms. 

3. Details of Important Symptoms. — (i) Convulsions are not common 
(pons, ventricles, cortex or corpus striatum lesions). 

(ii) Conjugate deviation is a phenomenon in which the lateral muscles 
of the head and eyes are paralyzed; their fellows on the sound side con- 
tract, so that " the patient looks at his lesion" (Prevost) ; in left hemiplegia 
the eyes and head look toward the right side of the brain. The centres 
paralyzed are the gyrus angular is and gyrus supramarginalis. It disap- 
pears in a few days because the sound side of the brain compensates 
or because it is a distant pressure symptom. Conjugate deviation may 
also be due to irritation or Jacksonian epilepsy when the patient "looks 
away from his lesion" (Landouzy), i. e., toward the side affected with 
convulsions. These differ from the deviation in localization in the pons 

(?• ?;)• 

(iii) The hemiplegia is due (75 per cent.) to a lesion of the internal cap- 
sule (v. p. 757). During deep coma it is often difficult to determine which 
side is paralyzed. The affected side is usually flaccid and the mouth 
shows greater puffing on the hemiplegic half. If the coma is not pro- 
found the sound arm and leg may move. Sometimes, especially with 
hemorrhage into the lateral ventricle, the paralyzed side exhibits early 
rigidity. The temperature is at first lower on the hemiplegic side from 
paralysis of a cortical centre. Later, during reaction, it is higher on the 
side of paralysis. After consciousness returns the contralateral hemi- 
plegia is more clearly seen. The lower two-thirds of the face (nose, 
mouth, cheek) are paralyzed; the nasolabial fold is obliterated, the lips 
cannot be puckered as though to whistle, the mouth is oblique or a little 
triangular when the teeth are shown. The upper third (eye and fore- 
head) is unaffected because it is innervated from both hemispheres or 
has two distinct centres and paths; in peripheral facial paralysis all 
branches are involved, with atrophy and the reaction of degeneration. 
If the optic thalamus (q. v.) is intact, the paralysis is not apparent on 
laughing. The tongue, when protruded, deviates slightly toward the 
diseased side because the sound genioglossus muscle pulls the tongue 
forward and over toward the hemiplegic side; the base of the tongue is 
higher on the paralyzed side which may lead to some difficulty in the 
external speech mechanism (dysarthria), while internal speech is not 
often disturbed unless there is psychical alteration (aphasia). The 
palate may hang lower on the paralyzed side, but this is of little impor- 
tance because it varies physiologically. Deglutition, mastication and 
phonation are but little or only transitorily involved; marked difficulty 
in mastication is usually associated with total hemianesthesia. In the 
trunk paralysis of the trapezius and levator anguli scapulae causes 
sagging of the shoulder; certain cerebral fibers of the spinal accessory 
may be involved. Hughlings-Jackson finds respiratory movement 
greater on the paralyzed side in automatic breathing and greater on the 
sound side in forced breathing. Early, the paralysis of the arm and leg 
is often absolute, sometimes partial (hemiparesis). In the typical 
49 



770 DISEASES OF THE BRAIN 

case the arm is most involved, though all parts on one side usually are 
somewhat paralyzed. The arm abductors, hand flexors and finger exten- 
sors, the extensors of the leg, dorsal foot flexors and knee flexors are most 
implicated. The paralysis is flaccid. In rare linear lesions the arm, leg 
or face remains free (see page 757) ; monoplegia is much less common than 
in cortical and subcortical disease. The hemiplegia is almost invariably 
contralateral, i. e., opposite to the side of the lesion; Lederhose collected 
45 cases of collateral hemiplegia due to more than one lesion, to a focus 
pressing on the other side of the brain, or to mistaking the early rigidity 
of the paralyzed side for the normal side. 

(iv) Sensory disturbance (v. page 757) is less important, less frequent, 
less complete and less stable than hemiplegia. Some hemianesthesia 
is frequently found in early cases after careful examination-, as disturbed 
tactile sensation, stereognostic sense and sometimes muscle sense, pains 
and hyperesthesia or paresthesia. A large lesion only can cause a com- 
plete hemianesthesia. It affects the skin and mucosa of the nose, mouth, 
palate and eyes, but not the cornea. Cortical hemianesthesia is usually 
partial and most often associated with monoplegia; lesions just above 
the capsule, may produce hemianesthesia, involving the fibers from the 
thalamus to the cortex. It also occurs in lesions of the crus, pons, 
medulla and cord (q. v.). 

(v) Special senses. Hemianopsia, due to pressure on the optic thal- 
amus, usually occurs with conjugate deviation, is temporary and is often 
overlooked. 

(vi) The reflexes of the skin, cornea, pupils, mucosae and tendons are 
suspended during complete coma, in which the central nervous system 
is almost wholly paretic. After the stroke they return slowly, first on 
the sound side. On the hemiplegic side they return more slowly; the 
periosteal, tendon and patellar reflexes often become exaggerated from 
interrupted inhibition; the skin reflexes return slowly, especially the epi- 
gastric, cremasteric, scrotal and mammillary, a point of early diagnostic 
value. 

Babinski's toe sign usually indicates organic pyramidal disease and 
may be found very early; when a sharp object is slowly drawn over the 
outer part of the sound sole there is plantar flexion of the large and some- 
times of the other toes; when drawn over the diseased sole there is great 
dorsal flexion (extension) of the great toe. 

4. Chronic or Secondary Symptoms. — The indirect symptoms, 
inflammatory reaction and collateral edema disappear. 

(i) If the hemiplegia is indirect, from a lesion without the capsule, 
marked improvement or rarely, recovery ensues. Complete lasting 
hemiplegia follows total division of the pyramidal tracts, due to hemor- 
rhage from the anterior choroid artery (Kolisko). The face often recovers 
rapidly ; Broadbent held that the intercostals , masseters and trunk muscles 
used in pairs, innervated from both hemispheres and having little differ- 
entiation in function, escape permanent paralysis. The functions of the 
arm and hand are especiajly complicated, are more often used alone, are 
innervated mostly from one hemisphere and therefore suffer the greatest 
permanent damage. The legs are much used together and often show 



CEREBRAL HEMORRHAGE 111 

improvement. The bilateral, spinal and bulbar nuclei enable "paired 
muscles" to be innervated from the sound hemisphere, or possibly uncrossed 
fibers in the anterior (and lateral) columns explain thephenomenon. 
Compensation is offset by the fact that the sound side is reduced in 
strength in 50 per cent, of cases. In the arm the residual paralysis affects 
functionally associated muscle groups rather than individual muscles, 
as the muscles supinating the forearm, those abducting and lifting the 
arm and shoulder, those moving the elbow, opening the hand and appos- 
ing the thumb. The shoulder improves a little, the elbows considerably, 
the hands very little. In the leg the flexors, dorsal flexors of the foot 
which shorten the leg in walking, abductors and internal rotators of the 
hip are most involved. The hemiplegic gait is awkward, the foot is 
swung out in -a half -circle and scrapes the ground. The power of the 
paralyzed leg is greater when it is used with the sound leg, as in walking, 
than when it is used by itself. 

(ii) The contracture, the important posthemiplegic manifestation, fixes 
a joint in an abnormal posture. Early contractures are often regarded 
as myotatic irritability. The typical late contracture develops in two 
to four weeks; the shoulder is lifted, the arm adducted to the chest, the 
elbow rigid, the forearm pronated, the wrist flexed and the fingers flexed 
even violently into the palm. When the wrist is passively flexed the 
fingers can sometimes be extended. Contractures involve both extensors 
and flexors, but more often the latter, and occur in the least paralyzed 
muscles. In the lower extremity, the contracture is not marked, in the 
thigh there is often only a trace, the knee is extended, plantar flexion 
of the foot occurs ("pes equinovarus) , and the great toe is dorsally flexed. 
Locomotion is difficult, perhaps painful, for there is bending of the trunk 
to the sound side, lifting of the pelvis because of the abduction paralysis 
and swinging of the paralyzed foot over the sound foot. The sound leg also 
suffers slight contracture. Contracture may occur in the face, platysma 
and sternomastoid, but rarely in the trunk. In rare cases, largely in 
children, the paralyzed side remains lax (hemiplegia flasque of Bouchard). 

(hi) Associated movements are explained as movements reflected to the 
associates of the paralyzed muscles or as due to bilateral representation 
in the hemispheres; an effort to grasp with the sound hand produces a 
similar movement in the one paralyzed; movement of the diseased 
side occurs after passive movement of the sound one, etc. 

(iv) Hemitremor is uncommon. The muscles are stimulated, but not 
enough vibrations occur for actual involuntary movement. 

(v) Atrophy may occur in spastic, though more in the flaccid, cerebral 
forms. Charcot referred it to degeneration of the anterior horns, while 
Quincke and Senator assume an injury to some trophic paths. It has 
no relation to the degree of paralysis, is often associated with disturbed 
sensation and muscle sense, affects principally the arm and occurs in 
large lesions which are cortical in the region of the third branch of the 
artery of Sylvius or central in the lenticulothalamic distribution. The 
skin may atrophy. 

(vi) Posthemiplegic chorea results in 80 per cent, of cases from lesions 
in the internal capsule or near it, in the optic thalamus, lenticular or 



772 DISEASES OF THE BRAIN 

caudate nucleus, from which irritation is reflected to the brain cortex. 
It develops months or years after small lesions, when the hemiplegia and 
rigidity are largely gone. It occurs especially in the arm, causes move- 
ments similar to but coarser than those of chorea and is often associated 
with pain and sensory disturbance (see page 757). It sometimes is pre- 
paralytic. In posthemiplegic athetosis the fingers and toes are incessantly 
moved; athetosis means " without fixed position/' a "mobile spasm" 
consisting of spasmodic, slow, coordinated movements in paralyzed 
members ; it is frequent in partial paralysis acquired early in life, appears 
long after the paralysis has regressed and has the same localization as 
hemichorea. 

(vii) In trophic and vasomotor disturbance (v. s.) the paralyzed members 
are usually cool, moist and sometimes edematous. The skin is glossy, 
even livid and fissured. In some cases paralysis of the cervical sym- 
pathetic causes redness, narrowing of the eye fissure, drooping of the 
upper lid, retraction of the eye-ball, lachrymation and narrow pupils. 
Sometimes there is overgrowth of the hair. Bed-sores were considered 
trophic by Charcot, but can usually be avoided by care regarding press- 
ure or heat and by cleanliness. Swelling of the joints and hypertrophic 
neuritis on the hemiplegic side are rare. 

(viii) Psychic disturbance, referable not to brain hemorrhage but to 
arteriosclerosis, is evidenced by self-concentration, weak memory and 
irritability and more when the left half of the brain is diseased. Laugh- 
ing and weeping are referable to disease of the thalamus (q. v.) or median 
fibers of the pons. 

Diagnosis of Brain Hemorrhage. — Two cardinal features, coma and 
hemiplegia, together with the typical insult, facilitate diagnosis. 

1. Coma. — In syncope the pulse is fast, weak and often irregular; 
in "cardiac apoplexy" (an insult from heart rupture, myocarditis, etc.) 
differentiation from rapidly fatal hemorrhage may be impossible. It 
is dangerous to make a diagnosis of alcoholic coma; an intoxicated indi- 
vidual may suffer basal fracture or actual apoplexy; an opinion should 
be withheld until such complications can be excluded, though the alco- 
holic coma is usually incomplete, the vomitus and breath smell of alcohol 
and violent struggling is frequent. Opium coma is characterized by slow 
onset, slow respiration, slow, hard pulse, flushed skin, contracted pupils, 
opium in the stomach washings and later Cheyne-Stokes's respiration, 
rapid pulse, clammy, cyanotic skin, and dilated pupils; in all intoxica- 
tions the focal symptoms and reflexes of apoplexy are lacking. Hemor- 
rhage in the pons produces narrow and often unequal pupils. While 
diagnosis of apoplexy during the coma is precarious, uremic coma rarely 
occurs without premonitory symptoms, as headache, drowsiness, delirium, 
restlessness, vomiting, myosis, retinitis or convulsions; the coma is often 
less profound. The cardiorenal findings of nephritis may also occur in 
apoplexy, of which nephritis is a frequent cause (33 per cent.) and the 
author repeatedly observed hemiplegia and crossed paralyses in uremia, 
sometimes with Babinski's sign. In deep coma rigidity may be observed 
in both uremia and apoplexy, but in uremia it is often variable. In 
diabetic coma the fruity, acetone breath, acetonuria, unrest, Kussmaul's 



CEREBRAL HEMORRHAGE 773 

breathing, granular casts, history of glycosuria, and absence of focal 
symptoms are characteristic. Symptomatic apoplexy, transient coma and 
hemiplegia sometimes occur in brain edema, congestion, progressive 
paralysis, multiple sclerosis, epilepsy and tabes. 

2. Hemiplegia. — This is a prominent finding in embolism and throm- 
bosis (q. v.); Kolisko states that most cases diagnosticated embolism 
prove to be hemorrhage and vice versa. When hemiplegia occurs in 
meningitis with coma, there are headache, general convulsions, rigidity, 
hyperesthesia, optic neuritis, fever, etc. In extradural hematoma and 
pachymeningitis the Jacksonian epilepsy followed later by cortical 
paralysis is distinctive. Hemiplegia may also occur in hysteria (q. v.), 
syphilis, brain tumor or abscess, trauma, chorea, paralysis agitans, 
alcoholism, plumbism, uremia, etc. 

3. Other Locations of Hemorrhage. — (a) Hemorrhage may occur 
in diseases of the meninges (q. v.). (6) It occurs rarely in the cortex; 
Jacksonian epilepsy and rigidity may be severe in subcortical lesions. 
(c) Ventricular hemorrhage is secondary to hemorrhage in the corpus 
striatum or thalamus and usually reaches all the ventricles; in rare 
cases it is primary from aneurysms or ruptured veins in the choroid 
plexus. One-third of all cases are in persons under forty years of age. 
It occurs usually with violent symptoms, convulsions (33 per cent.), 
early and sometimes bilateral rigidity. The conjugate deviation changes 
to the other side, the pulse is slowed, the temperature falls, the reflexes 
are suspended. Cheyne-Stokes's breathing, glycosuria and polyuria 
develop and death usually results within a day. (d) Hemorrhage in the 
crus (v. page 759) is usually descending, from bleeding near the internal 
capsule. Crossed paralysis may be observed, (e) Apoplexy in the 
pons (q. v.) occurs in 10 per cent, of cases. Paralysis and convulsions 
may occur in the arms or legs only; the trunk musculature is involved 
more frequently than in higher hemorrhages. The eyes look away from 
the side of the lesion. The pupils may be large from paralysis or small 
from stimulation of the third nerve, as in opium poisoning. Respiration 
is affected early, vomiting is frequent, there is often early high fever 
and death is usual within twenty-four hours (it has occurred in seven 
minutes). (/) Hemorrhage in the medulla will be considered later. 
It is rarely diagnosticated. Early or instantaneous death is frequent. 
(g) Cerebellar apoplexy occurs in 7 per cent, of cases. Vomiting is very 
frequent. The insult is sometimes less marked and the occasional hemi- 
plegia is due to indirect pressure or secondary ventricular hemorrhage. 
Cerebellar symptoms may result. 

Prognosis. — The prognosis concerns the immediate danger and ulti- 
mate outcome, (a) The immediate prognosis is always serious; 66 per 
cent, survive the first stroke, 33 per cent, the second and very few the 
third. When death occurs it is usual in one-half to two days, but the 
outcome is uncertain for a week, because light cases, even rare forms with- 
out coma, may rupture into the ventricle with rapidly fatal result. Coma 
lasting over thirty hours, early low fall of temperature or its early rapid 
rise is unfavorable, indicating a large focus. Conjugate deviation, 
relaxed sphincters, impaired breathing, bilateral or ventricular symptoms, 



774 DISEASES OF THE BRAIN 

glycosuria, albuminuria, decubitus and convulsions are unfavorable. 
The mode of death is as follows : the breathing becomes more rapid, irreg- 
ular and rattling from accumulated secretion and of the ominous Cheyne- 
Stokes's type; the slow ; regular pulse becomes rapid, small, irregular, often 
with a rise of temperature and finally ceases; death occurs in coma. 

(6) Ultimate Outcome. — The symptoms of shock disappear and the 
patient becomes partly conscious or delirious. Reaction begins usually 
within forty-eight hours after the onset; the pulse becomes faster, 
the temperature rises, pain develops in the head and limbs. Life hangs 
in the balance and the patient may die from hypostatic pneumonia, 
pulmonary edema, decubitus or a second hemorrhage. Reaction is over 
in one to six weeks. If the patient survives there is improvement, depend- 
ing on the extent and localization of the injury; if movement appears 
in three weeks the outlook is good; if it does not return in three or four 
months it is not likely to develop later. Disappearance of indirect 
pressure leads to bettering (i) of damage to the sensory nerves and 
those of special sense, (ii) of motility, first of the trunk and face, then of 
the leg, and less of the arm. Absolute recovery is improbable. Hemi- 
chorea and hemiathetosis are incurable. Broken neurones never unite 
and secondary degeneration results; exaggerated reflexes, developing a 
few weeks after the insult are forerunners of contractures and preclude 
full regression. The outlook is fairly good in children when the hemor- 
rhage is not due to blood affections, because some compensation is likely 
to occur. Recurrence is possible in decrepid and aged subjects, although 
less common than usually believed; the average expectancy is five 
years. 

Treatment. — 1. Prophylaxis concerns the causative factors. 

2. The Insult. — (a) Absolute quiet is indicated; movement, trans- 
portation or extended examination is avoided, (b) The head is slightly 
elevated, but flexion of the neck, tight clothes or any hindrance to the 
return venous flow avoided. Bowles thinks that stertorous breathing 
is due to the position of the paralyzed palate; turning the patient on his 
side relieves it more effectively than does venesection, (c) Venesection 
is indicated only in robust individuals with strong hearts and tense 
vessels; about 12 ounces of blood are withdrawn; the chief objection 
to venesection is the difficulty of differentiation; in thrombosis and 
embolism, venesection increases the anemia of the brain, and Gushing 
has shown that the high tension is a vicarious effort to keep the medulla 
supplied with blood. This objection holds to compression of the 
common carotid, (d) Leeches, sinapisms and the ice-cap cannot in- 
fluence the circulation in the brain, (e) Evacuation of the bladder and 
bowels is indicated. Croton oil was Hughlings Jackson's only remedy; 
two drops act in an hour or two and may be repeated. (/) The diet 
should be fluid and administered by the nasal catheter or by rectum. 
(g) Decubitus is prevented by change of posture and cleanliness; heat 
and sinapisms must be avoided because the hemiplegic side is prone 
to necrosis. (/?) Symptomatic treatment of cardiac failure is met by 
ammonia, etc; restlessness or convulsions are managed by chloral per 
rectum or morphine. 



CEREBRAL EMBOLISM 775 

3. The Reaction. — During the inflammatory reaction the treatment 
is expectant and if possible should be conducted without drugs. 

4. The Chronic Stage. — (a) Gentle massage of the muscles, move- 
ment of the joints and alcohol rubs are instituted as soon as the coma 
subsides, (b) Potassium iodide is indicated when the reaction subsides. 

(c) In four weeks, the patient should be encouraged to sit up and walk. 

(d) The faradic current is valuable after four weeks and, supplemented 
with massage of the paralyzed groups and their antagonists, minimizes 
the contractures, (e) Hydrotherapy: cool baths or rubs are efficacious 
except in poorly nourished individuals. Strychnine is contra-indicated 
in all cases. 

V. Cerebral Embolism. — Embolism and thrombosis of a cerebral 
artery result in brain softening (encephalomalacia), which, next after 
hemorrhage in importance and frequency, is one of the best-developed 
subjects in brain pathology. Brain softening from arterial occlusion is 
not the "softening of the brain" known to the laity who give that name 
to progressive paralysis of the insane. Encephalomalacia must not be 
confused with encephalitis. Softening was first recognized by Abercrombie 
(1818) and Rostan (1820). 

Etiology. — Embolisms involve the kidneys in 77 per cent., spleen in 
54 and brain in 22 per cent, (a) About 90 per cent, are due to heart 
disease, most commonly acute endocarditis. Calcareous fragments or 
parts of torn valves may be thrown into the brain. Of valvular diseases, 
mitral stenosis produces embolism most frequently because of stasis 
in the left auricle. Less frequent are cardiac clots formed in the weak 
hearts of decrepid, cachectic subjects, in myocarditis or acute diseases, 
as typhoid. (b) Atheroma of the arch and aneurysm are far less frequent 
causes, as are (c) lung lesions, as tuberculous cavities, abscess, gangrene 
or empyema (after irrigation), tumors, echinococcus, gumma or abscess 
of the heart, (d) In the rarest instances lung tissue, fat embolism from 
fractures, pigment embolism in malaria or liver cells in acute yellow 
atrophy may produce cerebral embolism, (e) With a patent foramen 
ovale, thrombi may reach the brain from the venous system, as in manual 
expression of the placenta. (/) Most cases occur in youth when acute 
infections are most frequent, as chorea, scarlatina or endocarditis. 

Pathology. — (a) The embolus first is grayish-red but later paler and fri- 
able; "riding emboli" straddle the point of arterial branching; they may 
by slipping produce another embolism farther on. Secondary thrombosis 
may occur at the infarction. (6) The artery beyond, save where the 
embolus retracts or softens, becomes a thin, hard, impervious cord. 
Behind the plug an aneurysm may form. If the embolus is septic, in- 
flammation intervenes in and around the vessel, (c) As to the fate of the 
brain tissue: (i) If the stoppage is partial, only stasis, edema and swelling 
occur; if total, necrosis results, (ii) The brain arteries are " end arteries," 
as Cohnheim pointed out, whence complete collateral circulation is 
unlikely, although the necrosis is rarely as extensive as the distribution 
of the artery occluded. There is more collateral compensation at the 
cortex than at the base and the least in the deep parts of the centrum 
ovale or basal ganglia. The brain tissue is ischemic, but a degree of 



776 DISEASES OF THE BRAIN 

collateral fluxion saves some tissue, especially if the heart is strong. 
With a weak heart or diseased collateral arteries, ischemic necrosis must 
follow. A marked hemorrhagic infarct is not common, being prevented 
by swelling of the nervous tissue. Microscopic changes are seen after 
one or two days; the brain becomes edematous, gelatinous, marbled, 
fusing with the slightly edematous brain tissue surrounding the focus; 
the brain rapidly becomes fluid and pulpy, although its remarkable 
cohesion is a matter of frequent comment; certain convolutions may 
waste or wholly disappear, as the hippocampus, lingual and fusiform 
lobules, especially after plugging of the posterior cerebral artery. The 
white matter often disappears and is replaced by lax cellular tissue, 
in whose meshes are cystic formations with turbid fluid and flocculi of 
brain tissue. Durand-Fardel described three forms of softening: (a) 
The red softening found most often in embolism is usually fresh and 
there is capillary extravasation; it is irregularly oval or wedge-shaped 
in basilar lesions; it usually measures but a centimeter or two; it is 
prominent on section from blood and serum; it is soft, but not fluid 
in the centre; it is mostly located in the cortex or central ganglia and 
lasts one or two weeks, (b) Yellow softening follows the red ; the yellow 
color is due to old blood pigment or fatty change ; it is sunken on section, 
from atrophy of the brain substance; is fairly demarked and may contain 
fluid, hydrops ex vacuo; it may last years and is found especially in the 
cortex, (c) White softening may represent (i) a fresh lesion about tumors 
or abscesses or in various cachexias, is sunken below the cut surface 
and occurs where few vessels are involved and little regurgitation from 
adjacent vessels occurs; (ii) old snow-white lesions, occurring when the 
blood and fat are absorbed ; if diffuse it gives rise to the spongy etat crible. 

Demarcation may occur after weeks, producing a "cyst." More 
rarely neurogliar increase may lead to shrinking and scarring. Myelin 
and fat drops, leukocytes laden with granules and fat, collapsed vessels 
and necrotic nervous relics are observed. Secondary degeneration occurs 
when the pyramidal tracts are involved (see page 776). 

Symptoms. — As in apoplexy, we consider the insult, the permanent 
symptoms, and those of the causal disease (mitral stenosis, etc.). 

1. The insult is (a) sudden and without prodromes (save when the 
embolism does not wholly occlude the vessel and symptoms appear only 
when secondary thrombosis develops) . Embolism in a small vessel 
may occur without symptoms. The patient may be stricken without 
coma and sit "astonished" at the stroke. The insult is caused by brain 
anemia, negative pressure and shock. In some cases (b) coma occurs, 
generally less profound and less protracted than in hemorrhage; irritative 
symptoms, as (c) convulsions, tonic spasms and conjugate deviation are 
more common; convulsions are often unilateral, corresponding with the 
hemiplegia. (d) Intermediate types are observed; cases with vertigo; 
tendency to fall to one side ; hemianopsia, alexia, hemianesthesia, aphasia 
or only confusion and delirium, (e) The pulse is full but not slow. 
(/) The temperature rarely suffers initial depression and later may rise. 

2. The permanent symptoms and secondary degeneration are the same 
as in hemorrhage. 



CEREBRAL EMBOLISM 



i i i 



Localization of Embolism. — 1. The Artery of the Fossa of Sylvius. — 
This most frequently involved (80 per cent.), largest and most direct 
branch of the middle cerebral is practically a continuation of the internal 
carotid. Convulsions occur in 33 per cent., with or without loss of con- 
sciousness, and are most frequent when the smaller branches are em- 
bolized. High temperature is common. The clinical picture varies 
with the site of infarction; embolism at A (Fig. 57) where the perforat- 
ing branches (P.P.) are given off to the internal capsule, corpus striatum 
and anterior part of the thalamus, must involve (a) these structures, 




Fig. 57. — Embolism of artery of the fossa of Sylvius: I.C., internal carotid; P.C., post, 
communicating; A.C., anterior cerebral artery; A.S., art. fossse Sylvii and 1, 2, 3, 4 and 5, 
its main branches. CR, corona radiata from cortex to internal capsule. (See text for 
explanation of lesions at A, B, C, D, E, F or G.) 



and (b) the motor and sensory cortex, with hemiplegia, hemianesthesia, 
motor aphasia (alexia), deafness and word-deafness (if it occurs on the 
left side). Convulsions are absent, because the injured internal capsule 
cannot convey the cortical irritation to the extremities; the large areas 
rendered anemic may cause marked reaction, sometimes death. In rare 
cases, only the central perforating branches are involved and the cortex 
obtains the blood by anastomoses with the posterior and anterior cere- 
brals. The left Sylvian artery is more frequently involved (63 per cent.) 
because the left carotid comes directlv from the arch. If the lesion is at 



778 DISEASES OF THE BRAIN 

(B) (Fig. 57), the motor speech area, F z , the anterior and posterior motor 
convolutions A.C.C., P.C.C. (hemiplegia), the gyrus angularis and 
gyrus supramarginalis P 2 (alexia) and the temporal convolutions T± 
and T 2 (deafness or word-deafness) are involved. Somnolence and 
delirium are common; convulsions occur, because the internal capsule 
escapes. Convulsions and pain are most frequent in embolism of the 
smaller vessels. Little hemianesthesia is observed. A lesion at C 
is the most frequent site. It affects the island of Reil (IR) in part; 
cortical convulsions, hemiplegia, monoplegia, sensory aphasia (7\, T2), 
alexia (P 2 ) and sometimes sensory disturbance occur. It is seen how an 
isolated lesion at D could produce motor aphasia; at E, monoplegia; 
at F 3 alexia; or at G, word-deafness. 

2. Posterior Cerebral Artery. — Embolism (in 2 per cent.) comes 
from the vertebral artery and often occurs with embolism of the Sylvian 
artery; it supplies (a) all the ventricles, the thalamus, ant. corp. quad- 
rigemina, the geniculate body and the peduncle by its central branches, 
and (6) the mesial aspect of the occipital, part of the parietal and most of 
the temporosphenoidal lobes. The most common general symptoms are 
convulsions, coma, vertigo, conjugate deviation and nystagmus; while 
the most important focal symptoms are sensory hemianesthesia, sensory 
aphasia and hemianopsia. The lesions are sometimes symmetrical. 

3. Anterior Cerebral Artery. — Few clear cases are recorded, since 
the artery originates at a right angle to the carotid. 

4. Internal Carotid Artery. — In this embolism (4 per cent.) the 
plug must be large to produce damage, for if the vessels of the circle of 
Willis are normal, only transient hemiplegia results. Disease of these 
vessels, abnormalities in size or secondary thrombosis may produce 
permanent or fatal results. Sepsis is a frequent factor. 

5. Basilar Artery. — Embolism occurs in 6 per cent.; the clot never 
fills the vessel, because it first passes the smaller vertebral artery; 
symptoms occur more frequently when secondary thrombosis occurs — 
convulsions, trismus, paralysis of the third, fifth and seventh nerves, 
crossed hemiplegia, diplegia, narrow pupils and ' conjugate deviation. 
The temperature often falls low and then rapidly rises. Death may 
follow in two to five days from respiratory failure. 

6. Vertebral Artery. — Involvement of the tongue, larynx, lips, 
pharynx and spinal branch of the fifth nerve results in anesthesia, dys- 
phagia or other signs of acute bulbar palsy. Hemianesthesia, hemiplegia 
and hemiataxia may develop. It is often fatal. 

7. Cerebellar Arteries. — This is the rarest of all embolisms. 
Diagnosis. — The main points are (a) recognition of the cardiac cause; 

(b) absence of prodromes; (c) sudden insult, frequent convulsions and 
infrequent coma (see page 781). 

Prognosis. — The outlook depends (a) on the primary disease, being 
most favorable after acute infections and in youth; (b) on the intensity 
of the onset itself, during which death may occur; (c) on the localization. 
The initial symptoms may improve; the outlook is more favorable than 
in hemorrhage. Psychical symptoms are cortical in origin, while the 
vegetative or trophic are due to a lesion in the basal ganglia; basilar 



CEREBRAL THROMBOSIS 779 

and vertebral embolisms are most unfavorable, (d) Recurrence is pos- 
sible, although it is less likely than usually stated, (e) The condition of 
other organs, as the vessels of the circle of Willis, the strength of the 
heart muscle, etc., determine the prognosis. 

Treatment. — (a) The insult is treated as in hemorrhage in regard 
to diet and quiet. (6) All derivative measures, as drastics and vene- 
section, are absolutely to be avoided, (c) The heart must be stimulated, 
if hemorrhage is excluded, to relieve the brain ischemia by a strong 
collateral circulation and to strengthen the heart to avoid recurrence. 
Digitalis acts too slowly, and camphor, strychnine and ammonia are 
preferable, (d) Convulsions should be treated by chloral given by rectum, 
avoiding alcohol; more than a dram of chloral in three hours is very 
dangerous, (e) The after-treatment is as in the corresponding stage of 
apoplexy. 

VI. Cerebral Thrombosis. — It is more common than embolism. 

Etiology and Pathology. — 1. Changes in the Vessel Wall. — (a) 
Arteriosclerosis (q. v.) is the most important cause. Blood plaques are 
deposited on the rough intima of the tortuous, inelastic, calcareous 
vessels, with their unequal caliber; layer after layer of fibrin is deposited, 
aided by local slowing of the blood stream and weakening of the heart. 
Tumors, abscesses and traumatic meningitis may initiate thrombosis. 
Brain atheroma usually occurs with general atheroma. The vessels 
most involved are, in order of frequency, the carotid, middle cerebral 
and its Sylvian branch, basilar, vertebral and posterior cerebral, (b) 
In syphilitic endarteritis the initial proliferation may of itself, without 
thrombosis, obliterate the vessel lumen (see Brain Syphilis). The 
pathological sequence is the same as in embolism; ischemia, necrosis 
(softening) and loss of function occur, save that in gradual thrombosis 
the focus is less homogeneous than in the sudden lesion of embolism. 
The foci are often multiple. 

2. Changes in the Heart. — Sudden cardiac insufficiency in arterio- 
sclerosis may precipitate thrombosis, as brought out especially by 
Kolisko. An acute infection in the aged, low arterial tension from 
exhaustion, grief and similar causes may induce encephalomalacia. 

3. Changes of the Blood. — This constitutes the smallest class of 
cases. Burns, poisoning by carbon monoxide and illuminating gas, 
gout, chlorosis, leukemia, metallic poisons, jaundice and marasmus in 
very young children or in extreme old age may cause thrombosis. Acute 
infections and heart weakness are frequent factors in this class. Throm- 
bosis affects the smaller vessels and is usually multiple. 

Symptoms. — In some cases thrombosis is found at necropsy without 
previous symptoms ("latency"). 

1. Prodromes. — These are frequent and may appear hours, days, 
even months before focal symptoms develop. The most common are 
headache, which is severe in the syphilitic variety, vertigo, numbness 
and weakness in a limb or in one-half of the body, disturbance in 
sight, mind, articulation or character. 

2. Onset. — The onset varies; (a) an acute insult is not frequent. 
If consciousness is lost, the coma is less deep and protracted than in 



780 DISEASES OF THE BRAIN 

hemorrhage; a " stroke" indicates thrombosis in one large or in several 
vessels. Conjugate deviation, flaccidity and paralysis are frequent 
during the coma. Consciousness is usually preserved in the syphilitic 
type, (b) The onset is usually gradual. Layer after layer is added 
to the clot but strengthened heart action may for a time maintain 
collateral circulation. When the heart weakens, the clot increases 
and the collateral blood supply decreases, so that, after alternating 
advance and regression, the final thrombosis results, with irreparable 
softening. The cardiac strength and the number and size of the vessels 
involved determine the acuity or chronicity of the course. Reaction 
may be marked, especially in the aged, (c) In the chronic or long latent 
variety, prodromes are absent, psychic alteration is apparent and focal 
symptoms develop. 

3. Chronic Stage. — Focal symptoms are common. Apoplectiform 
seizures mark the advance of the process in new vascular areas. The 
motor or sensory paralysis presents much the same picture as hemorrhage 
and embolism in their chronic stage. 

Localization. — Localization is impossible when multiple foci exist, as in 
the Sylvian artery of one side and the posterior cerebral artery of the 
other; to the few reported cases Senator adds one in which left-sided 
hemiplegia was associated with aphasia. 

1. Sylvian Artery. — The most common cause is syphilis or atheroma. 
When the main trunk is involved, the same symptoms appear as in em- 
bolism, viz., hemiplegia, etc., with this modification — the focal symptoms 
are more severe in thrombosis, because other vessels are somewhat dis- 
eased; the general symptoms are less severe. Prodromes appear first, as 
tingling, then hemiplegia, possibly with delirium or loss of consciousness; 
the symptoms may improve, then there may be recurrence with aphasia 
and coma. The course is a "step-like" progression and regression. 
Monoplegia is more common than in embolism, because thrombosis seeks 
the cortical vessels, whence the face and arm may be affected; aphasia 
may exist alone, or alexia, mind-blindness or deafness. 

2. Anterior Cerebral Artery. — This artery is rarely totally 
occluded. A clot beyond the anterior communicating vessel produces 
crural monoplegia with arm paresis. Very gradual ischemia produces 
wasting without softening; sudden ischemia produces softening. The 
frontal lobes present the "worm-eaten" atrophy, with abundant hydrops 
ex vacuo; its close arterial connection is obvious. 

3. Posterior Cerebral Artery. — Thrombosis may result in hemi- 
plegia alternans oculomotoria, hemihypesthesia and optic changes varying 
as the optic radiation, cuneus or other parts are affected. 

4. Basilar Artery. — If the thrombosis is acute the symptoms are 
like those of embolism. If slow, ophthalmoplegia which is rarely lasting, 
or other motor paralyses, hemiplegia with alternating palsy of the fifth, 
sixth and seventh nerves, may develop. 

5. Vertebral Artery. — Acute bulbar palsy, with stormy symptoms, 
cannot be distinguished from embolism. Subacute bulbar palsy, with 
dysphagia, dysarthria, hemianesthesia, homolateral ataxia, contralateral 
hemianalgesia or hemiplegia with crossed paralysis of the tongue may result. 



CEREBRAL THROMBOSIS 



'81 



Hemorrhage. 



Thrombosis. 



Embolism. 



(1) Predisposing etiology. Before 
third year (glioma) ; 80 per cent, 
after fortieth year. 

Miliary aneurysms; atheroma and 
cardiac hypertrophy. 



Heredity. Nephritis; cause in 33 
per cent., "granular kidney." 

(2) Attack precipitated by heavy 
meal, acute alcoholism, high art. 
tension (excitement, effort, shock) . 

(3) Prodromes unusual, unless from 
causal arteriosclerosis. 



(4) Insult: Usually sudden; with- 
out prodromata; long duration 
(fatal if more than two days). 
Cause; positive pressure produc- 
ing brain anemia. 

(5) Intra-cranial pressure: "Press- 
ure symptoms" present, polyuria, 
albuminuria, glocosuria, red face, 
beating arteries, Cheyne-Stokes's 
breathing; slow, hard pulse is the 
fundamental difference (Brissaud) ; 
bruit de gallop speaks strongly for 
hemorrhage. Irregularity, if com- 
bined with strength not against 
hemorrhage. Pulse may be fast 
(Brissaud) . 

(6) Temperature: Rectal tempera- 
ture usually depressed at first, 
may fall till death. May rise later 
(inflammatory reaction). Early 
rise (pons, medulla, ganglia). 
Sudden rise of bad omen; rises 
before death. 

(7) Coma: More frequent, greater 
in degree, longer in duration, usu- 
ally complete. If lesion seems 
small, coma speaks for hemorrhage. 
Deep and prolonged speaks for 
hemorrhage and usually fatal if 
over twenty-four hours. 

(8) Paralysis, sudden, complete, 
hemiplegic, non-progressive after 
first seizure. Foot gains more 
rapidly than hand. Persistent 
aphasia exceptional. Spasmodic 
laughing and weeping common. 



(9) Convulsions: Usually general- 
ized; very rare from cortical irri- 
tation or in corpus striatum; post- 
hemiplegic are rare. 

(10) Sensation: Anesthesia usually 
transient. 

Postplegic chorea, trembling, athe- 
tosis, common. 

(11) Atheroma retinal arteries, hence 
retinal hemorrhage (not signifi- 
cant unless large). Aneurysms 
very rare but speak strongly for 
hemorrhage. Retinitis albumin- 
urica. 

(12) Secondary reaction; not much. 
Psychical symptoms; far less. 



After eightieth more year frequent 
than hemorrhage. Twentieth to 
fortieth year syphilis (84 per cent, 
occur between these years). 

Weak, irregular heart; fevers, cach- 
exia. Atheroma, especially syphilis, 
alcoholism, plumbism. 



Rare. 
Rare. 

Low arterial tension; by sleep, grief, 
exhaustion, fatigue. 

Very common, mental irritability, 
weak memory, headache, vertigo, 
numbness, tingling, weakness in 
extremities. 

Rarely acute onset (unless in a large 
vessel) ; usually gradual, especially 
in senile softening. If an insult, 
focal and general symptoms usually 
appear during the coma. 

None. 

Pulse soft, weak. 
(Wassermann test) . 



Initial depression, usually lasting. 
Seldom temperature unless lesion 
in pons. More probably early 
reaction. Especially in the aged. 



Less frequent and shorter. Recovery 
possible after several days of coma. 
None in syphilitic thrombosis. If 
lesion seems large, consciousness 
speaks for softening. If coma, usu- 
ally focal symptoms are then seen. 
Coma in large bilateral lesions. 

Gradual, incomplete, monoplegia, 
hemianopsia; repeated, often sym- 
metrical paralysis. 

Converse. 

Aphasia common. Absence of focal 
symptoms rather more common 
(central ganglia). Laughing and 
weeping exceptional. 

Less than in embolism. More local- 
ized, Jacksonian epilepsy speaks 
for softening. May recur. Post- 
plegic frequent. 

Paresthesia persists and more 
marked. Cerebral pains (hyper- 
esthesia dolorosa). 

Less common. 

Arteriosclerosis. 



Greater secondary reaction. 
Often greater; intelligence, memory 
aphasia, word- deafness, etc. 



Youth; hemorrhage practi- 
cally never in youth. 



Endocarditis (rheumatism, 
sepsis), especially mitral. 
Weak, fatty, dilated heart. 
In heart disease Eichhorst 
found in 60 per cent, hem- 
orrhage and in 40 per cent, 
embolism. 

Rare. 

Rare. 

By exertion, dislodging clot. 



Absolutely none. 



Sudden, shorter and less 
severe than in hemorrhage. 
Cause; negative pressure. 
Slow insult only with sec- 
ondary thrombosis. 

None (pallor rather than 
congestion) . 



Temperature may rise high 
at once without bad omen. 
Temperature no absolute 
guide; occurs especially 
when large trunk embol- 
ized. 

No coma usually. 



More like hemorrhage. 
Monoplegia rare. In 63 
per cent, it is in the left 
side of the brain. 

Fairly common. 



More common (33 per cent.) 
than in hemorrhage or 
thrombosis (lesion corti- 
cal.) 
Paresthesia persists and more 
marked. Cerebral pains 
(hyperesthesia dolorosa). 

Less common. 

Optic retinitis sometimes 
from endocarditis (Broad- 
bent and Mackenzie) . 

Occasionally embolism in 
retinae. 



Very seldom; after attack 
may be some delirium. 



Diagnosis and Differentiation. — The prodromes, gradual onset and 
cortical location are most distinctive, although the differentiation may 
be wholly theoretical or impossible (page 781). In brain tumor the 



782 DISEASES OF THE BRAIN 

course is slower, and stabile focal symptoms less frequent — that is, 
headache, vomiting, choked disk and Jacksonian epilepsy are far more 
frequent than permanent paralysis. We may consider hemiplegia in 
the aged, Marie's les lacunes de desintegration cerebrale; multiple degenera- 
tion clefts occur, chiefly in the large basal ganglia, sometimes in the in- 
ternal capsule, pons, or centrum ovale. Marie holds that the lesion is a 
rarefaction (cavity formation) of brain tissue due to chronic sclerosing 
encephalitis, without vessel occlusion. It is said to cause 90 per cent, of 
" insults" in the aged, usually with partial paralysis; sometimes with 
aphasia, dysarthria or dysphagia; rarely with loss of consciousness; 
and never with sensory disturbance or contractures. The gait is the 
demarche a petits pas. The patient may live ten years. 

Prognosis. — The prognosis depends on (a) the cause; it is unfavorable 
in arteriosclerosis, because collateral vessels are probably diseased. If 
the other vessels are sound, enormous disease may be compensated, 
as in KussmauTs case of occlusion of both the subclavian and carotid 
arteries. In recent syphilis the prognosis is more favorable, though 
old specific thrombosis is incurable. The younger the patient the better 
is the outlook. (6) The onset; most cases with a brusque beginning 
die. Coma indicates thrombosis in large vessels or in both hemispheres. 
If there is no insult the focal symptoms are irreparable, i. e., there are 
no indirect symptoms. The first seizure does not usually threaten life. 
(c) The location and extent of the lesion. The number of vessels involved 
is obviously important. In Sylvian thrombosis involving the branches 
to the central ganglia, the patient dies in four to six weeks with involun- 
tary evacuations, cachexia and bed-sores. Cortical lesions are prone to 
produce psychical alteration. Basilar or vertebral thrombosis is directly 
dangerous, (d) The focal symptoms are likely to persist and recur. Oph- 
thalmoplegia may regress, (e) The condition of other organs, above all 
the heart, is of prognostic import. 

Treatment. — (a) The general treatment is the same as in hemorrhage. 
(6) The causal treatment relates to the iodides, valuable in atheroma 
and syphilis, (c) The heart must be stimulated with digitalis; absolute 
quiet in the prone position and free administration of food and fluid by 
rectum or by nasal catheter are indicated. Drastics and depleting 
measures must be avoided. On the heart devolves the entire possibility 
of collateral compensation, (d) In the period of reaction alcohol only 
accentuates the inflammation. For delirium and headache, bromides 
are most useful; no cardiac depressants, e. g., chloral or coal-tar products 
may be used, (e) The chronic stage is treated as in hemorrhage. At all 
times catheterization must be conducted antiseptically and great care 
exercised against bed-sores. 

VII. Intracranial Aneurysms. — Etiology. — Aside from miliary aneur- 
ysms, aneurysms may occur in the large brain vessels, more frequently 
in males (60 per cent.), and more (53 per cent.) before than after the 
fortieth year. The causes are (a) atheroma in whose causation alcohol 
is particularly important; (b) trauma, initiating arteritis, especially in 
the internal carotid, as after basal fracture; (c) syphilis, especially pro- 
ductive of basilar aneurysm, often within a year after infection; (d) 



SINUS THROMBOSIS 783 

embolism, the most frequent cause in early life; endocarditis is the usual 
cause when trauma and syphilis are excluded. The embolus produces 
arteritis from which the vessel dilates. The clot may later disappear. 

Pathology. — Location. — Statistics show the following frequency; 
middle cerebral, 29 per cent.; basilar, 26; internal carotid, 14; anterior 
cerebral, 8; anterior communicating, 6 per cent. They are rather more 
frequent on the left side, in 20 per cent, are multiple, are usually saccu- 
lated, of the size of a pea or walnut (rarely as large as an egg) and are 
genuine aneurysms involving all coats. Beadles collected 555 cerebral 
aneurysms with autopsy (1907). 

Symptoms. — In only 37 per cent, are symptoms present. They are 
(a) general, as headache, which is the most common sign, or convulsions, 
which result from aneurysm of the Sylvian branch; a systolic murmur 
was found in but 21 per cent.; in a personal observation, cured by 
operation, a continuous murmur over half the head was associated with 
exophthalmos, (b) Local symptoms; according to their location, hemi- 
anopsia, ocular paralysis, hemiplegia, optic neuritis (extension of inflam- 
mation from the sac), aphasia and symptoms referable to the pons or 
medulla may be noted. Rupture occurs in 67 per cent., into the men- 
inges, brain substance or ventricles, from which death rapidly results; 
healing has been observed. 

Diagnosis. — Rupture is generally the first symptom and differentiation 
from apoplexy is therefore necessary; cerebral hemorrhage in a young 
individual with a history of trauma, heart disease or syphilis suggests 
aneurysm, especially when the location is basilar; iodides and mercury 
usually are not beneficial in aneurysm. The suggestive murmur is 
rare and may be found in tumors wdiich compress vessels or in very 
vascular brain tumors. Aneurysm is most often embolic in the Sylvian 
and specific in the basilar artery. Loss of sight in an eye, sometimes with 
impairment of smell, rather indicates aneurysm of the anterior cerebral 
or, if the eye muscles are paralyzed, of the internal carotid artery. Oculo- 
motor paralysis without loss of vision suggests aneurysm of the posterior 
communicating artery. Some cases closely resemble arterial thrombosis. 

Treatment. — The indications are rest and iodides. Ligation of the 
carotid is occasionally opportune. 

VIII. Sinus Thrombosis. — Lebert (1854) diagnosticated the first case 
and with Tonnele built up its clinical recognition. 

Etiology and Pathology. — There are two varieties, the marantic and 
the inflammatory types. 

1. Marantic thrombosis of the sinuses and veins is the primary non- 
inflammatory type, due to altered blood states and weakened circulation. 
It occurs (a) in children mostly, especially in the first six months of life 
and after acute infections, particularly infective diarrheas; (b) less fre- 
quently in the aged from weak heart and venous stasis; (c) in cachexia; 
(d) in chlorosis; (e) compression, as by tumors, is rare. Its most frequent 
site is the superior longitudinal sinus, especially in children, because the 
sinus is fixed, its lumen is triangular and irregular, crossed by trabecular 
and compressed by the Pacchyonian granulations; the tributary veins 
ascend against the current of the sinus and their stream is very weak. 



784 



DISEASES OF THE BRAIN 



Simple slowing of the current is not sufficient for coagulation and the 
vessel wall must be altered. In the aged, marantic thrombosis elects 
the cavernous or transverse sinus. The marantic clot may enter the 
tributary veins which are seen as firm cords over the hemispheres. 

2. The inflammatory thrombosis, thrombophlebitis, is secondary to 
disease near the sinus; as (a) ear disease, chiefly chronic, suppurative 
otitis or caries of the bone; infection reaches the sinus by (i) infecting 
the mastoid cells, which infect the transverse sinus; (ii) by infecting 




COMMUNICANS WITH THE NECK 



Fig. 58. — Diagram showing the connections (*) of the transverse and cavernous sinuses 

(Leube) . 



small communicating veins or (hi) its passage along the petromastoid 
canal, (b) Acute infections, with otitis media; sepsis; trauma, tuberculous 
meningitis, disease of the orbit, nose and face. The most common 
sites are the transverse, petrosal and cavernous sinuses, whence it may 
extend to their branches. The clot is puriform, fetid, soft, discolored 
and contains pyogenic organisms; the process is frequently associated 
with meningitis and brain abscess. 

Most frequently the thrombosis is bilateral; suggillations in the pia, 
bloody imbibition of the brain or reddening of the cerebrospinal or ven- 



SINUS THROMBOSIS 



785 



tricular fluid may occur. Simple or septic pulmonary infarcts occur in 
50 per cent. 

Symptoms and Diagnosis. — Clinical signs may be absent. 

1. Extracranial Stasis. — (a) In thrombosis of the superior longitu- 
dinal sinus, stasis in the nasal veins is often shown by epistaxis, an 
effort of nature to deplete the cerebral congestion. Gerhardt observed 
cyanosis in the anterior frontal veins and edema in the temples between 
the great fontanelle and ear (by way of the emissaria Santorini through 
the foramen parietale). Edema is often absent in chlorotic thrombosis. 
(b) In thrombosis of the cavernous sinus stasis develops in its tributaries, 
producing exophthalmos, edema of the lids and conjunctiva (vena oph- 
thalmica); retinal stasis, more rarely choked disk or retinal thrombosis, 



VEINS COMMUNICATING THROUGH 
THE PARIETAL FORAMEN WITH 
THE EXTERNAL SKULL VEINS. 




CONFLUENS 
SIN. 



\ /• 
VENA JUGUL.INT. 



VENA JUGULARIS EXT. 



Fig. 59. 



-Leube's diagram showing the connections (*) of the superior longitudinal sinus 
with the external veins. 



results from congestion of the vena centralis retinae. Sometimes edema 
of the forehead results, (c) In thrombosis of the lateral sinus, edema 
behind the ear and in the neck (communicating with the posterior auricular 
vein) occurs in over 50 per cent. Occasionally the sivollen thrombotic 
internal jugular vein may be felt. The external jugular collapses, or if 
the internal jugular is thrombosed it becomes overfilled (Gerhardt). 
In 33 per cent, the disk is hyperemic and in another 33 per cent, there is 
choked disk from complicating abscess or meningitis. 

2. Intracranial Stasis. — Progressive clouding of the mind, delirium 
in adults, convulsions in children, conjugate deviation of the eyes and 
head, stiff neck, vomiting, headache, irregular pupils, nystagmus or 
strabismus are noted. Bilateral symptoms, as paraplegia, are due 
to the involvement of the veins in both hemispheres or more often to 
50 



786 DISEASES OF THE BRAIN 

meningitis. Bouchut thought that antemortem convulsions in children 
were often thrombotic in origin. The fontanelles, sunken at first in 
infantile diarrhea, may later become prominent (increased cerebrospinal 
fluid). Sometimes chlorotic thrombosis may extend to the vena Galeni 
magna, producing hydrocephalus internus, stupor, coma and death. 
Irritation or paralysis of the third, fourth and sixth nerves may occur 
because of their intimate relation to the cavernous sinus; involvement 
of the first branch of the fifth nerve may result in ophthalmia neuro- 
paralytica. 

The temperature is often normal in the simple, or in the thrombo- 
phlebitic variety attended by fever, chills and sweats. 

Differentiation. — Differentiation from meningitis (q. v.) and brain 
abscess (q. v.) is often impossible; the cause, the extracranial stasis and 
evidences of sepsis are of diagnostic importance. Korner held that 
metastases occur in the lungs from sinus thrombosis and in the bones 
and joints from mastoid caries. 

Prognosis. — Death occurs in the second week, possibly later. Few 
recoveries from either type are on record. 

Treatment. — Prophylaxis relates chiefly to the otitic variety; discharges 
from the ear are too lightly regarded by the laity. In marantic throm- 
bosis stimulation and avoidance of constriction of the neck are the 
chief indications. In septic types operation is indicated; recovery is 
most likely when there is early diagnosis with early operation. Opening 
and packing the lateral sinus was first performed by Zaufal in 1884. 
Ligature of the internal jugular veins, as first performed by Thersley 
and Lane in 1888, gives recovery in 50 per cent, and in 72 per cent, of 
Macewen's series. 

IX. Infantile Cerebral Paralysis. — Cerebral infantile palsy is classed 
under circulatory diseases because of the frequent etiological hemorrhage, 
embolism and thrombosis. Pathologically, it is sometimes encephalitis, 
sclerosis or porencephalia. Clinically, it is variously classed according 
to the dominant syndrome, hemiplegia, diplegia, Little's disease, para- 
plegia, hemiathetosis and athetosis. 

1. The Hemiplegic Form. — Etiology. — It is equally frequent in either 
sex. Gowers finds 88 per cent, in the first five years of life. Infections 
as scarlatina, measles, pertussis and diphtheria are apparent, and hered- 
ity, maternal syphilis and trauma are doubtful causes. The causes may 
operate before, during or after birth. 

Symptoms. — (a) Initial symptoms, present in 66 per cent., are severe 
in character, consist of fever, vomiting and delirium, and last from a few 
hours to several days; convulsions, present in 50 per cent., are often 
unilateral and are usually followed by coma. In 33 per cent, of cases 
the onset is insidious, (b) The paralysis (hemiplegia) usually develops 
when consciousness returns. It is more frequently right- than left-sided. 
The lower face is involved, but usually soon improves; the leg improves 
more than the arm and hand; and the paralysis, at first flaccid, soon 
becomes spastic and permanent. Tactile and stereognostic sense may be 
reduced, but sensation is slightly implicated, (c) The residual symptoms 
are the same as in adults, with some exceptions; the paralysis is spastic 



INFANTILE CEREBRAL PARALYSIS 



787 



(spastic infantile hemiplegia, Heine) but also atactic and athetotic; re- 
tarded development appears, intellection is retarded or actual idiocy results 
and epileptiform seizures are common. Contractures are frequent, the re- 
flexes are increased and the gait is somewhat impaired — the foot-dragging. 
In rudimentary or benign cases the paralysis may almost disappear, and, 
after months or years, may be replaced by epileptic seizures, hemiathe- 
tosis, hemichorea, hemitremor (described under Hemorrhage) or hemi- 
hypertonia (rigidity with but little paralysis). Aphasia is rarely lasting; 
(a) reflex aphasia is very common in childhood from fever or digestive 
difficulties; (b) the brain readily compensates in childhood; (c) per- 
manent aphasia indicates great or total loss of intelligence. Trophic 
changes are in part a moderate atrophy and in part a lack of later devel- 
opment; they are most common in porencephalia (v. i.). Epilepsy 
increases in frequency after the paralysis and is rated at from 13 per cent, 
to even 66 per cent. ; it occurs at the onset with the paralysis or a year 
or two later; it is more marked in rudimentary palsy; it is most often 
like the Jacksonian type, but may end in total loss of consciousness; 
there is less violence, initial cry, foaming and involuntary evacuations 
than in ordinary epilepsy. After a decade or more it often becomes 
very marked. 

Diagnosis. — Its separation from poliomyelitis is thus made: 





Cerebral type. 


Spinal type. 


Tendon reflexes. 


Increased. 


Decreased or abolished. 


Muscular atrophy. 


Only after a long time. 


Rapid. 


Electrical reaction. 


Normal, or little quantita- 


Partial or total reaction of 




tive decrease. 


degeneration. 


Distribution of paralysis. 


Hemiplegic — -diplegic . 


Chiefly monoplegic. 


Intelligence. 


Often involved. 


Usually not. 


Epilepsy and hemichorea. 


Common. 


Rare. 



2. The Double Hemiplegic or Diplegic Form. — Etiology. — (a) Prenatal 
causes, apparent in 20 per cent., include fright, trauma, malnutrition 
or syphilis, especially in cases which develop athetosis. (6) Anomalies of 
labor include difficult or long labor, malpresentation, resistant maternal 
tissues, twin pregnancy, version and cord prolapse; delivery by forceps 
is less important than the causes calling for their use. Asphyxia is an 
important etiological factor. In premature delivery the soft skull may be 
injured or venous stasis occurs, (c) Extra-uterine causes include trauma 
and acute infections. 

Pathology. — The initial lesion cannot always be determined, (a) In 
the traumatic class, meningeal hemorrhage causes 66 per cent, of the diplegic 
cases; it is promoted by asphyxia and the sliding of the skull bones of 
one side under or over those of the other side. The blood is absorbed 
slowly, if the brain is lacerated, resulting in atrophy of both motor areas. 
(b) Vessel disease (18 per cent.) may be arterial (thrombosis, embolism 
or hemorrhage) or venous (in the cortical veins), (c) Striimpell ad- 
vanced the views that acute poliencephalitis in the motor cortex causes 
the acute onset, an argument largely based on analogy (poliomyelitis in 
children) . 



788 DISEASES OF THE BRAIN 

Chronic Lesions. — The most important are diffuse lobar sclerosis 
and porencephalia, which are peculiar to infantile brain palsies: (a) 
Diffuse lobar sclerosis and atrophy of the brain occur in 55 per cent. 
About the atrophic areas and in the ventricles the cerebrospinal fluid 
is increased. The lobe affected is shrunken, hardened. The convolutions 
are wasted and smooth or " worm-eaten." The nervous tissue is wasted, 
the neuroglia increased and the bloodvessels tortuous and thickened. 
The nature of the initial lesion is disputed; it may be encephalitis, 
poiiencephalitis or embolism, (b) Porencephalia (Heschl, 1859) consists 
of loss of brain substance and cavity formation. It occurs in 26 per cent. 

of cases. The initial lesion is ascribed to 
agenesis, encephalitis or meningo-encepha- 
litis, trauma or anemic necrosis (Kundrat), 
the most widely accepted view. It is most 
frequent in the distribution of the Sylvian 
or occipital vessels. Most often it is con- 
genital and then the convolutions radiate 
from the defect, while in postnatum cases, 
the convolutions stop short of the defect 
"as though cut off." Sixty per cent, are 
bilateral and somewhat symmetrical, (c) 
The hypertrophic, nodular sclerosis, de- 
scribed by Bourneville, consists of multiple 
discrete, prominent, often umbilicated 
nodes the size of a quarter- or half-dollar. 
They are overgrowths of the neuroglia. 

Symptoms. — Diplegic cases are half as 
frequent as the hemiplegic. Freud de- 
scribes the following forms: (a) General 
rigidity, or Little's disease, 33 per cent, 
of which are caused by asphyxia. The 
main characteristics are (i) predominance 
of the rigidity over the paresis, and (ii) 
predominance of the leg paresis over that 
of the arms, the converse of adult cerebral 
-- An „ ,. , . paralvsis (hemorrhage occurs most often 

.biG. 60. — bpastic paraplegia, cross- i i \ r^ 

legged progression. (Dercum.) over the leg centres). Convulsions often 

usher in the symptoms, which appear after 
birth or a few months later. The rigidity is general but most conspicuous 
in the flexors and adductors, leading to unusual postures. The face is 
slightly involved, the maximum manifestation being spasm of the mouth ; 
in rare cases the child cannot nurse or swallow. Speech is slow in develop- 
ment and stuttering is common. In 33 per cent, the head cannot be lifted 
or the trunk flexed, due to involvement also of the uncrossed pyramidal 
tracts. The arms may be but slightly paretic, but the legs suffer extensor 
spasm on movement and the toes turn down (talipes equinus or equino- 
varus). The child learns to walk late, if at all, because of the adductor 
rigidity, which may cause crossing of the legs. The reflexes are greatly 
increased. The intellect is somewhat affected in 66 per cent. Nutrition 




MAIN TUMORS 789 

in the paretic members is usually intact. Later epilepsy is uncommon. 
The paresis may regress and the mind improve, but the legs remain 
spastic. (6) Paraplegic rigidity resembles type (a) except that the arms 
are but little or not at all affected and the legs alone are rigid. The 
name Little's disease is also given to this form. Strabismus is common. 
Premature delivery is a factor in 50 per cent, of cases, (c) Paraplegia 
is rare and is referred to extra-uterine causes or infantile infections. The 
legs are rigid and paralyzed. In severe types there may be strabismus 
and imbecility, id) In bilateral spastic hemiplegia (spastic diplegia), 
mental degeneration, nystagmus, convergent strabismus, bulbar symptoms 
and speech involvement (60 per cent.) are frequent, (e) General infantile 
chorea is also called "choreic diplegia"; asphyxia is a factor in 25 per 
cent. Its clinical characters are paralysis, rigidity and chorea-like move- 
ments which are irregular, slight in degree and wide in distribution. (/) 
In bilateral athetosis the mind is less involved than in the preceding types. 
The paralysis may precede it or it may be primary. 

In all forms epilepsy may (i) replace the regressing paralysis; (ii) 
overshadow the paralysis; (iii) paralysis may appear only after years 
of epilepsy, or (iv) may not appear at all, "cerebral paralysis without 
paralysis." 

Diagnosis. — Separation from the family spastic paralysis (q. v.) may 
be difficult or impossible. 

Treatment. — In the initial stage convulsions may be treated by chloral. 
Some regression in the paralysis is frequent, but the hemiplegia, mental 
changes and epilepsy are incurable. Marked improvement can be 
expected in the syphilitic cases alone. Orthopedic devices are valuable. 
The resulting epilepsy is usually intractable and bromides with opium 
are of little avail. Twenty-five per cent, die from operations, but the 
surviving cases seem to improve, especially in regard to the convulsions. 

BRAIN TUMORS. 

Etiology and Pathology. — Eichhorst found brain tumors in J of 1 
per cent, of his cases. Sixty-six per cent, of tumors occur in the male 
sex, especially glioma and tubercle. Age. In the first decade, 18.5 
per cent, of cases are observed; in the second, 14; third, 20; fourth, 
18.5; and in the fifth, 14 per cent. Trauma may act as the "agent pro- 
vocateur " in glioma, gumma, sarcoma, tubercle or aneurysm. The author 
has seen endothelioma of the dura develop years after and directly at the 
seat of an unhealed skull fracture. 

Classification. — 1. The Infectious Gkanttlomata.. — (a) Tubercle con- 
stitutes 50 per cent, of cerebral tumors, 75 per cent, being found in the 
first and second decades; 33 per cent, occur in the cerebellum, 33 per 
cent, in the cerebrum and the remainder in the pons, central ganglia, 
crus, etc. With equal frequency they are single or multiple (even 20 or 
80). They are firm, rounded tumors, with grayish-red periphery and 
yellow, caseated centre. Tubercles range from the size of a pea or walnut 
to that of an egg or the fist, from fusion of many small growths. They 
grow along the lymph vessels, cause vascular thrombosis, present the 



790 DISEASES OF THE BRAIN 

degenerations of tubercle of other tissues and may be shelled out of the 
brain tissue, which is compressed and atrophied, but neither infiltrated 
nor softened. (b) Gummata (see Brain Syphilis) in the adult are the 
most common type of tumor. They are most frequent in the cerebral 
hemispheres and pons and are rare in the cerebellum and central 
ganglia; they are most often the size of a pea or hazel-nut. Their centre 
is yellowish-gray and their periphery is reddish-gray, gelatinous, rich in 
cells and ultimately cicatricial. Gummata are usually multiple. The 
adjacent brain tissue is not infiltrated, but commonly softened and 
compressed. Microscopically, they closely resemble tubercle, but are 
more nodose, irregular, more distinctly connected with the dura, even 
when deeply located, more gelatinous and less caseated. 

2. Neuroepithelial Growths. — (a) Glioma constitutes 25 per cent, 
of brain growths; 50 per cent, occur in the hemispheres, especially the 
cortex; 25 per cent, in the cerebellum and the balance in the central 
ganglia, pons, medulla, crus, etc. They occur more frequently in the 
brain than in the cord or retina, to which three structures they are peculiar. 
Gliomata are, in 90 per cent., single and are seen most frequently in adults, 
largely in the gray substance, which they so closely resemble in tint that 
detection is difficult at operation or indeed at autopsy. Their size 
varies from that of a pea to that of a hemisphere. Glioma infiltrates 
without sharp demarcation rather than compresses the brain tissue. The 
cells resemble the neurogliar structure and usually have round or oval 
nuclei; Klebs found ganglionic cells. Their processes are fine ; numerous 
and branched delicate band-like lines result from fiber degeneration. 
(b) The rare cerebroma of Hayem is heterotopic gray matter, (c) Ade- 
noma of the pineal gland and hypophysis, growths from the plexuses 
and neuromata may be brought under this heading. 

3. Connective-tissue Tumors. — (a) Sarcoma consitutes 20 per cent, 
of brain tumors; it may develop in the meninges, periosteum or vessels. 
It is most common in adults. Though it infiltrates more than tubercles 
or gummata, many are well demarked. Its structure and degenerations 
are those of sarcoma elsewhere. Though commonly single, diffuse 'or 
multiple sarcomatosis is sometimes encountered. Endothelioma, cylin- 
droma, angiosarcoma and melanosarcoma are but varieties. The sand 
tumors (psammomata) are sometimes described as angiolithic sarcomata. 
The "pearly tumors" (cholesteatomata) are formed of flat endothelial 
cells, (b) Lipoma, fibroma and osteoma are very infrequent. 

4. Metastatic Tumors. — Cancer is not infrequent (7 per cent.), 
especially from mammary or lung carcinoma. It often invades the 
hemispheres and basal ganglia and may attain huge dimensions. Like 
sarcoma, it infiltrates. Cancer is very rarely primary. 

5. Cystic Tumors. — Cysts may result from hemorrhage or soften- 
ing, degeneration in neoplasms, porencephalia, trauma or inflammation 
in the choroid plexus. Dermoids and teratomata are most rare. 
Eclrinococcus cysts may be single or multiple, chiefly on the surface 
of the brain or in the meninges. Cysticercus cysts develop mostly on 
the pia and arachnoid over the cortex along the sulci or in the ventricles. 
Diamond could collect but 8 cases from the American literature; they 



BRAIN TUMORS 791 

Vary from the size of a pea to that of a hazel-nut, are usually multiple 
(200 in Snell's case) and contain clear fluid with black dots, the heads 
of the parasites. 

6. Aneurysms. — Aneurysms have been considered. 

Localization. — The localization is: cerebrum, 42 per cent.; cerebellum, 
25; base, 11; pons, 8; central ganglia, 7 ; medulla, 4; corp. quadrigemina, 
2; and cms, 1 per cent. 

Symptoms. — In rare instances, tumor is found at autopsy without 
clinical symptoms (latency), due to location in a "silent" or tolerant 
brain area. Symptoms result from the following mechanisms: (a) 
Direct pressure on the brain, which may flatten the convolutions, ob- 
literate the sulci, force open the skull fissures in children, absorb or 
perforate the cranium, conspicuously in growths of the posterior fossa 
closed by the rigid tentorium. (b) Internal hydrocephalus, distention of 
the ventricles, may follow closure of the aqueduct of Sylvius or 
compression of the veins (choroid plexus and vena Galeni magna), 
especially by tumors of the cerebellum and corp. quadrigemina. (c) 
The brain may be softened by pressure on its vessels, or hemorrhage may 
develop (as in glioma) . (d) Infiltration or destruction of the brain matter. 
(e) Meningitis, local as in gumma, or general as in tubercle. (/) Auto- 
intoxication from the growth, (g) Distortion of the cerebral or spinal 
nerves may cause their degeneration, or changes in the posterior columns 
of the cord and its roots. 

1. General Symptoms. — General symptoms usually introduce the 
disease and include the following: (a) Headache is present in almost all 
cases, is usually constant, with accessions (especially in the morning), 
is general, severe, is increased by alcohol, exertion and coughing, and 
rarely corresponds with the tumor's site except when the pain is per- 
sistently local and the tumor near the surface. Headache is best explained 
by stretching of the dural branches of the fifth nerve. It may be pulsating 
in aneurysm, (b) Choked disk, the most important general symptom, 
consists of a grayish-red swelling of the disk to even two or three times 
its normal dimensions, which lessens its sharpness of outline and physio- 
logical cupping; the arteries become less lustrous and smaller, the veins 
turgid and tortuous, extravasations of blood and white patches of fatty 
degeneration or exudation appear. (See Plate IV, Fig. 3). It is due to 
increased intracranial tension, which causes mechanical hydrops of the 
optic sheath or to inflammation from choking of the veins by toxic 
products. It is bilateral, although more marked on the side of the lesion, 
is not an early symptom and does not depend on the size of the tumor. 
It is constant in growths of the corp. quadrigemina, is present in 90 per 
cent, of cerebellar growths and in 35 per cent, of those of the pons, medulla 
and corp. callosum. There is often limitation of the field of vision (sco- 
toma for color). In many cases it develops into atrophy, oftener still 
into stasis and blindness, perhaps suddenly, while in some it may regress. 
Transitory amaurosis results from compression of the optic tract or chiasm 
by the distended third ventricle, (c) Convulsions occur in 50 per cent., 
are called the "signal symptoms" by Seguin and may be general; general 
tonic precede clonic convulsions in no special order; the pupils react 



792 DISEASES OF THE BRAIN 

poorly, the skin reflexes are increased unless deep coma develops, the 
tendon reflexes are not suspended and respiration is labored. Convulsions 
are more frequently late than early. Slight seizures, like the petit mal 
of epilepsy, may occur. Jacksonian epilepsy belongs to the focal symp- 
toms, {d) Vomiting is usually an early general symptom, indicating 
irritation of the vomiting centre (in the medulla it is a focal symptom). 
It is of the cerebral type, occurring without effort, nausea or pain, often 
on an empty stomach, as in the morning, or at once after eating, regard- 
less of the kind of food ingested. Vomiting is due to increased intra- 
cranial pressure or meningeal irritation. It is rarely absent in growths 
of the cerebellum or medulla, is very frequent in disease of the corp. 
quadrigemina and occurs in 25 per cent, of tumors in the hemispheres. 
(e) Sensorium. The most common change is dulness, which often deepens 
into stupor and coma. Tumors affecting the association fibers and avoid- 
ing the motor centres may cause disturbance of intelligence, judgment 
or memory only; they are frequently discovered at autopsy in the frontal 
or temporosphenoidal lobes in subjects committed to asylums for psy- 
choses or general paralysis. (/) Vertigo is an early symptom; it may be 
mere "giddiness" or it may affect the labyrinth, pons or cerebellum and 
be a sense of actual rotation. It is present in 31 per cent, and as a focal 
symptom when the middle cerebellar peduncle is implicated, (g) Slowed 
pulse results more often from indirect pressure on the vagus fibers behind 
and lateral to the hypoglossal nucleus. The vagus fibers become accus- 
tomed to pressure and the heart rate increases. It is often associated with 
yawning, hiccough, Cheyne-Stokes's breathing, glycosuria or polyuria. 

2. Focal Symptoms. — Focal symptoms may be absent when the 
disease is limited to "silent" or "tolerant" areas, when the tumor does 
not destroy nerve structures and when vicarious compensation by other 
parts is possible. Focal symptoms of irritation or paralysis may result 
directly from actual lesion of a centre or its fibers, or indirectly from 
"distance pressure" upon them. They are most significant when no 
particular increase of intracranial tension exists. 

(a) Frontal Lobes. — Early observers claimed that mental changes were 
no more frequent in frontal localization than in localization elsewhere. 
A dementia with characteristic irritability and excitement, a tendency 
to make jokes, apathy and suffering are described. Homolateral tremor 
and contralateral loss of the abdominal reflexes are described by Granger 
Stewart. Mental alteration sometimes follows other localizations. 
Tumors in the frontal lobes may be thought to be in the motor areas 
from indirect pressure upon the latter. The head and eyes may deviate 
and the neck and back are sometimes rigid; frontal tumors may induce 
cerebellar ataxia, caused by unequal innervation with disturbance of the 
sensorium or involvement of the trunk centres. Bradyphasia is probably 
psychical and differs from the separation of syllables sometimes seen in 
tumor of the pons. In "laryngeal aphasia" the patient moves his lips 
and attempts to speak, but finds the voice lacking. 

(b) Motor Cortex. — (i) Jacksonian convulsions (50 per cent.) are often 
dissociated, and follow a given sequence (see page 751). The convulsions 
may run into the hundreds (17,000 in eleven months). When the con- 



MAIM TUMORS 793 

ducting fibers are destroyed they cannot occur, whence they may be 
observed in the part nearest the seat of greatest damage. As long as 
convulsions are present the motor centres cannot be wholly destroyed. 
Tapping the skull may initiate spasms, (ii) Cortical paralysis is usually 
monoplegic and associated with cortical spasm; at first a weakness from 
exhaustion follows the spasms; later it becomes more marked. Slowly 
progressive hemiplegia without other symptoms may suggest tumor 
(Williamson) and paresis may be the first sign of tumor, perhaps narrowly 
localized, as in the thumb alone, fingers or great toe ; paralysis is accom- 
panied by increased reflexes and rigidity. Surgical extirpation has relieved 
both spasms and paralysis. In infrequent instances the paralysis may 
be bilateral, as when a cortical tumor near the median line presses on the 
opposite hemisphere or, when there are bilateral symmetrical growths. 
(iii) Sensory changes are less frequent, because the sensory is larger than 
the motor area, extends posterior to it and possibly is bilateral. Hyp- 
esthesia, especially for tactile and muscular sensibility and paresthesia, 
are not rare. 

(c) Parietal Lobes. — Sensory disturbance is fairly common. Inco- 
ordinate movements, ataxia, conjugate eye movements and sensory 
aphasia, hemianopsia, deafness and word-deafness are observed. 

(d) Temporal Lobes. — Hemianopsia, disturbed eye movements toward 
the opposite side, ptosis and agraphia are recorded. Uncinate "fits" 
are characterized by subjective — and usually disagreeable — sensations of 
smell and taste, of which Mills collected 12 cases (1908). 

(e) Occipital Lobes. — Hemianopsia is the most constant finding. Optical 
hallucinations indicate a cortical occipital localization. Alexia, optic 
aphasia and psychical blindness are seen. 

(/) Pons. — Focal may precede the general symptoms, as enumerated 
under Cerebral Localization. Hemiplegia with alternating paralysis of 
some of the first eight cranial nerves is the most common type (50 per 
cent.) . Foci in the substance of the pons involving the sixth nerve usually 
involve the opposite third nerve; foci near the surface involving the 
sixth nerve do not involve the third nerve. Sometimes the nerves may 
be involved without hemiplegia (25 per cent.), but rarely without crossed 
motor irritation or hemianesthesia; hemiplegia alone occurs in 25 per 
cent. Unilateral tumor may compress the opposite motor tracts (para- 
plegia or diplegia) and cranial nerves. Motor irritation is not uncommon, 
as trismus, facial spasm, trigeminal neuralgia, convulsions in the contra- 
lateral limbs, etc. Sensory disturbance is usual, as hemianesthesia cruciata 
(in arm and leg of one side and in the face of the opposite side when the 
focus is low in the pons), hemianesthesia of face, arm and leg of the 
same side (tumor in the upper pons) and anesthesia of one or perhaps of 
both sides. Dysarthria, dysphagia, difficult urination or defecation and 
disturbed respiration on change of posture have been observed. 

(g) Medulla. — It is remarkable that tumors may produce no symptoms 
or only such that localization in the pons or cord is first suggested. In a 
small number of cases only are the symptoms not ambiguous. Bilateral 
paralysis of the ninth to twelfth nerves with degeneration and atrophy 
of the lips, tongue, palate, pharynx or larynx is characteristic and presents 



794 . DISEASES OF THE BRAIN 

a picture like progressive bulbar palsy. Alternating hemiplegia is rare. 
Sensory, motor, atactic and nerve involvements are usually bilateral. 
Stern (1907) collected 72 cases of cysticerci of the fourth ventricle and 
50 of tumors, characterized by suboccipital pain, bowing of head forward, 
paroxysmal attacks of vomiting, headache and cervical rigidity. Growths 
outside the medulla may cause paralysis of the neck muscles. Slowed 
or rapid pulse, singultus, embarrassed breathing, glycosuria and polyuria 
are not uncommon. 

(h) Cerebellum. — Cerebellar ataxia, referred by Nothnagel and Gowers 
to lesions of the vermis in 85 per cent, of the cases, occurs but half as 
frequently in disease of the cerebellar hemispheres. Compression of the 
pons, medulla, corpora quadrigemina and fifth to twelfth cranial nerves 
is somewhat characteristic. Extra-cerebellar tumors may, in the ponto- 
medullocerebellar angle, involve hearing and also the eighth, fifth or 
sixth nerves (disturbance of hearing, paralysis of winking and tardy 
corneal reflex). Of the general symptoms, choked disk is almost in- 
variable; occipital headache and rigid neck are very frequent. Con- 
vulsions are common and opisthotonos with tetanic rigidity of the body 
and extremities is most suggestive. 

(i) Optic Thalamus. — Moderate hemiplegia (transient and without con- 
tractures), hemichorea, hemiathetosis, hemianesthesia (always marked 
as to deep sensation), slight hemiataxia, marked astereognosis and 
persistent pains (hemiplegie douloureux) constitute the thalamic syndrome 
of Roussy (1907). Less common are Nothnagel's mimetic paralysis, 
unilateral convulsions, forced movements or postures, contralateral 
hemianopsia, paralysis of the eye muscles, widening of the opposite 
pupil and monoplegia. 

(j) Corpus Callosum. — According to Bristowe, dementia (in 90 per 
cent.), absence of initiative in speech and action, paraplegia, dysarthria 
and few general symptoms, as choked disk, are characteristic. Oppen- 
heim holds that there are no distinctive symptoms. 

(k) Corpora Quadrigemina. — Paralyses of the third nerve are common, 
sometimes associated as double ptosis, and bilateral paralysis of the 
internal recti. The pupils are usually free. There may also be crossed 
hemiataxia, disturbed hearing, amblyopia and intention tremor. No 
paralysis, except of the third nerve, is present unless the tumor extends 
beyond the corp. quadrigemina (Oppenheim). 

(I) Pineal Gland. — The symptoms are the same as when the corp. 
quadrigemina are affected, save that the fourth and sixth nerves are 
involved more than the third and compression of the pons or medulla 
is more common. There may be obesity or genital hypertrophy. 

(m) Tumors at the Base. — These include osseous tumors, aneurysms, 
hypophysis growths and those from the nerves or meninges, (i) In 
the anterior fossa, hypophysis tumors (see Acromegaly) disturb vision 
and produce bitemporal hemianopsia with amblyopia or sometimes 
irregular or transverse hemianopsia. Usually there is no choked disk, 
but simple optic atrophy: The third nerve is paralyzed in most cases, 
sometimes other ocular trunks. Exophthalmos is occasional and the 
growth may perforate externally into the eye, pharynx or nose. Loss of 



BRAIN TUMORS 



795 



smell (anosmia) and mental symptoms are observed, (ii) In the middle 
fossa, mental symptoms and convulsions are less common. The Gasserian 
ganglion may be compressed and result in neuroparalytic ophthalmia. 
Other cerebral nerves, as the third and sixth, sometimes suffer. Syphilis 
and sarcomatosis may be diffusely basal, (iii) Lesions in the posterior 
fossa may simulate bulbar palsy. The lower eight cranial nerves usually 
suffer more readily and earlier than the pyramidal tracts; the grouping 
of the cranial nerve implication is different; thus paralysis of the sixth 
nerve is rarely associated with the conjugate fourth nerve, as occurs when 
the lesion is central. The seventh and eighth nerves are often conjointly 
paralyzed in disease of the posterior fossa and but rarely so in central 
tumors. The symptoms often resemble those of lesions of the pons, 
medulla, etc. 

Diagnosis. — Four general groups of cases are encountered: (1) 
Absolute clinical latency; (2) general and focal symptoms, the typical 
case; (3) general but not focal symptoms; (4) definite symptoms of 
some brain disease but of equivocal significance. According to Bruns, 
80 per cent, of cases can be detected. 

Analysis of the General Symptoms.— (a) Headache is suggestive 
when it is severe and when the skull is tender to percussion. Organic, 
irritative brain disease, as abscess or inflammation, may cause headache. 
Headache may result from migraine, neurasthenia, hypochondriasis, 
eye disease, intoxications (uremia, gastro-intestinal disorder and poison- 
ing by nicotine, opium, alcohol or lead), and from arteriosclerosis. (6) 
Choked disk in 85 per cent, of cases indicates brain tumor (Oppenheim) 
and if very marked it is seldom due to other causes. It is less frequent 
in abscess and meningitis, in which neuritis optica is more frequent. 
It is most rare in embolism, softening, hemorrhage, hematoma durse 
matris, arteriosclerosis, poliencephalitis, encephalitis, the acute fevers, 
lead poisoning, neuritis multiplex or alcoholism. Uremia and tumor 
have, in common, headache, epileptiform or apoplectiform attacks, 
hemiplegia, aphasia and slow pulse, yet neuroretinitis is more common 
in nephritis. The rare^ choked disk of chlorosis responds to iron, (c) 
General epileptiform convulsions occur in meningitis, pachymeningitis, 
abscess, vascular disease, syphilis, alcoholism, plumbism, multiple 
sclerosis, paretic dementia, uremia, etc. 



Epileptic Convulsions. 



More coarse; more biting of tongue; more 
frequent cry; more sudden, complete 
loss of consciousness, frequently an epi- 
gastric aura; usually longer interval 
between attacks. 



Convulsions resulting from organic brain disease. 



Convulsions more orderly, slow, clonic, 
broken by tonic contractions; often with 
gradual local commencement, without loss 
of consciousness, and with paresis in the 
Jacksonian type. 



(d) Vomiting is probably cerebral and due to tumor, if hysteria, 
migraine, toxemia and gastric disease can be excluded. 

Combination of General Symptoms. — Headache and choked disk 
occur in chlorosis, plumbism (also with delirium, convulsions and coma, 



796 DISEASES OF THE BRAIN 

but distinguished by the lead line on the gums) or in uremia, in which 
special examination for albumin, casts and cardiovascular changes are 
definitive. The same combination may prevail in hypermetropia in 
anemic girls, in amenorrhea and in injuries of the head, but care 
usually distinguishes them from the slow onset and focal signs of brain 
tumor. 

Topical Diagnosis. — Focal symptoms usually follow the general, 
whereas, in apoplexy, for example, the focal hemiplegia is early. In 
tumor with hemiplegia, contracture or spasticity accompanies rather than 
follows the paralysis, as usually occurs in hemorrhage or embolism. 
Hemiplegia from a tumor is less pure, less circumscribed, less systematic 
(Fournier). A tumor at the base may cause hemiplegia from pressure 
on the middle cerebral artery with encephalomalacia. Jacksonian epi- 
lepsy with paresis is due to cortical tumors in 50 per cent, of cases. It 
is also produced by hemorrhage, softening and inflammation and is then 
earlier, is not confined to as small an area and is not as progressive as in 
neoplasm. 

Nature of The Growth. — {a) Location. Cortical growths are prob- 
ably gumma or tubercle (possibly glioma, cysts, cysticercus or sarcoma) ; 
subcortical, glioma or sarcoma; pons, tubercle, gumma, glioma; cere- 
bellum, tubercle or glioma; extracerebral, sarcoma; multiple occurrence, 
tubercles or gummata. (b) Course. A rapidly growing tumor is probably 
glioma or sarcoma. An apoplectic attack indicates glioma or ruptured 
aneurysm. Growth with remissions is characteristic of tubercle or 
glioma. A very slow course suggests fibroma or osteoma. Coincident 
meningitis indicates tubercle or syphilis. 

Differentiation. — Brain abscess: abscess and tumor may result 
from trauma, but brain abscess is almost always traumatic, otitic or 
metastatic; unilateral optic neuritis is more common than choked disk, 
and abscess is more prone to fever, chills, rapid course and apoplectic 
seizures than is tumor, while involvement of the cranial nerves is less 
frequent. Differentiation from paretic dementia, pachymeningitis, 
meningitis, syphilis, hysteria and hydrocephalus will be considered under 
each disease. 

Multiple Sclerosis. The pressure symptoms of tumor are absent and 
in the disk there is an incomplete optic atrophy. The tremor may be 
confused with incoordination tremor of tumor in the optic thalamus, 
pons or cerebellum. 

Course and Prognosis. — The first symptoms are usually general; the 
later are focal. The disease runs a fatal course in one-half to two years, 
in rare cases four to fourteen years. Exacerbations result from aneurysmal 
rupture, hemorrhage into a glioma, cyst formation, ventricular effusions, 
meningitis or local neuritis. Remissions are not uncommon; healing 
of parasitic and simple cysts, aneurysms, tubercles (in the young) and 
gummata is possible. Unfavorable symptoms are pronounced mental 
change, incoercible vomiting, irregular, rapid pulse, repeated fits, apo- 
plectiform seizures or festinating neuritis optica. The mechanism of 
death is exhaustion from vomiting, pain or cachexia; inhalation pneumonia; 
coma with disturbed respiration, circulation or other bulbar signs* 



ENCEPHALITIS 797 

sudden death in tumors of the base; meningitis or arterial disease; and 
intercurrent infections. 

Treatment. — Medical treatment is not encouraging save in syphilis, 
but every patient should be given a long course of mercury and iodide. 
Tubercle is sometimes arrested by increasing the physiological resistance 
by forced feeding, fresh air, cod-liver oil and arsenic. The headache 
is often relieved by iodide, the ice-bag, morphine, atropine, coal tars 
and decompression operations. Convulsions should be treated by chloral. 
Brain congestion from alcoholism, excitement, exertion, overeating or 
obstipation should be avoided. 

Surgical Interference. — Macewen, Horsley, Bennett, Ferrier and 
Godle are the pioneers in brain surgery, (a) In radical operation the 
outlook is not encouraging. Allan Starr estimates that but 18 per cent, 
of tumors are accessible, and but 7 per cent, removable. The best results 
are obtained in meningeal and cortical growths, especially of the motor 
and occipital zones. Duret found that 18 per cent, died, 64 per cent, 
improved and vision was completely restored in 60 and partially in 18 
per cent. Recurrence is common. Death occurs from hemorrhage, 
sepsis, dislocation of the brain, basal compression, brain edema and 
shock. Horsley and Macewen suggested two steps; first exposing the 
tumor and later removing it after the brain had accommodated itself to 
the change of relations, (b) Palliative decompression may be beneficial, 
often greatly relieving headache and blindness and permitting the tumor 
to grow outward when it cannot be removed. From lumbar puncture 
38 cases of sudden death are reported, the withdrawal of the supporting 
column of cerebrospinal fluid accentuating a hernia of the medulla into 
the foramen magnum. 



INFLAMMATION OF THE BRAIN. 

I. Encephalitis. — "Inflammation of the brain" as understood by the 
laity, is meningitis. Coswell and Hasse (1850) definitely distinguished 
between encephalomalacia and encephalitis. 

Etiology. — The three main factors are: (a) Intoxications, from alcohol, 
illuminating gas, sulphuric acid, ptomaines in decayed meat, nicotine 
and sunstroke, (b) Infections, as influenza, scarlatina, hydrophobia, etc. 
Some relation to chlorosis, chorea insaniens or maniacal forms of exoph- 
thalmic goitre is possible, (c) Trauma. 

Pathology. — The process begins as multiple disseminated foci, prin- 
cipally in the gray matter; these usually are the small " flea-bite" areas 
of capillary hemorrhage, which glisten and stain the adjacent tissues, 
show above the cut section and later become foci of softening. Micro- 
scopically, hyperemia, perivascular exudation of red and white cells, 
serous effusion, aggregations of mononuclear cells somewhat resembling 
a tubercle, and degenerated, fatty and swollen ganglion cells are observed; 
the medullary sheaths and later the axis-cylinders degenerate. Its issues 
are: (a) regression (recovery); (b) necrobiosis with softening; (c) cyst 
formation; (d) cicatrix formation or (e) possibly diffuse brain sclerosis 



798 DISEASES OF THE BRAIN 

or multiple sclerosis. Associated nervous changes are optic neuritis, 
multiple neuritis and poliomyelitis, and general changes are enlarged 
spleen, general hemorrhages and parenchymatous degeneration, etc. 

Special Pathology and Symptomatology. — 1. Porencephalitis Acuta 
Superior Hemorrhagica or Ophthalmoplegic a. — Wernicke (1881) 
described this affection in alcoholic adults; it attacks the gray matter 
about the third and fourth ventricles and aqueduct of Sylvius, whence 
it may spread upward or downward; it is analogous to acute polio- 
myelitis. The general symptoms are delirium tremens, or somnolence in 
non-alcoholics, headache, vomiting and rigid neck. The local symptoms 
consist of an early extensive ophthalmoplegia, which involves associated 
eye muscles, as the two internal recti, or the internal rectus of one eye 
and the external of the other and usually evades the pupil and levator 
palpebral superior. The gait is atactic from involvement of the corpora 
quadrigemina. Speech is frequently difficult. Neuritis is observed in 
the optic disk and sometimes in the peripheral nerves, as evidenced by 
the absent patellars, ataxia, tender muscles, etc. Sometimes there is 
hemiparesis or facial paresis. The temperature is usually normal or 
subnormal, though respiration and pulse are increased. Death occurs 
within two weeks after these violent symptoms. Some cases thought 
to be nuclear have been proved polyneuritic. 

2. Encephalitis or Poliencephalitis Hemorrhagica. — Striimpell 
(1884) described cases causing infantile paralysis (q. v.). In 1885 Leichten- 
stern saw cases following certain infections. Foci in the cortex, subcortex 
or central ganglia, contained pus cocci and influenza bacilli. The disease 
occurs mostly between the fifteenth and thirtieth years. After an in- 
fluenza (q. v.) there may be (a) general symptoms, as headache, vomiting, 
delirium, mental obscuration, convulsions, high fever, slow pulse, irreg- 
ular breathing, stiff neck or optic neuritis; (b) focal symptoms appear 
after a few days, as hemi- or monoplegia, aphasia, conjugate deviation, 
focal convulsions or hemichorea. The reflexes are affected as in apoplexy. 
The course lasts one-half to three weeks and is often fatal. This form 
may resemble hemorrhage, syphilis or softening, but the paralysis is 
preceded by fever, enlarged spleen, somnolence or convulsions. Menin- 
gitis is usually differentiated with ease. 

3. Subtypes. — These consist of the following: (a) poliencephalitis 
inferior acuta, involving the pons or medulla and giving acute bulbar 
symptoms; there is paralysis of the sixth or seventh to twelfth nerves 
when it occurs in various combinations or with types (1) and (2). Con- 
fusion is possible with softening, hemorrhage, the late hemorrhage of 
trauma or tumors, (b) With poliencephalomyelitis, inflammation and 
paralysis of the anterior spinal roots may coexist. Hutchinson's facies 
is observed, viz., fixed eyes, fallen lids, prominent eyebrows, obliterated 
nasolabial folds and atrophic paralysis of the arms. Differentiation from 
multiple neuritis is usually possible. 

Prognosis. — The peracute cases may die in two days; acute cases last 
one-half to three weeks and death is most frequent; Oppenheim instances 
recoveries. Much involvement of the mind, decubitus, alcoholic delirium, 
chlorosis, sinus thrombosis and weak pulse are unfavorable elements. 



ABSCESS OF THE BRAIN 799 

In children recovery is common, but epilepsy, paralysis and mental 
alteration are sequences. 

Treatment. — This is symptomatic. The causal factor must be elimi- 
nated, cerebral congestion avoided and the skin, bowels and bladder, 
delirium and convulsions, diet and patient's rest must be cared for as in 
brain hemorrhage. Mercurial inunctions and potassium iodide give the 
best results. Electricity is indicated in the chronic stage. 

II. Abscess of the Brain. — Encephalitis apostematosa is not a common 
disease. Eichhorst found three among 13,563 medical cases. 

General Etiology. — The streptococcus is the most frequent micro- 
organism, the staphylococcus coming next, then the pneumococcus and 
other bacteria. Mixed infections are common; old abscesses are often 
sterile. Sixty-six to 75 per cent, occur in men. Twenty per cent, occur 
in the second and 33 per cent, in the third decade. The cerebrum is 
involved in 75 and the cerebellum in 25 per cent. 

General Pathology. — The focus is single in 80 per cent, of cases. The 
average size is from one to two inches, but it may occupy nearly the entire 
hemisphere. The surrounding brain may be inflamed, or edematous. 
The right side of the brain is more often affected. Pressure is less common 
and less intense than in tumor; very large abscesses may produce internal 
hydrocephalus. The abscess consists of pus of variable consistency, 
yellow or green, acid; flocculi of disorganized brain tissue are common. 
The pus cells are often disintegrated and fatty needles, cholesterin 
crystals and sometimes corpora amylacea are found. Putridity is due to 
communication with the nose or ear or embolism from putrid lung foci. 
Encapsulation occurs in 50 per cent., chiefly in old cases, but rarely 
completely or permanently limits the abscess, which usually grows and 
often ruptures. 

Special Etiology and Pathology. — 1. Infective Foci near the Brain. — 
Infective foci near the brain are its usual causes, and for this reason brain 
abscess is seen by internalists, neurologists, surgeons and otologists, (a) 
Ear disease explains at least 25 per cent, of brain abscess. Insurance 
companies recognize the risk in these cases. Jansen found one abscess 
to 500 cases of chronic and one to 2650 of acute otitis. The ear disease 
may date back thirty or forty-five years and is especially dangerous 
when it recurs and when granulations and polypi exist. The acute 
infections thus indirectly cause brain abscess. Infection traverses the 
bone to the dura by way of the thin tegmentum tympani, by the 
roof of the antrum, sometimes through the petrosquamous suture (in 
children), mastoid cells, lateral sinus, labyrinth or aqueduct along the 
sheaths of the seventh and eighth nerves; in 42 per cent, there is a fistule 
between the abscess and the causal focus; in 15 per cent, the dura inter- 
poses between the two foci; in 15 per cent, there are dural adhesions 
and in 17 per cent, the intervening substance is softened brain tissue. 
Toynbee remarked that disease of the roof caused temporosphenoidal 
abscess, but disease of the mastoid cells chiefly produced cerebellar 
abscess. Of otitic abscess, temporosphenoidal constitutes 67 per cent. 
(75 per cent, under ten years) and cerebellar abscess 33 per cent.; the 
latter is rarely due to any cause other than otitis and almost invariably 



800 DISEASES OF THE BRAIN 

occurs in the anterior part of its hemispheres. Otitic abscess infrequently 
involves the occipital, frontal (two personal observations) or parietal 
lobes. The smaller the abscess the nearer it lies to the cortex. (6) 
Traumatism produces 25 per cent, of cases. Punctured wounds are more 
dangerous than open, compound fractures. Fractures of the base (by 
infecting the middle ear), splintering of the inner table (areas becoming 
infected through the blood) and operations on the brain are possible 
causes; 80 per cent, occur over ten years of age. Ninety-three per cent, 
are solitary abscesses. Infection travels along the perivascular and 
perineural lymph sheaths but may pass "retrograde" by the valveless 
veins, (c) Other contiguous disease is rarer, causing but 4 per cent, of 
brain abscess. Disease of the nose and communicating sinuses may cause 
abscess of the frontal lobes and in antrum disease sometimes of the 
parietal lobes. Disease of the orbit, as phlegmon or penetrating wounds, 
and still more rarely cranial osteomyelitis, ulcerative tuberculosis or 
syphilis may cause abscess by contiguity. 

2. Metastatic Abscesses. — Metastatic abscesses constitute 25 per 
cent, of brain abscess. The abscesses may number from 2 to over 100; 
they are multiple in 66 per cent. They are cortical or subcortical, less fre- 
quently in the central ganglia and almost never in the cerebellum alone. 
The causal embolus is seldom found, (a) Lung lesions: "pulmonal cere- 
bral abscesses" are due to empyema, putrid bronchitis and bronchiectasis 
(45 per cent.), gangrene, abscess and sometimes tuberculous cavities. 
This form rarely encapsulates. (b) Ulcerative endocarditis, pyemia, 
osteomyelitis, etc., are less common causes; paradoxical embolism may 
occur through a patent foramen ovale, whereby the clot escapes the 
lungs. 

Symptoms. — Symptoms are absent in 10 per cent, of cases. 

1. Symptoms of Sepsis. — (a) Fever is the most important general 
symptom; Eichhorst describes cases closely resembling typhoid; it is 
present in acute cases and during the last stages when the abscess 
spreads or meningitis or sinus thrombosis develops. Macewen's cases 
showed normal or subnormal temperature. (6) Chills are not frequent. 
(c) The pulse is often accelerated, but may later become slowed to 30 
or 40, the compression pulse. 

2. Diffuse Brain Symptoms. — These are due to increased intra- 
cranial tension, inflammation, meningitis or internal hydrocephalus 
and include (a) headache, which is most common and severe, though 
less so than in brain tumor; even the stiff, painful neck and headache 
are general rather than focal symptoms. It is frequently associated with 
(b) vomiting and (c) vertigo, (d) Mental symptoms are those of slow 
cerebration, (e) General convulsions are frequent only in the last stages, 
in cases of extensive abscess or rupture into the ventricle. (/) The 
pulse is often slowed, even with coexistent fever, to 40 (even 10) and 
sometimes with slow or irregular respiration. (</) Optic neuritis is more 
common than choked disk; it occurs in 53 per cent, and may produce 
amaurosis and atrophy. 

3. Focalizing Symptoms. — Focalizing symptoms are often absent 
and when present are less conspicuous than in tumor because they are 



ABSCESS OF THE BRAIN 801 

obscured by the primary affection or the general symptoms and occur 
in areas of less physiological dignity. They usually signalize advance of 
the abscess, softening or increased brain tension. 

Frontal or mental symptoms may occur (see Tumor), but foci as 
large as the fist may remain latent. They may impinge on the motor 
cortex. The symptoms are those of a cortical lesion, which extends 
more rapidly than tumor and is attended by Jacksonian fits, rigidity 
and increased tendon and decreased skin reflexes on the contralateral 
side; in subcortical lesions from traumatic and metastatic abscess, hemi- 
paresis occurs in 50 per cent., is sometimes progressive, usually incomplete 
and at times is apoplectiform in onset (three personal observations). 
If hemiparesis i-s early it indicates involvement of the internal capsule,- 
which also causes hemihypesthesia. Conjugate deviation is not common. 
Temporosphenoidal lesions are largely otitic, frequently latent and 
subcortical, whence the centres are less involved than the deeper associa- 
tion fibers. The more important left-sided lesions lead (in 42 per cent.) 
to sensory aphasia, partial word-deafness, alexia, agraphia, amnestic 
and optic aphasia. The right side concerns the memory for letters and 
figures. Occipital lesions or those deeper in Gratiolet's optic radiation, 
produce hemianopsia (more in traumatic or metastatic than in otitic 
abscess). Cerebellar abscess results almost exclusively from ear disease 
and is often latent. Occipital headache and stiff neck occur; there may 
be a tendency to fall forward or backward and hemiparesis or yawning 
may result from compression; cranial nerve paralyses are not frequent 
and result from coincident meningitis. Paralyses of the seventh and 
eighth nerves are often due to bone disease. Abscess of the pons, medulla 
(of which Cassier, in 1903, found only 16 cases) and crus is exceptional. 
(See Cerebral Localization.) 

Symptoms by Stages. — (i) The initial stage is observed mostly in 
acute traumatic or metastatic abscess. Pus formation usually requires 
ten to thirty days. The causal septic and general brain symptoms 
appear rapidly; death may occur from coma, fever and meningitis 
or the next stages appear, (ii) The latent stage has no fever, is seen in 
chronic abscess, probably corresponds with encapsulation and lasts for 
months or even decades, (iii) In the u manijest" stage septic, general 
or focal brain symptoms appear continuously or remittently, with 
evidence of extension. Most cases are seen in this stage. Gowers esti- 
mates that after nervous symptoms once develop, (iv) the next or terminal 
stage, appears in five days (20 per cent.), in ten days (33 per cent.), 
fourteen days (50 per cent.) and in thirty days (75 per cent.). 

Diagnosis. — Recognition is impossible in latent cases affecting " silent'' 
areas, whence "no brain disease of equal severity so often escapes 
recognition." Few cases can be detected without consideration of the 
etiology, which is definitive in 75 per cent., the sepsis, general and focal 
brain symptoms. 

Otitic abscess may be confused with the otitis itself, especially in 

children; otitis may produce headache, vomiting, convulsions, ODtic 

neuritis, nystagmus and diplopia, but all symptoms disappear under 

surgical care; otitic brain abscess runs an acute course; temperature 

51 



802 DISEASES OF THE BRAIN 

is often lower than in other forms, the headache may be local and 
edema may be seen over the temporal region, with tenderness on per- 
cussion and a higher percussion-note (Macewen). 

Serous meningitis is often mistaken for the suppurative form and is 
very important in ear disease. It is attended by slight temperature, 
internal hydrocephalus, paralysis of the basal nerves and gives a serous 
fluid on lumbar puncture. Extradural abscess was found in 78 per cent, of 
cases of brain suppuration by Jansen, sinus thrombosis in 18 per cent, 
and brain abscess in barely 3 per cent. Local symptoms, as edema and 
tenderness, are commoner than diffuse and focal symptoms. Sinus 
thrombosis (q. v.) is more often attended by pyemic symptoms, foci in 
the lungs, choked disk and external signs of altered brain circulation. 

Traumatic abscess is often suspected because of delayed healing of the 
wound. It is usually cortical (whence its focal symptoms) and often 
provokes fever and other general symptoms. It must be differentiated 
from traumatic hemorrhage, which occurs days or weeks after the injury 
and often in the corp. quadrigemina, pons or medulla; from acute 
encephalitis, whose course is more rapid; from concussion, in which the 
symptoms are more diffuse and may involve the brain nerves or arouse 
fever, though cortical symptoms are absent. The late traumatic abscess 
is subcortical (affecting the conduction or association fibers). Cerebral 
tumor (q. v.). 

Abscess by metastasis; localization is largely in the hemispheres, thus 
obeying the topography of embolism. The Sylvian district and occipital 
lobes are most often affected and the multiplicity of localization should 
be remembered. The course is usually precipitate. 

Prognosis. — Spontaneous recovery by demarcation, inspissation, calcifi- 
cation or external rupture is very unusual. Without operation, death 
is practically inevitable, from (a) rupture into the lateral ventricles, 
chiefly in metastatic and otitic abscess and into the membranes 
(cerebellar abscess), (6) hydrocephalus internus, (c) sinus thrombosis, 
(d) pressure on the medulla, or (e) brain edema. Sudden death may 
occur without adequate postmortem explanation. 

Treatment. — (a) Prophylactic therapy concerns the etiological factor. 
Adequate drainage is always necessary, although granulations in the 
middle ear are protective and should not be curetted in any routine 
manner (precisely as uterine curettage is discountenanced in puerperal 
sepsis). (6) Palliative treatment is that of brain tumor and meningitis. 
Special care regarding vomiting is indicated, lest it rupture the abscess, 
(c) Surgical intervention. Successful cases were those of Morand 1868, 
Roux 1848, and Schede 1866. The contra-indications are metastatic 
abscess, a fatal etiological disease, ventricular rupture and diffuse 
meningitis, although in the last 2 cases isolated recoveries are recorded. 
Sinus thrombosis, circumscribed meningitis and incipient pyemia do 
not contra-indicate operation. In Korner's otitic abscesses, 51.6 per 
cent, recovered, Wheeler's series gave 87.5 per cent, and Macewen's 
96 per cent. 

III. Dementia Paralytica. — It is also known as paretic dementia, pro- 
gressive paralysis of the insane and among the laity as softening of the 



DEMENTIA PARALYTICA 803 

brain. Bayle, 1822, and Calmeil, 1826, first accurately described the 
affection. It is so important in every-day practice and constitutes such 
a large proportion (10 to 25 per cent.) of all insanities that its description 
is in place. 

Definition. — Dementia paralytica is a chronic inflammation or degen- 
eration of the brain, characterized by progressive vasomotor, motor 
and psychical disturbances. 

Etiology. — (a) Syphilis is the cause, Noguchi and Moore finding the 
spirochete in 25 per cent, of cases; dementia is syphilis and not a para- 
syphilitic affection. (6) Other causes are modern life, with its strenuous- 
ness, competition, hurry, worry, short sleep, dissipation, overwork and 
city life; Krafft-Ebbing summarized the etiology as " syphilization and 
civilization." These causes may cooperate with heredity and alcoholism. 
Generally speaking, the higher classes and certain occupations (officers, 
artists and actors) are more subject to it. Krafft-Ebbing found no 
clergymen among his 2000 patients. It occurs between the thirtieth 
and fiftieth years, and is 7 to 10 times as frequent in men as in women. 

Pathogenesis. — Lues probably produces (a) vasomotor paresis in the 
forebrain, followed by (b) lymph stasis in the cortex and pia, (c) degen- 
eration and atrophy of the brain and cord, and (d) interstitial inflam- 
mation. All cases end in brain atrophy but some regard chronic 
meningo-encephalitis as primary, and others hold that it is secondary 
to encephalitis parenchymatosa. 

Pathology. — (a) The calvarium is thickened in 33 per cent, (b) The 
dura in 50 per cent, is thick, opaque, vascular and adherent to the skull 
(pachymeningitis, which is often hemorrhagic). In attempting to strip 
off the pia it is found adherent to the brain cortex (in 80 per cent.), 
especially over the frontal and motor areas, supplied by the internal 
carotid artery, (c) Gross brain changes are constant. The brain in the 
early stages is swollen and hyperemic, in the later stages, wasted; it 
may weigh but a third or quarter of the normal (1260 gm.) ; atrophy 
affects largely the zones supplied by the internal carotid artery, especi- 
ally the frontomotor cortex and island of Reil. The gray matter is 
yellowish-gray, soft and wasted, but the atrophied white substance is 
firm. The convolutions are greatly narrowed and the sulci are widened, the 
degree of atrophy corresponding to the 6 or 8 ounces of serum which fills 
the deficit (hydrops ex vacuo). In 80 per cent, granulations are seen on 
the ependyma of the lateral ventricles, resembling the back of a "cat's 
tongue," and the ventricles contain hydrops ex vacuo, (d) The minute 
alterations in the brain are as follows : the ganglion cells are early swollen 
and cloudy; the later findings are vacuolated and atrophied ganglion 
cells; wasting of the medullary sheaths and axis-cylinders, especially the 
association or tangential nerve fibers running parallel to the cortex which 
waste before any inflammation can be seen; corpora amylacea repre- 
sent what is left of them; the same changes occur in the cranial nerves; 
the bloodvessels show mural proliferation, exudation, colloid or hyaline 
metamorphosis, thickening, atrophy and obliteration; the lymph vessels 
show proliferation, transudation and compression of the cortex, where 
cystic degeneration occurs from snaring off of lymph vessels ; the neuroglia 



804 DISEASES OF THE BRAIN 

increases even sevenfold (sclerosis), (e) Alteration of the sjrinal cord 
is present in 90 per cent.; the lateral columns often show descending 
degeneration, but more commonly changes like those of tabes (q. v.) ; the 
cerebrospinal fluid contains globulin and mononuclear cells and exhibits 
the Wassermann reaction. 

General Symptoms. — As a rule, the symptoms are vasomotor, psychical 
and motor, in the order of their usually slow development. The leading 
symptoms are referable to alteration in the frontomotor cortex. (1) In 
the prodromal stage, the first symptoms are equivocal or point to (a) neu- 
rasthenia because of the "irritable weakness/' ready fatigue in mental pro- 
cesses, headache, cephalic pressure, introspection and "rheumatic" pains. 
Again, the initial symptoms are (b) congestive, as headache, migraine or 
attacks similar to petit mal. (c) Most important are mental changes. The 
patient is "not himself" but "he does not remark his own alteration" 
(Schule). "The patient is confused as to time, and comes too early to 
work or remains after time ; he confuses places and may smoke in church ; 
his observation is faulty as well as his judgment; he confuses dreams with 
actualities and he forgets entire epochs, especially recent impressions. 
Esthetic and social lapses are common; the subject becomes vulgar, 
careless, neglects duties, disregards amenities and from lack of will-power 
may steal or dissipate most openly. Emotional outbreaks occur, as violent 
or brutal conduct or maudlin sentiment over soon-forgotten incidents" 
(Krafft-Ebbing) . The patient is often perniciously active, (d) Focal 
symptoms, especially amnestic aphasia, may appear, (e) General findings 
are noted after a time, as small and unequal pupils or other tabes-like 
findings, double vision, fibrillary contractions of the tongue, tremor, pains, 
headache, vertigo, congestive attacks, slow pulse, unmodulated voice, skip- 
ping of words in reading and incorrect writing. This stage covers months 
or years. In rare instances the symptoms follow tabes, "the ascending 
form of general paralysis." (2) At the height of the disease, (a) the 
psychical symptoms take various types, as maniacal exaltation, melan- 
cholia or simple dementia, (b) Congestive, apoplectiform attacks are 
frequent and immobile and unequal pupils, hesitant speech with elision 
of syllables, altered expression, trembling or paresis of the face, inco- 
ordination of the hands and gait, disturbances in writing and reading 
become more distinct. (3) The terminal stage is characterized by total 
dementia (the final type of all initial varieties), complete disorder of 
speech, incoordination so extreme as to necessitate feeding the patient 
and keeping him in bed, sensory, vasomotor and trophic complications 
and death from pyelonephritis, bed-sores or bulbar symptoms. 

Symptoms in Detail. — 1 . Psychical Symptoms. — The weakness, alter- 
ation in character, loss of memory and reason and the ethical, esthetic 
and moral deficit have been described. During the height of the disease 
there is one of three main mental manifestations: (a) megalomania, 
which classical expansive type occurs in 66 per cent., associated anatom- 
ically with the characteristic meningo-encephalitis, and characterized by 
ideas of grandeur, the patient believing he is a king, God, a millionaire, 
an athlete, etc. He makes ridiculously large plans, buys extravagantly, 
lacks will-power, indulges himself excessively, changes with great "facil- 



DEMENTIA PARALYTICA 805 

lty" from one thing to another, is optimistic, friendly, even philanthropic 
and rapidly runs through his capital. He loses himself, forgets names 
and confuses the real with the unreal. Periods of acute mania, with fever 
and grinding of the teeth are expressions of brain congestion; complete 
dementia is the final outcome, though remissions occur, (b) The melan- 
cholic or hypochondriacal form is thought to occur with cystic degenera- 
tion of the cortex. It may be of the dull or agitated type. The patient 
may dwell on the condition of his bowels and think they would "burst 
and flood the world." There is often micromania, characterized by 
"self-belittlement," in which the individual fears everything and thinks 
himself a "dot, nothing, or denies his existence." These cases may 
commit suicide, (c) Simple primary dementia may be present from the 
beginning; this type is increasing in frequency, while megalomania 
is decreasing. It is anatomically simple cortical atrophy in which in- 
flammation is absent or late. These subjects are often deceptive in the 
early stage, being quiet, urbane and optimistic. In the ultimate dementia 
of all types, "there is no sense of time, place or identity," and the patient 
babbles or is speechless. 

2. Motor Disorder. — This usually occurs with mental changes, is 
constant, though variable in its expression, incomplete in degree, exten- 
sive as to parts involved and progressive, (a) Speech is pathognomonic- 
ally disturbed as a result of mental change, wasting of association fibers 
and later bulbar atrophy. It is incoordinate, involving letters ("literal" 
ataxia) or syllables. In pronouncing such words as "electricity" the 
patient characteristically stutters over syllables. Loss of word-memory 
is the primary trouble; the patient forgets expressions, speaks ungram- 
matically and "does not notice it." Speech becomes atactic, there is 
paraphasia, the voice is unmodulated, gives out suddenly, is sometimes 
hoarse, nasal or slow, but never scanning. Later, speech is disturbed 
from bulbar alteration, causing dysarthria from disease of the facial and 
hypoglossal nuclei; it is ultimately unintelligible (absolute aphasia). 
Closely associated with speech disturbance is (b) disordered reading 
(paralexia) (c) Writing is disturbed first because of the mental alteration; 
the patient has difficulty in collecting his thoughts, although he does not 
realize the cause (the ataxia by which he drops syllables, repeats words 
or sentences — paragraphia)) and it is disturbed secondly because of 
tremor. The writing is uneven, up and down or zig-zag. These changes 
are diagnostic, (d) Paralysis of the eye muscles (in 6 per cent.) is usually 
partial and transitory. When total, syphilis or tabes is the probable 
cause, (e) The pupils: Myosis may occur, often just before maniacal 
outbursts. Mydriasis is frequently unilateral and results from sym- 
pathetic irritation. In 60 per cent, of cases the pupils are now large, 
now small, which is considered especially sinister. They are often 
irregular or triangular. The Argyll-Robertson pupil, responding to 
accommodation but not to light, is marked in 47 per cent., partial in 20 
per cent, and absent in 33 per cent.; it is due to degeneration in Bech- 
terew's column (between that of Goll and of Burdach). (/) The facial 
nerve: The paresis of the lips is cortical, as are fibrillary twitchings, 
automatic chewing movements and almost constant grinding of the teeth. 



806 DISEASES OF THE BRAIN 

The " fatuous" or "masked" expression is psychical. Salivation results 
from cortical irritation. There may be difficulty in swallowing, (g) 
The limbs: (i) The cortical changes cause the small- waved, rapid, con- 
stant tremor, the ataxia, loss of muscle sense and the uncertain, 
awkward, tripping paralytic gait, (ii) The gait may be tabetic, with 
absent knee-jerks, immobile pupils and vesical symptoms; or it is 
more often spastic with early increased patellars, ankle-clonus, con- 
tractures and arthropathies, (iii) Neuritic atrophy of the cranial nerves 
may occur as in tabes, (h) Apoplectiform and epileptiform attacks, (i) 
Apoplectiform seizures result from vasomotor paralysis and brain edema 
and differ from apoplexy in their incompleteness, evanescence, increased 
temperature and increased reflexes. They last part of an hour and may 
produce temporary hemiplegia, but especially aphasia with paresis of 
the right arm. (ii) Epileptiform attacks occur later, result directly 
from cortical disease, are usually partial (involving the face or arm), 
and either Jacksonian or attended by partial loss of conscious- 
ness. 

3. Sensation and Special Senses. — Coincident tabes and pachy- 
meningitis may emphasize the sensory manifestations, as lancinating 
pains. Sensation is often dulled and, like the analgesia, is cortical in 
origin. Perhaps the hypochondriacal complaint that certain organs, as 
the bowels, are absent, is due to visceral anesthesia. Migraine, first 
appearing late in life, may indicate an organic origin; Charcot described 
a form with hemianopsia and symptoms like glaucoma. Migraine is 
cortical when associated with paresis of the face, tongue or arm. There 
may develop optic neuritis and atrophy (4 per cent.), optic hallucinations 
and psychical blindness. 

4. Other Symptoms. — (a) Vasomotor changes occur in the skin 
(lividity, edema and sweating) and in the brain, lungs, bladder, intestines 
and stomach (resembling the so-called bilious attacks), (b) Trophic 
symptoms are sweating of blood, rough skin, phosphaturia, perforating 
ulcer of the foot (3 per cent.), bed-sores and friability of the bones, which 
may be broken without the patient knowing it. The "insane ear" is 
frequent. 

5. General Symptoms. — The pulse is often slow and monocrotic, 
the temperature low, although the heat centres may be involved in 
congestive seizures with great febrile elevation, and the body weight 
is often reduced in the early and late stages, though at the height of 
the disease it often increases, especially before the congestive seizures. 
The sexual instinct, at first increased and sometimes perverted, later 
declines. Insomnia may be severe, protracted or absolute. 

Diagnosis. — The diagnosis depends upon (a) the etiology, as syphilis 
with mental strain or excesses ; (6) the grouping of the psychical symptoms, 
as character, esthetic or ethical changes with (c) motor symptoms, as the 
speech, writing or tremor; (d) vasomotor symptoms, as migraine or 
apoplectiform insults, and (e) the progressive course. 

The Wassermann test (v. page 219) of the blood is positive in 80 to 
98 per cent.; the spinal fluid shows lymphocytosis, globulin and the 
Wassermann reaction. 



DEMENTIA PARALYTICA 807 

Differentiation. — 1. Diffuse Bkain Disease. — (a) Cerebral syphilis 
may be confused with diffuse meningoencephalitis. (b) Senile dementia 
seldom occurs under sixty years of age. Its course is longer, the symp- 
toms more gradual and less intense, memory is maintained longer and 
there is less megalomania than fear of persecution and poisoning, 
(c) Multiple sclerosis occurs earlier, is complicated by late and mild 
mental symptoms and an intention tremor, which is wider in amplitude 
and ceases during repose. The speech is scanning, staccato, and there 
is no literal ataxia. Nystagmus is common, while it is rare in general 
paralysis. Motor symptoms are largely referable to lateral column 
disease. 

2. Focal Brain Disease. — (a) Although migraine, headache, apop- 
lectiform attacks and sensory or motor irritation of the Jacksonian type 
may occur in brain tumor, it does not cause difficulty in pronouncing 
syllables, peculiar mental alteration or immobile pupils; it is character- 
ized by general symptoms, as choked disk or vomiting and focal symptoms, 
which are foreign to general paralysis. In tumor there is dementia only 
with marked internal hydrocephalus. (6) Hemorrhagic pachymenin- 
gitis complicates 20 per cent, of cases of dementia paralytica; when it 
exists as an independent affection, it often leads to intense local headache, 
vomiting, recurrent hemiplegia or monoplegia, cortical irritation and 
more rapid course, (c) Softening usually produces focal symptoms. 

3. Psychoses and Neuroses. — (a) Every case of mania or hypo- 
chondriasis between the twenty-fifth and forty-fifth years, not due to 
alcoholism or to acute somatic disease should arouse suspicion of general 
paralysis (Mendel). (6) In neurasthenia the onset is more acute; the 
memory is fatigued but never lost and the patient recognizes his in- 
capacity. In dementia paralytica there are hypochondriasis with absurd 
conceptions, changes in the pupils, disk and field of vision, alterations 
in character, speech and intellect which are never seen in neurasthenia. 

4. Intoxications. — These may cause the forms known as general 
pseudoparalysis, (a) Chronic alcoholism is not progressive, recovery is 
frequent, delirium tremens and convulsions are common, the course is 
acute and the alcoholic tremor, headache, hallucinations and neuritis 
are found, (b) Chronic plumbism (saturnine encephalopathy) is often 
progressive, and in its last stages almost indistinguishable from dementia 
paralytica. It is more acute and 80 per cent, of cases recover. There are 
headache, cardiac distress, anemia and a gingival lead line, (c) Chronic 
bromism is distinguished by its dementia, bromide acne, fetid breath, 
coated tongue, pharyngeal anesthesia, weak heart and acute and usually 
favorable course. 

Prognosis. — The disease is fatal in 66 per cent, of cases within two 
years, though remissions may occur. Krafft-Ebbing saw no recoveries 
in 2500 cases; recovery indicates an incorrect diagnosis, pseudoparalysis 
generalis. The following courses are distinguished : (a) acute or galloping 
form, which lasts months to a year; (b) classical, expansive type, three 
or four years; (c) the depressive type, two or three years; (d) dementia 
forms, four or five years; (e) circular form, in which depression alternates 
with mania; (/) female variety which has a longer course than in males; 



808 DISEASES OF THE BRAIN 

(g) spinal form, with a relatively long course; (/*) juvenile or adolescent; 
and (i) senile form. Death results in 50 per cent, from the disease itself, 
by apoplectiform seizures, suicide, inanition or bulbar symptoms. In 
50 per cent, it results from complications, tuberculosis (18 per cent.), 
bed-sores, with sepsis (10 per cent.), lung gangrene (6 per cent.), pneu- 
monia (5 per cent.), choking (10 per cent.) and cystitis. 

Treatment. — Hygienic treatment, as rest, protection from heat, and 
quiet surroundings, is indicated. The patient should be committed to 
an asylum, for suicide or other violence is always possible. In simple 
dementia alone, may the patient be treated at home. Hydrotherapy 
is valuable within limits; cold rubs lessen excitation; full cold baths are 
contra-indicated. Medicinal treatment (v. Syphilis). 



CHRONIC BULBAR PARALYSIS. 

First thoroughly described by Duchenne (1860), as labioglossopharyn- 
geal (laryngeal) paralysis, Trousseau made the first autopsies, Charcot 
and v. Leyden demonstrated alteration in the bulbar nuclei. 

Etiology. — Most cases occur in males between fifty and seventy years 
of age. Heredity is a factor only when the disease is associated with 
progressive muscular atrophy. 

Pathology. — To the naked eye the medulla usually appears normal. 
Microscopically, (a) the motor nuclei are symmetrically and bilaterally 
wasted. The hypoglossal nucleus suffers most and few normal cells 
remain; its accessory nucleus is usually normal. The spinal accessory 
nucleus is next most frequently affected, but the vagus nucleus suffers 
less. Atrophy may invade the glossopharyngeal or exceptionally the 
facial and fifth nuclei. In some cases perivascular exudation occurs 
within the nuclei and the nerve elements are degenerated (the parenchy- 
matous form), but in others increase of connective-tissue or vascular 
thickening may be seen, (b) The respective nerve trunks in their course 
or in their terminal endings show parenchymatous and interstitial change, 
even within the medulla, and the posterior longitudinal fibers waste in 
direct ratio to the hypoglossal nuclear atrophy, especially those which 
form the anterior fundamental fibers of the spinal cord. Sometimes the 
loop of the seventh nerve wastes, (c) The muscles supplied by the above 
nerves waste, as those of the lips, tongue, palate and larynx (the process 
sometimes extends to the neck and arms). The greatest change is in the 
tip of the tongue. The changes are those of progressive muscular atrophy 
(q. v.). (d) In all cases pyramidal tract degeneration may be traced down 
into the cord or up into the cms. 

Symptoms. — Labioglossopharyngeal paralysis, the name proposed by 
Duchenne, designates the parts paralyzed by the wasting of the motor 
nuclei. It is bilateral, but one case showing unilateral disease. It is slow 
in onset, afebrile and painless. The first symptom is usually paresis 
of the tongue (hypoglossus) which first shows fatigue and much later 
actual paralysis. It is difficult to protrude or move up, down or trans- 
versely. The Unguals, L, N, R and S are formed with difficulty and also 



CHRONIC BULBAR PARALYSIS 809 

later the lingual palatines, as T and D. The tongue is wrinkled and 
wasted. The lips become weak and whistling and formation of the labials 
(O, U, P, B, M) become impossible. The tongue and lips are more 
closely associated than any other muscles of the body; anatomically the 
facial fibers for the orbicularis oris probably originate in the hypoglossus 
nucleus. Later the mouth cannot be closed, the lower lip sags and the 
zygomatic muscles overcome the weak fibres of the upper lip and accen- 
tuate the nasolabial furrow. The lips are frequently thin. The expression 
is peculiar, the forehead is corrugated, the eyebrows somewhat lifted, 
but the mouth is "dead" and laughing and emotional displays produce 
a strange effect, which Trousseau compared to the mask of the Greek 
actors. The original descriptions picture the patient constantly holding 
a handkerchief before the lips to collect the free flow of saliva from the 
open mouth ; the salivary secretion is probably also increased from disease 
of its bulbar centre. Swallowing becomes difficult from the inability of the 
tongue to propel the food to the pharynx so that the subject must push 
the food back with the finger, and again the palate (controlled by the 
spinal accessory and vagus nerves) is weakened, producing a nasal 
voice and allowing food to regurgitate into the nose. The pharynx is 
paretic (glossopharyngeal and vagus nerves). Semisolid food can best 
be swallowed, because fluid more easily regurgitates into the nose and 
solids more easily reach the larynx. The larynx is often involved (spinal 
accessory and vagus nerves). The adductors are more often affected 
than the abductors. Talking and coughing are difficult or impossible. 
Fibrillary twitchings are very common, sensation is normal, but the 
reflexes of the skin and mucosa are usually lost. There is sometimes 
a partial reaction of degeneration. The intellect is normal. Forced 
laughing and weeping are not uncommon. The general nutrition suffers 
from the dysphagia. In some cases the eyes may be involved, as in pro- 
gressive nuclear ophthalmoplegia (an identical process in the pons); 
occasionally the cervical, facial, masseteric, temporal and pterygoid 
muscles are involved. Bulbar paralysis, frequently coexists with pro- 
gressive muscular atrophy of spinal origin, affecting the limbs or trunk, 
and Kussmaul pointed out that the two processes are identical in nature. 
The spinal disease may progress upward to the medulla, causing secondary 
bulbar palsy, or the bulbar palsy may be primary. In typical forms, 
there are wasting, paralysis and absence of the reflexes; in some atypical 
forms there is no wasting; at times the reflexes are increased (clonus 
in the muscles of mastication), probably from a supranuclear lesion, "the 
bulbar analogue of amyotrophic lateral sclerosis of the cord." 

In the progressive course of the malady the pulse becomes rapid and 
irregular and the heart tones run together, which Duchenne compared 
to the "heart beating in water." Dyspnea develops and the expiration 
is weak. 

Diagnosis. — This is based on (a) the distribution of the process in 
the motor nuclei; (b) its bilateral symmetry; (c) gradual onset, and 
(d) chronic progression. Neuritis of the bulbar nerves is very rare; 
the lips escape, because the nerve fibers to the orbicularis oris, arising 
in or near the hypoglossus nuclei run to the pons and leave it by the 



810 DISEASES OF THE BRAIN 

facial nerve fibers; there is more atrophy, more rapid course, more 
sensory disturbance and the reaction of degeneration is present. It 
occurs in acute infections. Brain tumor within the medulla, growths 
without the medulla and multiple sclerosis and syringomyelia rarely 
produce bilateral or symmetrical paralyses. Pseudobulbar paralysis; 
bilateral disease, more often in or near the internal capsule, especially 
when due to arterial lesions, may cause dysarthria (Joffroy, 1872). 
One lesion may be in the cortex and the other in the lenticulostriate 
area. Pseudobulbar palsy causes mental change, aphasia, hemiplegia, 
double facial paralysis and hemianopsia; one side is involved after the 
other and it is attended by no wasting, no loss of reflex action and no 
reaction of degeneration. 

Prognosis. — The disease is fatal in one to three years, especially in 
advanced life or with coexistent spinal muscular atrophy. In the rarest 
instances the disease may be arrested. Death results from inanition, 
inhalation pneumonia, intercurrent disease or paralysis of the cardiac 
or respiratory centre. 

Treatment. — Treatment is discouraging. Nutrition must be main- 
tained by feeding with the nasal catheter. Iron and strychnine may be 
given. Electrotherapy is of little value. 

Asthenic Bulbar Palsy; Myasthenia Gravis. — Chronic bulbar palsy 
without anatomical lesion was first described by Wilkes (1877), Erb 
(1879), Goldflam (1891) and Oppenheim. It is also known as the Erb- 
Goldflam syndrome. Starr collected 250 cases. It most often occurs in 
person's under the thirtieth year. The cardinal feature is extreme exhaustion 
{myasthenia) after the slightest exertion. Weakness develops in the eyelids, 
face, palate, masseters, pharynx, vocal cords and tongue, although but 
slightly expressed by ptosis (the first symptom in 33 per cent, of cases), 
dysphagia, dysarthria and difficult mastication, and disappears after 
rest, to return anew after a few muscular efforts. Myasthenia may be 
confined to the eyes. From these bulbar symptoms the affection is 
called asthenic bulbar paralysis. In some cases the arms, legs and trunk 
are similarly involved, so that walking or arm movements become im- 
possible after short exertion — myasthenia gravis pseudoparalytica. The 
symptoms are symmetrical. The myasthenic reaction of Jolly consists 
of normal tetanic response to faradic stimulation, becoming weaker 
with each repetition, until at last no reaction is elicited. The reflexes 
soon become exhausted. Some atonicity of the digestive tract is common. 
Collins noted a rapid exhaustion of the special senses and Buzzard re- 
remarked sensory alterations. Remissions are usual, sixteen years being 
the maximum clinical duration. About Jfi per cent, of cases die from 
exhaustion of the cardiac and respiratory centres but the autopsy findings 
are negative (in 66 per cent.) or doubtful; Kalisher found hemorrhages 
in the medulla, and C. Mayer found vascular and nuclear alterations. 
Lymphoid cells were found in the heart and between the muscle bundles 
(Weigert, 1901), and Weigert, Hun and Blumer describe lymphoid and 
glandular hyperplasia in the thymus gland. The diagnosis is based on 
(a) absence of atrophy, of the reaction of degeneration and of twitch- 
ings and sensory phenomena; (6) the presence of muscular adynamia 



HYDROCEPHALUS 811 

recurring remittently; (c) Jolly's myasthenic reaction and (d) the slight 
involvement of the hypoglossus. 

Treatment. — Rest and massage are helpful; iodides, calcium, adrenalin 
and strychnine are less useful. Galvanization is recommended by Gold- 
flam, who reported recovery under its use. 

Apoplectiform Bulbar Paralysis. — Sudden bulbar paralysis deserves 
discussion in this place for the sake of topical differentiation. Its usual 
causes are hemorrhage, embolism, thrombosis and less frequently bulbar 
encephalitis or neuritic trauma. 

Symptoms. — (a) The onset is apoplectiform with symptoms which are 
rarely focal, as vertigo, vomiting, dyspnea, yawning, slowed heart, and 
often without coma, (b) Motor symptoms are frequent, as double hemi- 
plegia; monoplegia is possible, or if the lesion occurs at the pyramidal 
decussation there may be hemiplegia cruciata, i. e., paralysis of one arm 
and the opposite leg. A unilateral focus may produce bilateral symptoms 
rarely, however, symmetrical. The pyramidal tracts in the medulla 
are supplied by the inferior cerebellar artery, (c) Sensory symptoms 
may develop, as hemiataxia or hemianesthesia (d) The bulbar nerves may 
be affected ; paralysis of the tongue, pharynx, masseters, larynx and, 
because of the vascular supply, frequently of the eyes, face and other 
pons centres may result. The reflexes of these parts are often suspended, 
though in the extremities they are increased. The lesion may be at the 
level of the nuclei or supranuclear. The hypoglossal and spinal acces- 
sory nerves are supplied by the anterior spinal and vertebral arteries; 
the vagus, glossopharyngeal and auditory nerves by the vertebral; the 
fifth, seventh and eye nerves (third, fourth and sixth) by the basilar 
artery. There may be hemiplegia with paralysis of the opposite side 
of the tongue if the lesion is in the anterior part of the medulla. 

Diagnosis. — Chronic bulbar palsy is excluded by the acuity of onset 
and the asymmetry and irregularity of the bulbar symptoms, as double 
hemiplegia, which is unequal on the two sides, or dysphagia without 
paralysis of the tongue or lip. Differentiation between hemorrhage, 
embolism and thrombosis is frequently impracticable. Pseudobulbar 
paralysis of cerebral origin (v. s.). 

Prognosis and Treatment. — The prognosis is most grave at the onset. 
Improvement and even recovery are possible. Treatment concerns chiefly 
the underlying vascular disease. 

Progressive Nuclear Ophthalmoplegia. — An atrophy of the oculomotor 
nuclei, (v. Affections of the Third Nerve.) 



HYDROCEPHALUS. 

Acute hydrocephalus is an acute accumulation of fluid between the 
dura and the brain (acute external hydrocephalus) or in the ventricles 
(acute internal hydrocephalus). In some cases the fluid is a transudate, 
being part of a general edema, resulting from cardiac or renal disease, 
or due to local causes, as sinus thrombosis. In most cases it is an exudate. 
Acute meningitis, the only certain cause, is tuberculous in 80 per cent.; 



812 DISEASES OF THE BRAIN 

it is less often serous meningitis. Quincke thinks some cases are angio- 
neurotic. 

I. Chronic External Hydrocephalus. — Fluid between the dura and 
brain is caused by (a) compensatory hydrops ex vacuo, occurring where 
brain development is arrested (congenital form) or when the brain wastes 
(paretic dementia, softening, hemorrhage, senile atrophy, porencephaly). 
(b) Stasis, as in sinus thrombosis; and (c) chronic diseases, as cancer, 
nephritis or alcoholism. The symptoms are indeterminate. 

II. Chronic Congenital Internal Hydrocephalus. — Etiology. — Possible 
causes are fetal meningitis, obstruction of the choroid plexus, branches 
of the vena Galeni, lymphatics, lateral apertures of the fourth ventricle 
near the glossopharyngeal roots, aqueduct of Sylvius or in the foramen 
of Magendie or Luschka. 

Symptoms and Pathology. — The large head may be an obstacle to 
labor. It may measure 167 cm. in circumference. If it appears after 
the seventh year the head is not enlarged, and in cretins the head may 
be undersized. Often the head cannot be held upright. The skull is 
even membranous and translucent to the candle test. If the disease halts, 
the bones may thicken and Wormian bones develop. The head projects 
beyond the base, the sphenoid is luxated forward and downward, the ear 
meatus points downward, the occiput is forced back, the sella turcica 
is flattened and widened, the roof of the orbit may be pushed down so 
as to become palpable, the fontanelles are large, the fissures gape and 
fluctuation may be felt. The hair is thin, the veins are large and a systolic 
murmur may be heard, the cause of which is doubtful. The brain is 
pale and may be flattened almost beyond recognition. The ependyma 
are thick, granular and sclerotic. The average amount of fluid is 1 
quart, the maximum 13 quarts. The ventricles, especially the lateral, 
are enlarged; the enlarged third ventricle easily compresses the optic 
chiasm. The foramen of Monroe is often very large. The fluid is usually 
clear, and rarely blood-stained. It is neutral or alkaline, its specific 
gravity is 1.001 to 1.009; and the albumin is 0.2 to 2 per mille; more 
than 1.009 or 2.5 per mille of albumin indicates inflammation. 

The face is small, triangular, and the eyes are prominent. Much 
of the sclera is shown and the upper lid is small. The brain may be 
reduced to a small fraction of an inch in thickness and is a mere flask 
for the fluid. The demarcation between gray and white matter is lost 
and in marked cases the convolutions and sulci are obliterated, the basal 
ganglia flattened, the cerebellum forced into the spinal canal and many 
structures, such as the fornix or corpus callosum have disappeared. 
Mentality, as a rule, is impaired or abolished, speaking is learned late 
if at all, and irritability, epileptiform attacks, psychoses, headache and 
vomiting are fairly common. Eye symptoms are frequent, as diminished 
vision or blindness from optic atrophy, strabismus, nystagmus and wide, 
possibly reactionless, pupils. The limbs often present spasticity, con- 
tractures, paresis and increased reflexes. The child walks late, if at all. 
Sensation is normal. Puberty may be delayed or the infantile testes may 
persist. Lumbar puncture shows increased intraspinal pressure (36 mm. 
of mercury). 



HYDROCEPHALUS 813 

Complications. — Complications are largely anomalies of development, 
as syringomyelia, hydromyelia, meningocele, microcephaly, porencephaly, 
anencephaly and encephalocele. 

Course. — Some subjects die during or after birth. Many die in the first 
three years from increase of brain pressure with coma or intercurrent 
disease. In some cases temporary remissions, and in still rarer instances 
permanent arrest of the process occurs, the mind improves, the speech 
shows some defects or the gait remains paretic and spastic. In very 
exceptional cases rupture externally is observed after head trauma or 
spontaneous breaking into the ear or nose occurs, as in Lebert's case, 
which "leaked" for five years. Golis reported a case which lived seventy- 
one years. 

HI. Acquired Chronic Hydrocephalus. — Etiology. — The causes are 

(a) stasis, general (cardiac or pulmonary) or local (tumor or sinus throm- 
bosis); (b) cachectic transudation, as in carcinoma or nephritis; and 
(c) inflammation, beginning as acute meningitis of the sporadic or epi- 
demic type, or as slowly beginning chronic basal meningitis, especially 
in young children. The same points of obstruction may exist as in the 
congenital variety, (d) Rickets is a frequent associate. Some forms may 
be angioneurotic. 

Symptoms. — Meningitic symptoms usher in some cases in which 
after weeks new evidences of brain pressure appear, as alteration in the 
pulse and breathing, unequal pupils or coma. Headache, vomiting, 
visual disturbance, spastic paresis, epilepsy, altered mentality, idiocy and 
involvement of the cranial nerves are seen, as in the chronic congenital 
form. The shape of the head, however, is not altered. 

Diagnosis. — Differentiation between chronic congenital and acquired 
forms is very difficult, without an accurate history, (a) From rhachitis: 
The two affections are often associated. The rhachitic head is square 
rather than globular, it protrudes more in front and laterally than 
behind, the sutures are less widely separated, the fontanelles are wide 
but do not bulge, and there are no signs of brain tension. The rhachitic 
head should be measured, because it seems larger than it actually is. 

(b) From brain tumor: The two conditions may be coincident. The 
congenital form is the more easily distinguished by the history and its 
slower course, but focal symptoms are less common, and spinal symptoms 
are more common than in tumor, (c) Hyperostosis of the skull, brain 
hypertrophy and acromegaly enlarge the head, but are separable by the 
same arguments as in rhachitis. 

Treatment. — Few therapeutic results can be obtained. Bandaging the 
head is sometimes helpful, but it may aggravate the brain compression. 
Puncture of the lateral ventricles dates from the time of Hippocrates. 
Isolated recoveries are recorded, but the evacuation must be slow. 
Permanent drainage is usually fatal. Attempts to effect anastomosis 
between the ventricles and the subdural space are sometimes successful. 
Lumbar puncture in acquired forms may be useful, but may cause death. 



814 DISEASES OF THE CEREBRAL MENINGES 



DISEASES OF THE CEEEBRAL MENINGES. 

Inflammation of the dura is termed pachymeningitis, and inflam- 
mation of the arachnoid and pia, leptomeningitis or meningitis. 

PACHYMENINGITIS. 

External pachymeningitis is secondary to skull disease, infections and 
cerebral atrophy. Its symptoms are indefinite, as pain, headache, possibly 
hemiplegia, or are those of the primary lesion. Surgery in Macewen's 
22 cases gave 100 per cent, recovery. 

Internal pachymeningitis is divided into (a) the purulent form, which 
follows bone disease or leptomeningitis; and (b) the pseudomembranous 
or serous type, seen chiefly in general paralysis or in children with peri- 
splenitis. More important is (c) pachymeningitis hemorrhagica interna, 
described by Heschl (1855). 

Etiology. — (a) Fifty per cent, occur in persons over fifty years of age 
and 40 per cent, over sixty, (b) Seventy-seven per cent, of cases occur 
in males, (c) Paretic dementia causes 19 per cent. Pachymeningitis is 
common in other dementias and chronic psychoses, whence its great 
frequency in asylums and poor-houses. It also occurs in arteriosclerosis 
and encephalomalacia. (d) Chronic alcoholism, frequently with cardiac 
and renal disease, is a frequent cause, (e) Trauma, as during birth, 
from forceps delivery or from small pelvis. (/) Hemorrhagic diathesis 
(scurvy, hemophilia, pernicious anemia), chronic nephritis, (g) Infective 
diseases, as typhoid, puerperal fever (9 per cent.), heart disease (18 per 
cent.), hereditary syphilis (11 per cent.), and tuberculosis (23 per cent.) 
are also causes. 

Pathology. — 1. Gross Pathology. — The inner surface of the dura is 
cloudy, yellow or brown from punctate hemorrhages or hematoidin 
deposits. In pronounced cases the dura shows membranous laminse, 
maybe a quarter of an inch thick, which are adherent by proliferation of 
bloodvessels and by organization. Those layers nearest the brain are 
the most newly formed. Repeated hemorrhage into the layers of the 
newly formed tissue or between them may be an inch thick or reach the 
size of an egg. The free hemorrhage may spread over the entire surface 
of the brain, even reaching the retina. Corresponding to the most fre- 
quent seat of pachymeningitis, the convexity of the brain is compressed, 
especially over the motor areas and bilaterally in 56 per cent. 

2. Minute Examination.- — The fresh fibrin and the exudation contain 
red cells and, nearest the brain, a covering of endothelial cells. Later the 
exuded fibrin develops capillaries, organizes and again hemorrhage occurs 
from the newly formed vessels. This organizes in turn, so that successive 
laminae develop. 

3. Pathogenesis. — Jores proved that two classes of cases exist: 
(a) The hemorrhage is primary and the simple clot organizes into firm 
connective tissue; this variety is called regressive and occurs in cases 
due to trauma, blood diseases, infections and arteriosclerosis, (b) In 



PACHYMENINGITIS 815 

chronic pachymeningitis proper, the inflammation is primary, the pro- 
cess is progressive, the connective tissue formed in layers is looser, more 
vascular, and its inner, successively formed layers are the seat of repeated 
hemorrhages. 

Symptoms. — Generally there are no symptoms, because the hemorrhage 
is slight or overshadowed by the original disease. 

1. Geneeal Symptoms. — The most frequent is headache, which is of 
little differential value, diffuse and most marked in alcoholics. There 
may be prodromal delirium, slow and irregular pulse, choked disk, 
moderate albuminuria or some fever. 

2. Focal Signs. — The most important is hemiplegia, which is pre- 
ceded for some time by coma (Fiirstner). The paralysis is contralateral, 
rarely complete, varies with increase or decrease of the clot, often involves 
the cortical facial and hypoglossal centres, is sometimes bilateral and 
associated with aphasia (33 per cent.), hemihypesthesia (hemiataxia), 
hemiamblyopia, contractures in the paretic members and Jacksonian 
epilepsy. Conjugate deviation of the head and eyes, nystagmus and 
forced postures may be observed. The patient may grasp at his clothes 
or at his hair or beard. The pupil contralateral to the lesion is usually 
larger; the pupils react poorly and later both are wide. The tendon 
reflexes are increased, but the skin reflexes are decreased or abolished 
during the coma. Basal nerve involvement, trismus and rigidity of the 
neck are uncommon. 

Course and Prognosis. — Death may occur in the first seizure or the 
symptoms may subside for months, possibly permanently. Residual 
signs include headache, ataxia, psychical alteration, paresis and aphasia. 
Recurrence is frequent, with stupor, coma and hemiplegia until death 
occurs from the fundamental disease, hemorrhage or intercurrent affec- 
tions. 

Diagnosis. — A correct diagnosis is rare. A patient with paretic 
dementia may die from a pseudo-apoplectic shock or pachymeningitis; 
a nephritic may succumb to pachymeningitis, apoplexy, uremia, brain 
edema or heart failure. A presumptive diagnosis can be made from 
the age, causal disease, preceding dulness or coma, hemiplegia, small 
pupils and convulsions, and recurrences. 

In pachymeningitis there is more cortical irritation than in cerebral 
hemorrhage, the coma and paralysis are more variable and temperature, 
narrow pupils and optic neuritis are more common. In encephalomalacia, 
the hemiplegia is more often attended by aphasia and hemianesthesia, 
and there is less cerebral irritation. Brain tumor is easily distinguished. 

Treatment. — Treatment relates to prophylaxis and the seizure. The 
use of the ice-cap, quiet, elevation of the head, application of leeches 
back of the ear, and possibly venesection are indicated. Nourishment 
should be given by rectum. Morphine and chloral relieve the headache, 
excitement or convulsions. Lumbar puncture has not proved beneficial. 
Operation was first performed by Ceci in traumatic and Annandale, 
Jaboulai, Monroe and Ballard in other varieties. 



816 DISEASES OF THE CEREBRAL MENINGES 

MENINGEAL HEMORRHAGE. 

Etiology and Pathology. — (a) Trauma may rupture the anterior, middle 
or posterior meningeal arteries, with or without fracture of the skull, 
usually at the site of trauma, but sometimes by contre-coup. The cor- 
responding veins may rupture, also the sinuses or the pial vessels, from 
the latter of which blood may percolate to the base of the brain or cord. 
The internal carotid may be ruptured and death then occurs. External 
hemorrhage results most frequently from middle meningeal rupture. 
The blood clot may weigh 3 to 17 ounces or reach the size of the fist, 
compressing the brain and dislocating the falx. During birth (see In- 
fantile Cerebral Paralysis) trauma may be a factor; large sym- 
metrical hemorrhage of the convexity is common, (b) Arteriosclerosis 
and rupture of cerebral aneurysms; (c) acute infections, hemorrhagic 
diathesis, sinus thrombosis and rarely heart and lung disease; (d) 50 
per cent, of cases occur under forty years of age. Small clots may be 
absorbed or microgyria, porencephalia, cysts or brain sclerosis may 
result. 

Symptoms. — Clinical latency is not rare in the newborn. Small hemor- 
rhage in the adult may produce no symptoms. Very large effusions 
result in early, sudden death. In rupture of the middle meningeal artery 
there are (a) symptoms of brain pressure with those of brain concussion 
or contusion, as loss of consciousness, irritative symptoms, increased 
breathing, slowed pulse, pallor, vomiting and fever of 100° to 101°. Either 
death or improvement may result, (b) In other cases improvement from 
the concussion and contusion occurs, but after an interval of hours or 
days, hemorrhage occurs or recurs, with coma, pressure symptoms, mono- 
or hemiplegia and convulsions, as in pachymeningitis. Rigidity is less 
frequent than in meningitis. Hemorrhage of the sinuses and pia are said 
to cause monoplegia. 

Prognosis and Treatment. — Ninety per cent, of cases die from ex- 
pectant treatment; 33 per cent, die in twenty-four hours and, when the 
hemorrhage is due to aneurysmal rupture, 30 per cent, die in ten hours. 
Early surgical treatment is indicated. 



ACUTE SUPPURATIVE LEPTOMENINGITIS. 

In 1768, Whytt noted the acute hydrocephalic symptoms of meningitis, 
but failed to recognize the meningitis, which Quinn (1779) described. 
In 1855 Rilliet and Barthez distinguished the suppurative, secondary, 
tuberculous and other forms. 

Etiology. — Suppurative meningitis is generally a secondary process. 

1. Trauma. — Microorganisms from the ear or nose may find ready 
access to the brain when its resistance is lessened by trauma. 

2. Regional Extension. — (a) Disease of the middle ear, antrum or 
petrous bone may result in suppurative or serous inflammation (see 
Brain Abscess), (b) Extension from the nose is less common. The 
disease may be spontaneous or operative, syphilitic, tuberculous, menin- 



ACUTE SUPPURATIVE LEPTOMENINGITIS 817 

gococcic, neoplastic or suppurative, of the nasal mucosa or of the eth- 
moidal, sphenoidal or antral cells. Infection may travel through the 
bone, along the veins to the dura or along the olfactory nerve endings. 

(c) From the eye, the avenues to the brain are numerous, and yet disease 
of the eye itself, even panophthalmitis is less important than orbital 
cellulitis or enucleation, which exposes the sheath of the optic nerve. 

(d) Extension may result from parotitis, carbuncles of the face, whose veins 
communicate with the cavernous sinus; scalp affections; erysipelas, etc. 

3. Metastatic or Secondary Extension. — (a) Septicopyemia, from 
lung suppuration, empyema, arthritis, endocarditis and kindred affections ; 
(b) pneumonia and rarely exanthemata may produce it ; in this group 
there is an intermediate link, as otitis media in scarlatina and empyema 
or lung infarct in typhoid. 

Bacteriology. — (a) The pneumococcic is the most frequent variety, 
being primary or secondary to pneumonia. (b) Pyogenic organisms, 
especially the Streptococcus pyogenes and the Staphylococcus pyogenes 
aureus ; (c) the typhoid, colon and influenza bacilli, pneumobacillus, actino- 
mycomata, and many other organisms have been found. 

Pathology. — 1. Macroscopically a purulent exudate effuses between 
the dura and leptomeninges and in the meshes of the arachnoid. The 
dura is tense. The leptomeninges are reddish, cloudy and often dotted 
with punctate hemorrhages. The exudate is purulent, yellow or whitish- 
green and succulent. The infection spreads rapidly, follows the peri- 
vascular lymphatics, as streaks of pus, imbeds the vessels and nerves 
in its meshes, obliterates the sulci and involves the brain and cord mem- 
branes. The brain is always swollen, springs out as the membranes 
are cut,- is vascular and sometimes locally anemic from compression by 
the exudate; its surface is most affected by small abscesses, punctate 
hemorrhages or minute islets of encephalitis, particularly in the meta- 
static form (convexity meningitis) : the base is most frequently concerned 
in ear disease. There may be primary or secondary sinus thrombosis. 
The ventricular fluid is increased, cloudy, purulent or sometimes serous. 
The apertures of the ventricles may be occluded; inflammation may 
be noted in the velum interpositum, choroid plexus or ependyma. In 
the spinal membranes the changes are similar and are most marked over 
the posterior part of the dorsal region. The process is usually diffuse. 
On incising the membranes the swollen cord bulges out and the same 
changes are seen as in the brain. 

2. Microscopically there are perivascular exudation of red and white 
cells and fibrin formation, even in those cases in which the membranes 
appear normal to the naked eye. Exudation is most marked over the 
cortex and near the ventricles, but may also occur deeper in the medullary 
substance. The ganglionic cells show degeneration. Analogous findings 
are present in the cord, on its surface or about the central canal. In the 
optic nerve, exudation, hemorrhage and edema are seen, possibly also 
in other cranial and spinal nerves. Various bacteria are found, as the 
pyogenic organisms, the pneumococcus and the meningococcus; patho- 
logically (though not bacteriologically), the suppurative and epidemic 
forms are identical. 
52 



818 DISEASES OF THE CEREBRAL MENINGES 

Symptoms. — Prodromal phenomena are ambiguous; otitis, pneumonia 
or pyemia may overshadow or totally obscure meningeal manifestations. 
Complete latency is possible, as in a convalescent pneumonia patient, 
who while dining, felt dizzy and died in a few minutes. The autopsy 
revealed a massive, purulent cerebrospinal meningitis, which had not 
produced a single sign or symptom. The onset may be sudden with chill 
and fever. Headache is usually the first and most prominent symptom, 
and is often associated with vomiting. The sensorium is disturbed, 
delirium is succeeded by stupor and finally by coma, in which headache 
still persists. Convulsions are particularly equivocal in children. Optic 
neuritis may develop if the course of the disease is not too precipitate. 
Rigidity of the neck and spine is soon noted, as well as hyperesthesia, 
hyperalgesia and muscular rigidity. Fever is usually present. It is 
usually higher than in other types, perhaps 104° to 105°, and more con- 
tinuous. Toward the end it may be 107° or may drop to subnormal. 
The pulse is faster and irregular. Irritation and paralysis of the cerebral 
nerves develop and are manifested by ocular paralysis, pupillary inequality 
and tardy reaction to light, if the inflammation is basal. If the process 
invade the convexity, cortical irritation may be manifested by Jacksonian 
epilepsy and mono- or hemiplegia. Lumbar puncture reveals purulent 
fluid and the organisms of suppuration. Kernig's sign is present. The 
abdomen is often retracted, there may be vomiting, the urine is febrile 
and frequently contains albumin and peptone. The course is generally 
rapid ; it lasts a few hours or more, usually two to ten days, and almost 
invariably results fatally in coma. The diagnosis, differentiation and 
treatment are considered under Cerebrospinal Fever. 

SEROUS MENINGITIS. 

This is more frequently seen at the bedside than at autopsy. It 
is often tuberculous. The membranes are glistening, clear or flocculent 
fluid is seen in the arachnoid meshes and ventricles, which may be the 
sole seat of the disease, and the pia especially shows exudation. It is 
often mistaken for edema of the brain. The microscope may be necessary 
to demonstrate inflammation. 

Symptoms. — No definite symptoms can be outlined. The disease is 
too frequently diagnosticated. Headache is common; vomiting, rigidity, 
fever, slow and labile pulse, optic neuritis, hyperesthesia, spasms and 
paralyses of the cerebral nerves are much less frequent than in the 
other forms of meningitis. The symptoms resemble those of brain 
tumor. Lumbar puncture in some instances gives absolute relief; the 
prognosis is most favorable in this type. 

CHRONIC LEPTOMENINGITIS. 

Etiology. — It may result from (a) acute leptomeningitis; (6) trauma, 
atrophic and sclerosing brain diseases, as paretic dementia, hydrocephalus 
and softening and in alcoholism, nephritis or plumbism or (c) suppuration, 
syphilis and tuberculosis. 



GENERAL ANATOMICAL CONSIDERATIONS 819 

Pathology and Symptoms. — The leptomeninges are diffusely or locally 
dense, opaque and fibrous. In the chronic suppurative form the pus 
loculi are situated in a firm, fibrous tissue. The symptoms, if cortical, 
are like those of the chronic tuberculous form; if basal, nerve paralysis 
and optic neuritis are common. In the chronic simple form (Gee and 
Barlow) the process may begin acutely and may persist, especially at 
the base and in the posterior fossa. Possibly it is a sequel of a localized 
epidemic or tuberculous type. This "simple meningitis of children" 
occurs in 76 per cent, in the first year of life. Rigid neck is the leading 
symptom. Paralyses, convulsions and rigidity are rare. Fifty per cent, 
of patients die. The alcoholic form is slight, diffuse and cortical; menin- 
gitic symptoms are obscured by alcoholic disease of the liver, kidneys, 
heart or peripheral nerves. Diagnosis is difficult, and therapy wholly 
etiological. 



DISEASES OF THE SPINAL CORD. 

GENERAL ANATOMICAL, PHYSIOLOGICAL AND SYMPTOMATIC 

CONSIDERATIONS. 

The nervous system is made up of numerous similarly constituted 
units, called neurones (Waldeyer) . Each neurone comprises (a) a central 
nerve cell; (b) protoplasmic processes or dendrites from the cell which 
conduct (cellulipital) impulses to the cell; (c) an axis-cylinder or axone 
arising from the cell and conducting impulses (cellulifugal) from the 
cell; and (d) the terminal ramifications of the axis-cylinder, known as 
arborizations. The axis-cylinder often gives off collateral branches or 
paraxones. The nutrition of the nerve cell probably depends upon the 
integrity of its nucleus, and the nutrition of the cell governs that of its 
neurone. Disease of the cell causes degeneration of the entire neurone; 
division of a process or axis-cylinder results in its degeneration below 
the point of separation from the nutrient cell. The neurones are mostly 
independent of each other ; at times, especially in the retina, some degree 
of anastomosis between the dendrites of different systems exists (Dogiel). 
The nerve cells are closely grouped in the gray cortex, gray substance of 
the cord and ganglia of the peripheral nerves. The axis-cylinders largely 
course through their white substance. To comprehend localization in 
spinal diseases, we must recognize that pathological processes are in 
general of two varieties: (a) those involving certain neurones, or system 
diseases and (b) those not involving given neurones, non-system diseases. 

The functions of the cord are (1) conduction of motor impulses to 
the muscles; (2) conduction of sensory impressions to the brain; (3) 
certain reflexes; (4) centres governing the bladder, rectum, etc., and 
(5) trophic influences. 

1. The motor tract is composed of two sets of neurones or segments. 
The upper segment has its origin in the cells of the motor cortex (Fig. 
61, A), runs through the corona radiata, internal capsule, cms, pons 



820 



DISEASES OF THE SPINAL CORD 



and anterior pyramids of the medulla (whence the name pyramidal 
tracts), and crosses to the opposite side (Fig. 61, B), running down in the 
lateral columns of the cord (C) and giving off branches (D,D) to the 
anterior horns, where the tract ends in 'fine terminal filaments, which 
surround the motor ganglion cells in the anterior horn. (See Fig. 56.) 
The lower segment begins with the motor cell in the anterior horn (E), 
the dendrites of which connect with the terminal ramifications of the 



FAC 




ARM 



FACE 



Fig. 61. — Illustrating the course of the two motor neurones: A, cortical cell of origin of 
motor tract; B, decussation in medulla; C, course in lateral columns of cord: D,D, branches 
to anterior horns in cord; in second (lower) neurone, E, cells of anterior horns, E", cells 
in pons; F, nerve trunks; G, motor end plates; H, muscles. 



axis-cylinder of the upper segment by contact (Ramon y Cajal) or by 
concrescence (Held); it extends along its own axis-cylinder into the 
anterior nerve roots and nerve (F) f and ends in terminal ramifications 
(G, motor end plates) in a muscle, e. g., of the arm or leg, which is on the 
side opposite to the origin of the cortical motor centre. From the cells of 
both segments the motor impulse travels downward (cellulifugal" con- 
duction). About 75 per cent, of the upper motor neurones cross as 
above described, are called the crossed pyramidal tracts (C.P.T., in Figs. 



GENERAL ANATOMICAL CONSIDERATIONS 



821 



61 and 62) and lie in the lateral columns of the cords; 25 per cent, of the 
motor fibers do not cross in the medulla, but pass down in the anterior 
columns of the same side — the anterior or direct pyramidal tracts (D.P.T., 




GANGLION CELL OF 

CORTEX. BEGINNING 

OF 1ST NEURONE 



AXIS CYLINDER 
OR AXONE 



C. P.T. 



TERMINAL FILAMENTS 
END OF FIRST NEURONE 




GANGLION CELL OF ANT. HORN 
BEGINNING OF 2ND NEURONE 



-END OF 2ND NEURONE 
IN MUSCLE PLATES 



Fig. 62. — Illustrating the general outlines of the upper and lower neurones and of the direct 
(D.P.T.), and crossed (C.P.T.), pyramidal tracts. 



lOCTS 




pos 

ROOT 



Fig. 63. — Showing the different tracts of the cord. (Gowers.) 



822 



DISEASES OF THE SPINAL CORD 



c 1. 



Dl. 



10., 



11. 



12., 



n 



"<& 



I 



Dl, 



in Figs. 61 and 62). The direct pyramidal tract probably crosses to the 
anterior horn of the opposite side by way of the white portion of the 
commissure of the cord. The upper segment is largely crossed, but the 

lower segment (or neurone) is a direct tract, 
the cells in the anterior horns supplying 
muscles of the same side of the body. 

The cord therefore contains parts of both 
neurones, the course of which has been ascer- 
tained by the secondary descending degneration 
which follows neurone lesions. Turck first 
fully described its occurrence and Flechsig 
and Bechterew added information from em- 
bryological studies. After a lesion, as hemor- 
rhage in the internal capsule, the fibers of the 
upper neurone below the lesion degenerate; 
granule-bearing cells appear and the axis- 
cylinders swell, degenerate and stain poorly 
by the Marchi method, because the axones 
are separated from the nutrient cortical cells. 
The neuroglia increases and corpora amylacea 
develop. Degeneration is seen in the opposite 
lateral pyramidal tract and in the anterior 
column on the same side as the brain lesion. 
Sometimes slight degeneration occurs in the 
lateral pyramidal tract of the same side, which 
probably has some connection with the anterior 
uncrossed pyramidal tract of the same side 
(see Broadbent's theory, page 770). Since 
the vitality of the neurone fibers decreases as 
their distance from their trophic cell increases, 
the degeneration is greatest in the most per- 
ipheral part of the axone. The degeneration 
usually stops at the end ramifications of the 
axone (see page 766 and Plate XX). 

Degeneration in the Lower Segment. — Dis- 
ease of the anterior horns or the nerve trunk 
causes degeneration of the nerve toward the 
periphery and trophic muscle changes. The re- 
action of degeneration is elicited. (See Neuritis.) 
The two neurones do not correspond in 
'number, because one neurone of the upper 
segment is connected with several lower 
neurones, i. e., various cells in the anterior 
horns at different levels are probably excited 
by a single pyramidal fiber. For complex 
movements, as of the hands, there are more 
Fig. 64. — Diagram from pyramidal fibers than for simple movements, 
Gowers, showing relation of ag f th i nte rcostal muscles. The anterior 

vertebral spines to their bodies . . . • i ni p 

and to the nerve roots. spinal root nerves 30m with fibers irom 



\ 



12 



LI 



■10 



"11 



1L 



.IS 



PLATE XX 



B 











A. Ascending degeneration in the posteromedian column and anterolateral 

ascending tracts from lumbar lesion. (After Gowers.) 

B. Ascending degeneration after injury to eauda. (After Sehultze.) 

C. Descending degeneration of pyramidal tracts from right-sided cerebral 

hemorrhage. (After Mott.) 



gMMal anatomical CONSIDERATIONS 823 

the posterior roots, and passing downward, leave the spinal cord 
between the vertebrse, thus forming the spinal nerves, whose area of 
origin in the cord is called a segment. The peripheral nerves often arise 
from several segments, which are sometimes considerably separated; 
muscles with similar function have similar spinal localization, because 
movements rather than muscles are localized in the cord, as well as in the 
brain. The table on page 824 gives the localization of the muscles, with 
special regard to their cells (the beginning of the second neurone), as 
well as of the skin and reflexes. The cord is shorter than the spinal canal, 
reaching only to the second lumbar vertebra. The nerve roots descend 
and therefore their level at the point of exit does not correspond with 
their level of origin. Fig. 64 shows this relation. 

2. The sensory tract conducts upward and is more complicated and 
less clearly understood than the motor tract, because the interpretation 
of experiments on animals is confusing. It is composed of three or more 
neurones. The cells of the first neurone are in the intervertebral ganglia, 
whose cells end in an axis-cylinder dividing into a branch to the skin 
and another to the cord by the posterior root; the branches from the 
skin (peripheral sensory nerves) represent the dendrites of the ganglion 
cells and the branch to the cord represents the axis-cylinder. All per- 
ipheral sensory fibers originate in the ganglia and almost all fibers of 
the posterior nerve roots come from these ganglia. From the posterior 
roots the fibers reach the cord, where (a) some pass into the posterior 
column, (b) some into the gray matter and (c) others run to the cells 
of the anterior horns (reflex arcs) . 

(a) The fibers entering the white substance (the posterior columns) 
divide into a short descending branch (probably concerned in reflex 
processes, giving off some collaterals and ending in the gray matter) 
and into a more important long ascending branch; by the entrance of 
new fibers at higher levels they become more centrally located in Goll's 
posterior median column in which the lowest fibers (e. g., the sciatic) 
are most posterior and the highest (e. g., the cervical) are most anterior. 
The posterior columns convey fibers for muscle sense (sense of posture 
and movement association) and possibly also for simple tactile sensation. 
"Sensations we do not feel" travel in these columns (Gowers). Goll's 
posterior median column ends in the nucleus gracilis of Goll (postero- 
median nucleus) in the medulla. It is uncrossed, i. e., direct. Burdach's 
posterior external column ends in the nucleus cuneatus of Burdach 
(posterior external nucleus) in the medulla. It is likewise uncrossed 
or direct. The first neurone ends in these nuclei. The second neurone 
crosses above the motor decussation in the medulla (interior arcuate 
fibers) to the opposite side and unites with fibers that have already crossed 
in the cord, thus forming the fillet (see below, 6). This neurone is crossed. 
The posterior nuclei communicate with the opposite cerebral cortex, 
with the cerebellum of the same and opposite side and with the external 
arcuate fibers. 

(6) The fibers entering the gray matter of the posterior horns also divide 
into ascending and descending branches. Some lie at the zona terminalis, 
the most posterior part (Lissauer's zone) of the posterior horn. All these 



824 



DISEASES OF THE SPINAL CORD 



Segment. 



Muscles. 



Skin: Sensation. 



Reflexes. 



2-3 Cervical. 

4 Cervical. 

5 Cervical. 

6 Cervical. I 

7 Cervical. 



8 Cervical. 



1 Dorsal. < 



2-12 Dorsal. 



1 Lumbar. 



2 Lumbar. < 



3 Lumbar. 



4 Lumbar. 



5 Lumbar. 

1-2 Sacral. 
3-5 Sacral. 



Sternocleidomastoid, trape- 
zius, scaleni, neck mus- 
cles. Diaphragm (3, 4, 5, 
6 cerv.). 

Lev. ang. scapulae, rhom- 
boideus, supra- and infra- 
spinatus, deltoid, supin- 
ator longus, biceps. 

Supinator brevis, serrat. 
mag., clavicular portion 
of pectoralis maj., teres 
minor. 

Pronators, coracobrachi- 
alis, brachialis ant., tri- 
ceps, long extensors of 
hand and fingers. Lower 
neck muscles and middle 
part trapezius, 6, 7, 8, C 
and 1 D. 



Costal portion of pectoralis 
maj., latissimus dorsi, 
teres maj. 

Long flexors of the hand 
and fingers. 



Extens, poll. long, et brev. 
Small muscles of hand. 



Muscles of back (also low- 
est part of trapezius) and 
abdomen. Intercostals D, 
1-10. 



Abdominal muscles, quad- 
ratus lumborum. Ileo- 
psoas. 

Sartorius (or third lumbar), 
flexors of hip. Quadri- 
ceps femoris (extensors 
of knee), cremaster. 

Internal rotators of thigh. 



Adductors of hip. 
Sartorius (?). 
Abductors of hip. 
Tibialis anticus. 
Calf muscles. 

Flexors of knee (?) , gluteals 
(extensors of hip) . 

External rotators of hip. 
Flexors of foot (?). 
Extensors of toes. 
Peronei. 

Flexors of foot and toes. 
Small muscles of foot. 



Muscles of perineum. 



Neck and occiput. 



Shoulder (anterior part, 
Dana) . 



Radial side of arm (volar 
and dorsal surfaces) to 
the insertion of deltoid. 
Post, surface of shoulder? 

Dorsal and volar surfaces of 
radial side of hand to mid- 
line of middle finger, and 
up to base of hand, nar- 
row strip on volar and 
dorsal surfaces up to 
axilla, connecting with 
above area. 

Ulnar part of hand (dorsal 
and volar) from middle 
of the fourth to middle of 
third finger and connect- 
ing with it, a moderate 
strip on volar and dorsal 
surfaces of arm. 

Dorsal and volar surfaces of 
hand to middle of fourth 
finger, narrow strip on 
dorsal and volar surfaces 
of arm up to axilla. 

Narrow strip on ulnar sur- 
face of arm and forearm 
down to base of hand. 
(The upper part, perhaps, 
belongs to the second 
dorsal segment.) 

Chest, back, abdomen and 
upper gluteal region. 
(Umbilicus, tenth dorsal; 
ensiform, sixth to seventh 
dorsal) . 



Pubic area, anterior aspect 
of scrotum. 



Anterior and inner side 
of hip, inner side of leg 
to malleolus, inner 
side of foot, external 
surface of hip, lumbar 
regions. 

Posterior surface of hip, 
thigh, external surface 
of leg and foot. 



Back of foot. 



Skin of sacrum, anus, peri- 
neum, genitalia. 



Sudden inspiration by 
sharp pressure below the 
. ribs. 

Widening of pupil from 
irritation of neck, 4-7 
cervical. 

Scapular reflex (fifth cerv. 
to first dorsal). Tendon 
reflexes of this group of 
muscles. 

Tendon reflexes of muscles 
named. 



Volar reflex of hand, peri- 
osteal reflexes of radius 
and ulna. Tendon re- 
flexes of muscles named. 



Corresponding tendon re- 
flexes. 



Tendon reflexes. 



Abdominal reflex. Epi- 
gastric reflex (according 
to Dinkier, is at the ninth 
dorsal, the middle and 
lower abdominal at the 
tenth and twelfth, respec- 
tively) . 

Cremasteric reflex (1-3 
lumbar) . 



Patellar reflex (2-4 lum- 
bar). Erection (lumbar 
cord) . Uterus (lumbar 
cord) . 



Gluteal reflex (4-5 lum- 
bar). 



Plantar reflex; ejaculation 

(3-4 sacral). 
Achilles tendon reflex. 

Bladder and rectum reflex. 



The brackets to the left concern only the muscles, and indicate the origin of the muscles from several 
nuclei. 



PLATE XXr 




Scheme of Sensory Conduction. (Strumpell.) 



A. — Entrance of posterior sensory roots into lumbar cord: g.i., intervertebral ganglion; 
r.p., posterior root; part of the fibers end in the posterior horns, from whose cells other fibers 
arise and enter the lateral columns, partly on the same and partly on the opposite side; other 
fibers from the posterior roots, course upward in the posterior columns and form in: 

B (the cervical cord). — Goll's columns (G) ; B.C., Burdach's columns. 

C. — Medulla oblongata, G and B are the nuclei wherein Goll's and Burdach's columns end. 
From these, new fibers arise which decussate and form the fillet (lemniscus, L) in: 

D. — L, lemniscus; Py, pyramidal tract; 0, the olive; C.R., corpus restiforme. 

E. — Pons; IV, fourth ventricle. 

F. — L, lemniscus of fillet; n.r., nucleus ruber; Py, pyramidal tract in crus cerebri; nL, 
nucleus lenticularis ; Th, optic thalamus (beginning of new neurone to cortex?). 



GENERAL ANATOMICAL CONSIDERATIONS 825 

fibers end with terminal ramifications about ganglion cells in the gray 
matter; they form the beginning of a second neurone which crosses in the 
commissure of the cord and courses upward in the anterolateral column 
and anterior ground fibers of the opposite side (just anterior to the lateral 
pyramidal tracts) and they unite in the medulla with the fibers of the 
second neurone of (a) (v. s.). (See Plate XXI.) The fibers entering the 
posterior horn convey temperature and pain conduction and travel between 
the posterior median column and the central canal. Tactile sensation 
is probably conveyed in the anterolateral column, which conveys most 
of the upward sensory impulses, since their division causes anesthesia 
(Gowers). Both (a) and (b) then run in the median lemniscus of the 
fillet and in part of the longitudinal bundles of the formatio reticularis 
of the pons, tegmentum of the crus and posterior limb of the internal 
capsule, beyond which some fibers run directly to the motor cortex or 
parietal lobes, while others end in the optic thalamus, whence perhaps 
by a third neurone to the cortex. 

The sensory tracts degenerate upward (ascending degeneration). Plate 
XX, Fig. A, shows degeneration in the posterior and anterolateral 
columns. Most ascending degenerations stop in the medulla. The 
direct cerebellar tract, which begins at the first lumbar nerve, also de- 
generates upward; most of its fibers come from the lower dorsal and 
first lumbar nerves ; some of them come from the gray substance of Clark's 
columns to which collaterals are sent from the posterior fibers; Flechsig 
believes that it conveys muscular impressions from the lower part of the 
trunk and the legs; its destination is the middle lobe of the cerebellum 
by way of the restiform body. 

The spinal sensory nerves descend lower than do the corresponding 
motor nerves and skin sensation for a given area is often supplied by 
two, three or more nerves, whence anesthesia results only when all of 
them are diseased (Sherrington). (See Plate XXII.) 

Lesions of the conus medullaris down to the fourth sacral nerve pro- 
duce paralysis of the bladder and rectum and simultaneously saddle- 
shaped anesthesia on the anus, gluteal region, perineum, genitalia, 
undersurface of the thigh (pudendal and coccygeal plexuses), but the 
scrotum escapes because the spermatic plexus and external spermatic 
nerve connect with the lumbar plexus. Motor paralysis is absent because 
the limbs receive their supply from the lumbar and upper sacral segments. 
The cremaster reflex is normal. If sexual desire and erection are preserved 
with loss of vesical and rectal function, a conus localization is probable. 
Sensory dissociation, trophic changes and rapid advance of the disease 
argue for conus disease. Lesions of the cauda equina (where the roots lie 
closely together) are usually symmetrical. The onset is insidious and the 
progression slow; pain is prominent and usually the first symptom; 
then the leg reflexes are lost, followed considerably later by paralysis, 
atrophy and anesthesia (especially in the perineum, ext. genitalia and a 
narrow zone about the anus). For caudal lesions speak remission and 
improvement in the vesical and rectal functions and the slow appearance 
of muscular wasting, reaction of degeneration and trophic alteration. 
In its upper part, the above symptoms with paralysis of both legs are 



826 



DISEASES OP THE SPINAL CORD 



noted; paraplegia dolorosa is frequent (see Plate XX, Fig. B). A 
lesion below the third lumbar vertebra is usually limited to the pudendal 
and sciatic distributions. 

3. In the gray matter there are reflex centres enumerated in the table 
above. The reflex arc comprises the afferent sensory fiber with its 
termination in the gray matter and the motor nucleus with its efferent 
motor fiber. The fibers of the oculopupillary reflex run by way of the 
sympathetic nerve (rami communicantes) to the cord. Irritation of its 
centre produces mydriasis, especially in spinal caries. Paralysis from 
disease of the centre produces myosis, narrowing of the eye fissure, 
sometimes retraction of the eye-ball and flattening of the cheek; this 
paralysis is produced by section of the eighth cervical and first dorsal 
segments, i. e., the same localization as for paralysis of the forearm and 




Fig. 65. — Lesion at the level of the 
second lumbar segment (Striimpell and 
Miiller, from whom also following figures 
are borrowed). 



Fig. 66. — Lesion at third lumbar segment. 



anesthesia of the ulnar surfaces of the hand and arm. It occurs more 
often in disease of the nerve roots than of the cord itself. The tendon 
reflexes will be considered under the individual cord diseases. They are 
inhibited from the brain and probably also from the cord. There are 
muscular fibers to evacuate the bladder and rectum and sphincters to 
retain their contents. The former are stimulated by distention and the 
latter relax; they are controlled normally by the will. If inhibition fails, 
the bladder or rectum is evacuated, sometimes with the knowledge of the 
patient, as in disease of the pyramidal tracts, or unconsciously, as in 
coma or when the sensory nerves of these parts are diseased. As to the 
rectum, disease of the centre discloses itself by continuous evacuation 
and relaxation of the sphincter on digital examination; disease above 
the centre, by normal tonicity of the sphincter. 



GENERAL ANATOMICAL CONSIDERATIONS 



827 



In the above considerations, the leading points are given regarding 
the level of the lesion and the course of the chief systems. Total transverse 
disease of the cord produces paralysis of the muscles at and below that 





Fig. 67. — Lesion at fifth lumbar segment. 



Fig. 68. — Lesion at first sacral segment. 



level, and sensory interruption; it might be difficult to decide whether 
the cord were affected through a narrow horizontal level, or whether all 
the cord below it were diseased, unless the reflexes below were noted. 
Hyperesthesia usually discloses the level of the lesion. Lesions of the 




Fig. 69. — Lesion at second sacral segment. Fig. 70. — Lesion at third sacral segment. 



pyramidal tract (first neurone) produce motor paralysis at the level of 
the lesion, increased reflexes and spasticity (hypertonic muscular rigidity) 
but with no muscular atrophy, reaction of degeneration or sensory dis- 



828 



DISEASES OF THE SPINAL CORD 



turbance. Lesions of the anterior horns or anterior roots produce a flaccid 
paralysis, atrophy and the reaction of degeneration if the process is 
acute. (If it is chronic the atrophy is more marked than the paralysis 
and the reaction of degeneration is absent or atypical. The trophic 
cells are not specialized in the horn, but all cells are probably trophic.) 
The motor nerve (Nasse, 1839) and the muscle degenerate; the reflexes 
are abolished; the muscle tension (myotatic irritability) is lost, there is 
vasomotor paralysis (since the fine fibers of the anterior roots are vaso- 
motor) and contractures result (from sensory irritation). If the lesion 
is in the anterior horn there may be fibrillary muscular contractions. 
Irritation of the anterior horns may increase the reflexes and induce 
contractures. In lesions of the posterior columns the chief alteration is 
sensory disturbance, especially in the muscle sense, and therefore inco- 




Fig. 71. — Lesion at fourth sacral segment. 



ordination or ataxia. The reflex arc may be interrupted. In lesions 
of the posterior horns there are disturbance of the temperature and pain 
sense and some alteration of the tactile sense; the reflexes may be dis- 
turbed. In lesions of the posterior roots the reflexes are disturbed and 
there are anesthesia and ataxia. Irritation of these roots causes pain, 
hyperesthesia in the form of a girdle sensation around the trunk or lancin- 
ating pains in the extremities and reflex contractures. The importance 
of the spinal ganglion as the trophic centre must be remembered 
(Waller, 1852). Vasomotor fibers leave the cord through the anterior roots 
by the rami communicantes and course down in the lateral columns or 
in the intermediolateral tract from the centre in the medulla. Most 
of the vasoconstrictor fibers leave the cord between the third dorsal and 
second lumbar segments, while the vasodilator fibers are much more 
diffusely scattered through the cord. 



PLATE XXH 






,3 d" 
id 



X 



?d :/ 



J 2d' 



fail 



4 1 



5 s 



4 1 



2sJ 






These figures have been aevised by Wichmann in order to show the distribution of the sensory areas 
corresponding to the segments of the spinal cord. The colors used correspond to those of the normal spec- 
trum, red, orange, yellow, green, blue, indigo, and violet, with brown; respectively- — the first, second, third, 
fourth, etc., segments in each portion of the spinal cord- -cervical, dorsal, lumbar, and sacral. The last four 
segments in the dorsal region are left white. The advantage of the plate is that it shows very clearly the 
overlapping of the segments that has been demonstrated by Sherrington. The dark heavy black lines 
on the arms indicate the division between the two sides of innervation — that from the upper portion of 
the cervical enlargement and that from the lower portion. The heavy black lines of the legs indicate the 
divisions between the sacral and lumbar areas of innervation. The figures and letters indicate the seg- 
ments in which the supply has been drawn and have been introduced for the sake of making the diagram 
more available for ready reference. C — cervical, D — dorsal, L — lumbar, and S — sacral. The horizontal 
bands of color without dividing lines between them indicate that both segments innervate the areas 
involved. (Musser.) 



DISEASES OF THE SPINAL MENINGES 829 

DISEASES OF THE SPINAL MENINGES. 

Most diseases of the vertebra? and cord affect the meninges, but 
generally, meningeal symptoms excite little clinical interest. 

I. Hemorrhage. — (a) Between the vertebrae and dura, hemorrhage is 
frequent from rupture of the subdural plexus of veins. It surrounds 
the nerve roots and is most severe over the posterior cord; it results 
mostly from trauma and to a lesser extent from vertebral disease or 
aneurysmal rupture. (b) Arachnoid hemorrhage (hematorrhachis) 
results from the above causes, dystocia, or hemorrhagic diseases. The 
entire spinal canal may be filled with blood from brain hemorrhage, 
especially at the base. 

Symptoms. — Small hemorrhages cause no symptoms and meningeal 
apoplexy may be overshadowed by brain or traumatic cord symptoms. 
Pain in the back, rigidity, radiating pains from root compression, hyper- 
esthesia, painful reflex spasms, motor weakness, anesthesia, sphincter 
disturbance and abolition of the tendon reflexes are the common symp- 
toms. They affect the lower more than the upper cord, increase for a day 
or so, produce inflammatory reaction for a few days and subside in from 
four to eight weeks. Physical signs vary with the location; brachial 
paraplegia is present in cervical, and involvement of the legs in lumbar 
or dorsal, hemorrhage. 

Diagnosis and Treatment. — In diagnosis the most important symptom 
is irritation, while in hemorrhage of the cord (hematomyelia) paralysis 
prevails and pain is less frequent. In non-traumatic cases, diagnosis is 
impossible. The treatment is symptomatic. Absolute rest in the lateral 
decubitus or on the face should be enjoined. 

II. Pachymeningitis. — (a) This may be external (peripachymeningitis) 
and follows caries, penetrating bed-sores, deep cellulitis, psoas or retro- 
pharyngeal abscess. Its symptoms are those of compression. Root 
symptoms and fever are frequent. The prognosis is unfavorable and the 
treatment is etiological, expectant or surgical. (b) Internal pachymenin- 
gitis hemorrhagica. Its causes are those of the cerebral form (q. v.), 
(c) Charcot (1871) and Joffroy described a pachymeningitis cervicalis 
hypertrophica, in which the inner surface of the dura is thickened by 
annular concentric fibrous deposits. The dura adheres to the vertebras 
and leptomeninges and compresses the nerve roots, which indurate. 
Several cervical segments are involved. The process is most marked on 
the dorsal aspect of the cord, which is flattened anteroposteriorly and 
shows peripheral induration by extension of the process to it through the 
pial vessels (meningomyelitis) ; this causes ascending and descending 
degeneration. Cold, syphilis, alcoholism and trauma are probable 
causes. 

Symptoms. — Charcot described three stages: (a) the neuralgic stage, 
which corresponds to involvement of the posterior roots, in which pains 
radiate from the neck into the ulnar and median nerve supply. They are 
continuous, with paroxysmal exacerbations, with localization at times 
in the arm-joints, with rigidity, paresthesia in the arms and some motor 
weakness, (b) The second stage is atrophic paralysis of the arms, the 



830 DISEASES OF THE SPINAL CORD 

process involving the anterior roots. The pains are replaced by atrophy 
and paralysis in the ulnar and median nerve areas, while the radial area 
is usually unaffected; this produces flexor paralysis in the forearms 
and hands, and the claw-hand (main en griff e) results from contracture; 
the wrist is overextended, the first phalanges are extended, the second 
and third are flexed ; ulnar and median anesthesia and the reaction of de- 
generation are found. The shoulder and elbow muscles may be involved. 
Deviations from Charcot's complex are at times noted, as absence of 
atrophy and contracture, (c) In the third stage the legs exhibit spastic 
paralysis without atrophy; the bladder and rectal functions and some- 
times the sensory conduction are disturbed from secondary changes in 
the cord. 

Diagnosis. — The process is easily localized to the cervical region. 
Marked pain also occurs in tumors, cervical spondylitis, syphilitic meningo- 
myelitis and at times in syringomyelia. Amyotrophic lateral sclerosis 
(q. v.) and progressive spinal muscular atrophy cause no such severe 
pains and syringomyelia (q. v.) is characterized by dissociated anesthesia, 
muscular atrophy, painless felons and trophic changes in the joints. 
Tumors (q. v.) are difficult to differentiate. Neuritis causes symptoms 
limited to the limbs. 

Prognosis. — This is usually unfavorable and chronic progression, 
cystitis, etc., usually develop. Instances of recovery are recorded. 

Treatment. — Warm baths, counter-irritation, sedatives, narcotics, 
mercury, iodides and care of the skin and bladder are indicated. 



TUMORS OF THE SPINAL CORD AND ITS MEMBRANES. 

Of Schlesinger's 400 cases 126 were intramedullary and 239 extra- 
medullary (151 intradural and 88 extradural). 

I. Tumors of the Membranes. — These may arise from the dura or 
leptomeninges. In Horsley's extradural tumors there were sarcoma, 
lipoma, tubercle, echinococcus cysts, myxoma, fibrochondroma, car- 
cinoma and fibrosarcoma. Cysticercus often causes no symptoms. 
Intradural tumors include myxoma, sarcoma, fibroma, psammoma, 
tubercle, parasitic and syphilitic tumors. Lipomata, echinococci, cysti- 
cerci, neuromata and angiomata are rarer. Usually single, multiple 
occurrence may be noted in sarcomata, parasitic tumors and neuromata. 
This group compresses the cord or its nerve roots. There are edema 
of the cord, flattening, peripheral hardening, central softening and 
ascending and descending degenerations. The nerve roots atrophy. 

Symptoms. — Extradural growths produce more vertebral than cord 
symptoms. The first symptoms are usually those of compression of 
the nerve roots, e. g., radiating pains, first on one side, then on both, 
which run into the arms, trunk or legs and advance from one root to 
another; hyperesthesia; paresthesia; anesthesia, which is less common 
since it implies involvement of at least three roots; atrophic paralysis; 
rigidity; and spontaneous muscular contractions. Local tenderness is 
rare. The symptoms recall those of carcinoma of the spine aside from its 



TUMORS OF THE SPINAL CORD AND ITS MEMBRANES 831 

vertebral signs. Later, evidences of compression of the cord appear, as 
paresis, perhaps of one side first (Brown-Sequard's type, v. i.) or para- 
paresis with atrophy if the anterior horn is involved at that level, with 
increased reflexes (unless the arc is broken), with spasticity and contract- 
ures; and with sensory changes. As in carcinoma of the vertebrse, the 
paraplegia dolorosa of Cruveilhier is common, as is anesthesia dolorosa 
(the "eccentric projection" or reference of pain to the anesthetic areas). 
Finally, there are total paraplegia, anesthesia and bladder and rectal 
paralysis. 

II. Tumors in the Cord Substance. — They are less common than 
tumors in the membranes, and include glioma (cervical and upper dorsal 
regions), sometimes gumma, sarcoma (pia), tubercle (gray substance or 
posterior horn) and cysticercus. Most are circumscribed, though glioma 
tends to vertical diffusion. Unlike meningeal tumors, they are rarely 
metastatic. 

Symptoms. — In intramedullary growths, root symptoms are absent, 
especially in gliomata and, since there is gradual compression of the 
cord, the clinical picture may resemble chronic myelitis and syringo- 
myelia. The cord symptoms are disturbed conduction; spastic para- 
plegia; marked increase of reflexes (unless the arc is broken or absolute 
cord compression develops); bilateral symptoms, or if unilateral, they 
soon reach the other side; extensive muscular atrophy, if the cervical 
or lumbar enlargement is diseased, often then with the reaction of de- 
generation; and sensory changes involving all varieties of sensation or 
certain varieties only, as pain or temperature (dissociated or partial 
anesthesia). Bruns maintains that the lesion and symptoms are at first 
unilateral, followed by the Brown-Sequard complex (q. v.). As the tumor 
grows, total paraplegia and anesthesia may, in rare cases, develop below 
the level of the lesion. 

Localization. — Accurate localization is most important but rarely 
possible until the cord itself is compressed. The most common error 
is in locating the tumor too low. Atrophic paralysis, in the cervical 
or lumbar region, is the most certain aid. Sensory changes are less 
reliable; the actual lesion is two, three or four segments higher than 
the anesthesia because anesthesia results only from involvement of at 
least three roots (Sherrington's law). The hyperesthesia usually repre- 
sents the level of the lesion and local spinal tenderness, though rare, 
is very important. Finally, the spinal segments involved must be con- 
sidered in terms of the corresponding vertebrae (v. s., page 822). (a) 
In a tumor of the tipper cervical cord there are pains in the cervical plexus 
and perhaps anesthesia.; at first there may be a spinal hemiplegia differing 
from cerebral hemiplegia in that the face and hypoglossus escape and the 
anesthesia is contralateral to the paralysis ; then there is spastic paralysis 
of all four extremities, which rarely lasts long, since affection of the 
phrenic nerve causes early death, (b) In tumor of the cervical enlarge- 
ment there are atrophy, flaccid paralysis and pain in one arm, spastic 
paresis in the leg of the same side, anesthesia of the entire opposite half 
of the body and opposite limbs; and then paralysis of both arms and 
legs with anesthesia, (c) Localization in the dorsal cord often produces 



832 DISEASES OF THE SPINAL CORD 

unilateral signs, as paresis of one leg with its half of the trunk, and 
anesthesia of the corresponding parts of the other side ; spastic paraplegia 
of legs and abdomen, retention of urine and later incontinence; and 
then girdle pains, (d) In tumors of the lumbar enlargement there are 
unilateral pains in the lumbar plexus and atrophic paralysis in the 
ileopsoas, quadriceps and adductors; there is total anesthesia when the 
cord is involved in the region of the lumbar plexus ; later partial anesthesia 
(affecting the sense of temperature and pain) develops in the region of 
the sacral plexus; still later there is complete paralysis and anesthesia 
in the region of the lumbar plexus, with atrophy, absence of the patellar 
reflexes, the reaction of degeneration, spasticity of the legs and feet, 
and Achilles clonus, (e) If the localization is in the sacral cord there is 
atrophic paralysis of the leg and foot, posterior muscles of the thigh, 
gluteal and perineal muscles, anesthesia, total paralysis of the bladder 
and rectum, impotence, loss of the Achilles reflex (while the patellars 
may persist), early decubitus and cystitis. (/) If the tumor is in the 
cauda, the symptoms are usually bilateral from the beginning; para- 
plegia is rarely as symmetrical as in cord lesions; there is the reaction 
of degeneration; pain is violent, since many sensory fibers are in close con- 
tact; Minor described bilateral and even unilateral sciatica as an early 
symptom. The sacral plexus is chiefly or first involved, while growths 
of the lumbar enlargement affect both the sacral and lumbar plexuses. 

Diagnosis. — The diagnosis of meningeal tumor, always difficult, is 
based on (a) local pain and rigidity, which are especially marked in 
the extradural type; (6) hyperalgesia; (c) radiating pains, i. e., root 
symptoms which later gradually give way to (d) cord symptoms, often 
unilateral at first and then bilateral, as interrupted sensory and motor 
conduction and increased reflexes. Carcinoma of the vertebrae produces 
more pain on movement than other tumors. In caries there is less pain, 
local vertebral changes eventually appear, and the course is usually more 
rapid. In myelitis the arms are less often paralyzed; radiating pains 
are much rarer than in tumor and a girdle sensation is more common. 
The local pain sometimes suggests aneurysm, lung disease or peripheral 
neuralgias but the tender points of Valleix are absent. Root symptoms, 
early interruption of cordal conduction and absence of trophic disturb- 
ance in the bones and of dissociated anesthesia argue against syringo- 
myelia. A diagnosis of tuberadosis or syphilis is fortified by its presence 
in other organs. In youth, tubercle; at puberty, sarcoma and glioma; 
in the third and fourth decades, glioma, tubercle or sarcoma; and in 
advanced years gummata are most frequent. Diffuse sarcomatosis is 
usually cerebrospinal, rarely invades the cord substance, affects the 
posterior cordal surface most frequently and generally in the lumbar and 
lower dorsal regions; it occurs largely in the young and its course is 
rapid. Tabes in one remarkable case was simulated by multiple tumors 
of the posterior roots. Tumors of the cord are more difficult of differen- 
tiation, for root symptoms are often lacking. 

Course and Prognosis.— Slow development, progression either steady 
or "by starts," sometimes remissions and eventual compression of the 
roots or cord are usual, with death from cystitis or decubitus. Sudden 



CIRCULATORY DISTURBANCES 833 

paralysis is less common. The average duration is one to three years, 
but a longer course is possible (even fifteen years). 

Treatment. — 1. Therapeutics. — Narcotics are employed sparingly in 
the early stages, lest their effect fail later if the course is protracted. 
Syphilis is always a possible factor. 

2. Surgical Treatment. — Gowers first, 1887, localized a fibromyxoma 
which Horsley removed successfully. Tumors of the cord are less favor- 
able than those of the meninges. Intramedullary tumors may only crowd 
the nerve paths, but in their removal the attendant laceration or acute 
myelitis results in damage equal to that of the tumor. Accurate locali- 
zation is most important. Death may result from shock, escape of cere- 
brospinal fluid and infection. The operative mortality is 47 per cent. In 
Stursberg's 126 cases, 30 per cent, recovered. 



CIRCULATORY DISTURBANCES. HEMORRHAGE. TRAUMA OF 

THE CORD. 

I. Anemia of the Spinal Cord. — Paralyses referred to anemia of the 
cord are mostly due to neuritis, hemorrhages in the cord or nerve sheaths, 
and to degeneration. Paralysis following profuse hemorrhage from the 
stomach or uterus may be properly referred to cord anemia. Stenson 
(1667) demonstrated experimentally that compression of the aorta pro- 
duced paraplegia due to anemia of the cord, the motor cells of which 
appear to be especially susceptible to ischemia. 

II. Embolism and Thrombosis (Myelomalacia) . — Embolism of the spinal 
arteries is extremely rare, though observed in endocarditis. No separate 
clinical symptoms can be recognized. Thrombosis is very rare. Venous 
thrombosis is secondary to other lesions of the cord. Arterial thrombosis 
is rather more common; it has been found in syphilis, multiple sclerosis, 
senility and perhaps bears some relation to acute disseminated myelitis. 
It is often impossible to decide whether an area of softening is ischemic 
(myelomalacia) or inflammatory (myelitis). 

III. Hemorrhage (Hematomyelia). — Etiology and Pathology. — Most 
cases of this rare lesion occur in men between 20 and 40 years of age. 
Trauma causes 90 per cent, (a) Capillary hemorrhages occur in foci 
of softening, inflammation, etc. (b) The larger hemorrhagic focus from 
trauma, muscular effort, caisson-disease, etc., compresses and destroys 
the cord substance; it rarely exceeds the size of a hazel-nut but may 
extend the entire length of the cord (tubal form of Levier), following 
exactly the less resistant gray matter, while the firmer pyramidal tracts 
usually resist its lateral diffusion; if it invades the white matter, hemor- 
rhage usually occurs in the posterior columns; it occurs mostly in the 
cervical cord; all large non-traumatic hemorrhages occur in the gray 
matter. The nervous tissue is disorganized by large hemorrhages, which 
result eventually in a pigmented apoplectic scar or cyst. 

Symptoms. — (a) In the accessory form there is bleeding into a tumor, 
cavity, softening or inflammation; punctate hemorrhage may accompany 
purpura, stasis or convulsive disorders, and few or no symptoms develop. 
53 



834 DISEASES OF THE SPINAL CORD 

(b) The traumatic form is less important in spinal fracture than concussion 
(see Trauma); it may develop during dystocia or fetal extraction, (c) 
The spontaneous form is rarer than it is in the brain, because the cord is 
firmer, subject to lower blood-pressure, and most rarely the seat of miliary 
aneurysm; it results from sudden exertion in man (and more often in 
the horse), repeatd coitus or rarely arteriosclerosis. 

The onset is sudden, without prodromes or loss of consciousness. 
Local symptoms must vary with the structures involved and their 
level; they embrace paraplegia, monoplegia, the Brown-Sequard syn- 
drome, paralysis with or without atrophy or spasticity, anesthesia either 
total or partial ; pain at the level of the lesion ; less often eccentric pain, 
girdle sensation and muscular rigidity. In general the reflexes are in- 
creased in small and abolished in large hemorrhages. The symptoms 
advance rapidly and may be aggravated by secondary myelitis. Late 
death from cystitis or decubitus is more common than early death. 
Recovery is rare compared with cerebral apoplexy; it occurs most often 
in the punctate type; it is rarely absolute. 

Diagnosis. — The diagnosis is usually only probable, based on the 
sudden paresis and anesthesia and their rapid advance. For differ- 
entiation from hematorrhachis, see page 829. From acute myelitis, 
differentiation is often uncertain and of only academic interest; in 
myelitis and poliomyelitis elevation of temperature is distinctive. 

IV. Caisson or Divers' Paralysis. — According to Pol and Watelle 
(1854), this occurs in workers subject to pressure of at least 2, and usually 
3 or 4, atmospheres. Symptoms appear when the individual comes 
suddenly into the open air. They include transient pain in the ears, 
sometimes deafness, vertigo, headache and pains in the limbs, joints 
and epigastrium; in 35 per cent, there is paraparesis or paraplegia, some- 
times with anesthesia, and usually with urinary retention; much less 
often there is hemiplegia or involvement of both arms; epistaxis, mental 
symptoms; loss of consciousness and symptoms of brain-pressure, as 
vomiting or slowed pulse. Symptoms are not severe or are absent if 
the interval of work in the caisson does not exceed five hours. 

Pathology and Pathogenesis. — Hoppe-Seyler (1885) and Bert found 
that lessened atmospheric pressure liberated nitrogen in the blood and 
tissues, which ruptured the vessels and tissues. In the first autopsy 
v. Ley den found clots particularly in the posterior and lateral columns, 
surrounded by round cells (reactive disseminated myelitis) ; most changes 
were in the less compact, dorsal cord; secondary degeneration is found 
and changes in the gray substance from hemorrhage; Catsaris saw 
gas bubbles in the blood. Under moderate pressure the gas is given 
off to the lungs, while in extreme instances it is given off to the tissues 
(air embolism). 

Prognosis. — A few subjects die at once; 3-16 per cent, die from 
cystitis, as in myelitis; about 50 per cent, recover completely and the 
balance partially, with spastic paresis. 

Treatment. — The return to normal atmospheric pressure should be 
made gradually; recompression is successfully employed. Ergot and 
strvchnine are recommended. 



BROWN-SEQUARD'S PARALYSIS 



835 



V. Brown-Sequard's Paralysis. — According to Brown-Sequard's orig- 
inal statement (1850), on the side of section (cervical cord) there occur 
(a) paralysis of voluntary motion, muscle sensibility and vasomotor 
tonus; (b) hyperesthesia of trunk and limbs, to touch, pain, heat and 
cold; (c) vasomotor paralysis of face and eyes (higher temperature, 
narrow pupils and contracture of certain facial muscles). On the contra- 
lateral side there is anesthesia of all varieties of sensation, except muscle 
sensibility. 




Fig. 72. — Brown-Sequard's par- 
alysis from a left-sided focus : a, vaso- 
motor and motor paralysis; b and d, 
cutaneous anesthesia; c, hyperesthe- 
tic zone. (Erb.) 



VVS.M 




Fig. 73. — (Combined from Brown-Sequard.) 
F, focus in left side of cord; V, pyramidal fibers 
having crossed in medulla; V, vasomotor fibers, 
not crossing in cord; S.M, fibers for muscle sense, 
not crossing in cord; S S S' S', other sensory 
fibers crossing in the cord. The focus explains 
the classical signs and also how few of the 
crossed sensory fibers to the left side are in- 
volved (merely a zone of anesthesia), while all 
sensory fibers to the right side are severed 
(hemianesthesia) . 



Symptoms. — Exact hemiseclion of the cervical cord produces a spinal 
hemiplegia on the side of the section, but in injuries and experiments 
the trauma is rarely complete or strictly unilateral. (In some cases 
decussation of the uncrossed pyramidal tracts may occur in the cord 
lower down than the usual crossing point in the medulla (Flechsig) 
and spinal hemiplegia with contralateral monoplegia may result from uni- 
lateral lesion.) The characteristic clinical type is the mid-dorsal lesion, 
but in cervical section or in pathological foci, paresis of the arm with 
paralysis of the leg is more usual, because the cervical motor tracts 



i 



836 DISEASES OF THE SPINAL CORD 

are less compact than they are in the lower cord; paralysis of the leg 
may be incomplete, while that of the arm is complete, owing to the 
escape of fibers for the leg which cross lower down in the cord. The 
paralysis often decreases with surprising rapidity, and if the anterior 
cells are intact it gradually becomes simple weakness. There is an 
inactivity atrophy of the muscles without abolition of faradic irritability 
and without reaction of degeneration. Respiration is rarely affected. 
Involvement of the thoracic and abdominal muscles usually indicates 
a bilateral lesion. Swelling and edema in the paralyzed members and 
enlarged joints have been observed. The deep reflexes are exaggerated 
on the side of lesion; they are abolished in a sudden total transverse 
lesion of the lower cervical or upper dorsal cord. The skin reflexes are 
abolished or decreased on the side of paralysis and on the opposite 
anesthetic side they may be normal, absent or increased. 

Hyperesthesia occurs on the paralyzed side and also as a zone above 
the anesthetic area, near the level of the lesion. Hyperesthesia or hyper- 
algesia concerns tactile, pain and heat and cold sensation and their 
absence infers incomplete section. It usually disappears rapidly. The 
fibers involved lie in the lateral tracts. 

The zonular anesthesia on the side of the injury and of motor paralysis 
is explained since the lesion involves not only the sensory fibers (which 
are ready to decussate to the other side and produce the crossed hemi- 
anesthesia), but also sensory fibers from the contralateral side, which 
have just decussated to the side of section. Abolition of muscle sensation 
on the side of the lesion is in accord with the uncrossed course of the 
muscle sense fibers in Burdach's column, entering Goll's column higher 
up. Muscle sense is preserved on the side opposite to the lesion. Vaso- 
motor paralysis occurs on the side of section, as the vasomotor fibers 
course in the anterolateral columns. " Sensation is affected on the opposite 
side, but not quite up to the level of the lesion, because the decussation 
of the sensory tract is not immediate but occurs somewhat above the 
entrance of the nerve" (Gowers). Complete crossed hemianesthesia 
occurs in 60 per cent, and partial anesthesia (analgesia and thermo- 
anesthesia) in 40 per cent, of cases. 

Prognosis. — Almost complete restitution to normal is possible; it is 
not due to reestablishment of conduction in the severed tracts, in which 
ascending and descending degeneration occurs, but to assumption of 
function by the uninjured side of the cord. The prognosis and treatment 
of Brown-Sequard's paralysis vary with the etiology of this symptomatic 
syndrome, which may be syphilis, tumor, sclerosis, myelitis, tuberculosis, 
trauma, hematomyelia, fracture or luxation. 



INFLAMMATION OF THE CORD. 

Myelitis, inflammation of the cord, was described by Oliver and 
Abercrombie a century ' ago ; the term has been made to cover many 
affections not inflammatory, as compression paralysis. Oppenheim and 
Marie dispute the idea that myelitis is a frequent affection. 



ACUTE MYELITIS 837 

I. Acute Myelitis. — Etiology.- — The affection occurs largely in males 
between ten and forty years of age. 

1. Acute Infections. — Experimental myelitis has been produced by the 
B. pyocyaneus, B. diphtheria?, B. coli, B. typhosus, strepto- and staphyl- 
ococci, etc. It has followed epidemic meningitis, variola, measles, 
rheumatism and other infections, caused (a) by the germs themselves 
or secondary infection (focal myelitis resulting) or (6) by their toxins 
(disseminated myelitis resulting). 

2. Intoxications. — These include poisoning by alcohol, ergot and lead 
and perhaps auto-intoxications, as in cancer or severe anemia. 

All other causes are doubtful; trauma or compression by caries or 
cancer causes softening or hemorrhage, to which infection may be added; 
exposure to cold and dampness reduces the physiological resistance, thus 
indirectly favoring bacterial localization; syphilis (q. v.) may initiate 
meningomyelitis, but syphilitic myelitis is usually ischemic softening 
from endarteritis. 

Pathology. — On macroscopic examination we find redness and swelling; 
on cross-section, blurring of the cord tissues and decreased consistency, 
even to fluidity; "red softening" (hemorrhagic myelitis) and in older 
cases "yellow softening" from fatty change, or "white softening." 
After hardening in Miiller's solution, the normal tissue appears green 
and the diseased, yellow. In the ultimate stages, atrophy, cyst forma- 
tion, induration and very rarely abscesses are found. Microscopically 
there are, in fresh cases, degenerated, swollen axis-cylinders; disintegrating 
medullary sheaths from which myelin drops form; granule corpuscles 
(leukocytes or vessel endothelial cells); extravasated red and white 
cells; turgid vessels the nuclei of which proliferate; choking of the peri- 
vascular lymph spaces with cells; degeneration, blurring and vacuole 
formation of the nerve cells, the processes of which shrink and the nuclei 
vanish; amorphous deposits of coagulated albumin in and about the 
cells; in some cases the parenchymatous far exceeds the interstitial 
alteration (parenchymatous myelitis, or better, parenchymatous de- 
generation). The gray matter (poliomyelitis) is involved much more 
often than the white (leukomyelitis) . In older cases there are corpora 
amylacea, empty spaces corresponding to destroyed nerve fibers; Deiters's 
large "spider" cells with many processes; and interstitial proliferation 
is substituted for the destroyed tissue. In rare instances bacteria 
are found, but their toxins are more important. The microscope differ- 
entiates between inflammation and softening. The degree and the extent 
of inflammation vary greatly; transverse myelitis may destroy an entire 
cross-section; or disseminated foci may involve at random, various 
structures at different levels. Meningomyelitis (perimyelitis, annular or 
cortical myelitis) chiefly affects the periphery of the cord, whence con- 
centric invasion along the septa may split up the cord structures, par- 
ticularly in the syphilitic form. Poliomyelitis (inflammation of the gray 
substance) is a type of myelitis classified by itself. Degeneration and 
inflammation of the motor and sensory roots may follow myelitis in the 
cervical or lumbar enlargement. 



838 DISEASES OF THE SPINAL CORD 

Symptoms. — The symptoms vary with the extent, form and local- 
ization. The localized form, limited to a small segment, is called trans- 
verse, while the diffused form is known as disseminated myelitis. 

Acute transverse myelitis is the prototype. The cord symptoms are 
usually first in time and always first in importance and constitutional 
symptoms, as fever, chills, malaise and in children convulsions sometimes 
precede but usually attend the cord symptoms. Symptoms resulting 
from involvement of the cord are (a) paralysis, which is usually early, 
rapid but not apoplectic in onset and is prominent, paraplegic, progressive, 
flaccid and complete. The flexors are usually weaker than the extensors. 
The toes alone may be moved; twitching of the paretic muscles or 
clonic muscular spasms are sometimes present. The paralysis is often 
preceded for a short time by numbness, or moderate darting pains in the 
limbs, joints or back. The paralyzed limbs show a transient rise of tem- 
perature, followed by somewhat subnormal temperature. The limbs are 
often dry and may not sweat even after injection of pilocarpin. (b) 
Sensation is frequently involved. The initial tingling pain has been 
considered. Anesthesia may be complete but more often incomplete 
(hypesthesia) and rarely partial. It is higher anteriorly than posteriorly; 
a zone of hyperesthesia or "girdle pain" marks the upper level, caused 
by early irritation or late cicatrization. Severe pain suggests vertebral 
or root disease rather than myelitis; gastric crises like those of tabes, 
dysesthesia, i. e., diffuse vibrating sensations over the entire limb from 
local stimulation, and ataxia (usually obscured by the paraplegia) are 
much less common, (c) At the onset all reflexes may be lost, but they are 
usually increased below the focus, from lessening of cerebral inhibition 
(lateral pyramidal tracts). (See table.) (d) The sphincters are affected 
almost constantly and early; ischuria or urinary retention and later 
incontinence are usual; when the bladder is full it may dribble from 
relaxation of the sphincter, known as ischuria paradoxa or retention 
with incontinence; the patient may or may not be conscious of the 
retention, depending on whether the afferent sensory fibers are involved 
or not. The urine is at first alkaline and later ammoniacal on the advent 
of cystitis. The sphincter ani is spasmodically contracted or paralyzed 
(see table); the paresis of the bowel and abdomen are factors in con- 
stipation, (e) Trophic changes. Muscular atrophy and the reaction 
of degeneration are caused by disease in the anterior horns and the 
muscles also waste from inactivity. The skin is usually dry, sometimes 
glossy or vesiculated. The joints are sometimes swollen and the limbs 
edematous. Bed-sores are frequent over the sacrum, trochanters, heels, 
between or even over the knees, from the bed-covers; they result from 
neglect or in lumbar myelitis from trophic disturbance (disease in the 
gray matter or posterior horns). The same factors cause cystitis, ulcera- 
tion in the bladder or urethra and the tendency to cellulitis. 

Course and Prognosis. — The onset covers a few hours (the apoplectic 
form), or several days to a week (the subacute form). Four stages are 
described: the acute initial stage; the advancing degeneration; the resti- 
tution; and the stationary stage. Complete paraplegia and anesthesia 
may persist, but more often sensation returns after some weeks, while 



ACUTE MYELITIS 



839 



movement returns slowly, incompletely and usually with some residual 
spastic paraplegia. Contractures may develop, especially in the ad- 
ductors and knee flexors, which indicates profound disease. Contractures, 
muscular contractions and increased reflexes are caused by secondary 

Cord Symptoms Grouped According to Localization. 



i In order of 
frequency. 


Dorsal myelitis most 
frequent. 


Then lumbar myelitis. 


Lastly, cervical myelitis. 


Paralysis. 


Trunk, back, intercos- 


Trunk and arms nor- 


Neck muscles, dia- 




tal and abdominal 


mal. Paraplegia flac- 


phragm, arms, trunk 




muscles (favoring 


cid throughout (ant. 


and legs paralyzed. 




mucous stagnation in 


horns involved). 


Typically but rarely, 




lungs) . Arms normal. 




atrophic flaccid par- 




Paraplegia, first flac- 




alysis of arms (ant. 




cid then spastic (lat- 




horns involved), with 




eral columns in- 




flaccid, later spastic 




volved) . 




paralysis of legs (lat. 
columns involved). 


Atrophy. 


In trunk; difficult to 


None in arms or trunk. 


Atrophy of neck mus- 




elicit. In legs; only 


Atrophy in legs (ant. 


cles if high lesion 




from inaction. 


horns involved) . 


(rare) . Usually of 
arms only (ant. horns 
involved at level of 
lesion). In legs only 
from inaction. 


Reaction of de- 


Present in trunk mus- 


Present in legs or in 


Present in arms (rarely 


generation. 


cles; absent in legs 


mild cases quantita- 


in neck). 




(or only quantitative 


tive reduction. 






reduction) . 






Sensation. 


Girdle pain and hyper- 


Pain in loins or legs; 


Pain and hyperesthesia 




esthesia, between en- 


hyperesthesia in 


in arm nerves (with 




siform and navel. 


loins. Anesthesia of 


highest localization) ; 




Anesthesia corre- 


of legs. 


anesthesia in arms 




sponding with motor 




(lower localization) ; 




paralysis. 




and the trunk and 
legs. 


Reflexes. 


Superficial reflexes, ini- 


Lost. 


Superficial reflexes; ini- 




tial loss, rapid return 




tial loss, rapid return 




and increase. 




and increase. 




Deep reflexes, initial 


Lost. 


Deep reflexes; initial 




loss, slow return and 




loss, slow return and 




increase. 




increase. 


Sphincters. 


Bladder, initial reten- 


Incontinence from be- 


Same as in dorsal mye- 




tion, later intermit- 


ginning (sphincter 


litis. 




tent overflow or in- 


paralysis) . 






continence. Cystitis 








common. 








Bowels; usually spasm 


Incontinence (sphinc- 


Same as in dorsal mye-» 




of sphincter ani; con- 


ter paralysis) dis- 


litis. 




stipation. 


guised, perhaps, by 
constipation. 




Trophic changes, 


Decubitus from ne- 


Decubitus, cystitis, etc., 


As in dorsal lesions. 


etc. 


glect, etc. 


from neglect and 


(Occasionally very 






trophic alteration. 


high temperature.) 


Pupils. 


Klumpke's paralysis 


Absent. 


Paralysis of pupil (low- 




of pupil (if in upper 




est cervical region) . 




dorsal) . 




Optic neuritis in iso- 
lated cases. 


Priapism. 


Often present and 
painful. 


None. Impotence. 


Priapism often present. 


Mode of death. 


Cystitis, decubitus. 


Decubitus, cystitis. 


Medulla symptoms; in- 
volvement of phrenic 
nerve with early death. 



840 DISEASES OF THE SPINAL CORD 

degeneration. The immediate outlook is uncertain and depends (a) 
on the etiology, the prognosis being best in acute infections; (b) on the 
intensity of inflammation; (c) on its transverse or vertical dimensions, 
and (d) on the rapidity or tardiness of improvement. Complete recovery 
in circumscribed forms is possible, since indirect symptoms, due to 
collateral edema, may disappear. Death results from extension to the 
medulla, phrenic nerve phenomena, and sepsis following cystitis, pyelitis 
or pyelonephritis. 

Diagnosis. — The early onset of retention of urine, paraplegia and 
anesthesia, is especially significant after acute infections. The upper 
level of the myelitis corresponds to that of the paralysis or anesthesia. 
The lower level may be determined by the condition of the reflex 
centres. Anterior poliomyelitis (q. v.) does not involve sensation as it 
rarely extends back of the anterior horns. In compression by caries or 
cancer local vertebral and root symptoms usually precede cord symptoms. 
The so-called syphilitic myelitis (myelomalacia) begins acutely without 
pain and is rarely relieved by antisyphilitic remedies. Hemorrhage in 
the cord produces most sudden symptoms and acute spinal pain without 
prodromes. For differentiation from Landry's paralysis, see page 842, 
and from midtiple neuritis, see page 872. Meningeal hemorrhage and 
meningitis produce unmistakable root symptoms. Of abscess of the cord, 
few more than a dozen cases are reported; its symptoms are those of 
myelitis plus meningeal symptoms. Hysterical paraplegia is characterized 
by motiveless variability of the symptoms, little myotatic irritability, 
little extensor spasm (and then both legs move together when one spas- 
modically extended leg is lifted) ; rarely by incontinence of urine or feces, 
no trophic changes, no cystitis, no reaction of degeneration and no 
decubitus. 

In the chronic stage the diagnosis is usually provisional and pachy- 
meningitis, tumor and multiple sclerosis should be considered. 

Treatment. — In the acute stage the indications are (a) absolute rest 
in bed for at least two weeks, keeping the. patient on one side or on 
the face. Blisters should be avoided lest they develop decubitus, (b) 
Gowers recommended spt. etheris nitrosi with digitalis to equalize the 
circulation and promote diuresis, (c) Mercury and iodides are usually 
without effect in syphilitic myelitis (softening), although their use 
is rational, (d) Care of the skin. Though bed-sores may be trophic, 
care greatly reduces their frequency and extension. Pressure and heat 
should be avoided by change of posture, rubber cushions, soft, thick pads 
of cotton or the water bed. As in typhoid, the use of two beds is very 
beneficial and the sheets should be stretched smooth. Alcohol rubs are 
antiseptic and harden the skin. Moisture and filth are most dangerous; 
the bowels should be irrigated if they move involuntarily; incontinence 
of urine is more dangerous, especially in women; hard urinals, if left 
between the legs, may cause equal damage ; the urine should be gathered 
in bags of oiled silk filled with cotton; in women mild antiseptic gauze 
and impalpable boric acid should be disposed about the genitalia, (e) 
Cystitis develops in most cases in which the catheter is used; residual 
urine is easily infected, infection ascending the dribbling, patent urethra; 



CHRONIC MYELITIS 841 

the urethra should be irrigated before the absolutely clean catheter is 
introduced; lavage with Thiersch's solution in cystitis with retention 
or incontinence and grs. v-x, each of urotropin and salol, t. i. d., are 
indicated. 

In the subacute stage, tonics, massage after four weeks, mild faradism 
of the bladder and rectum are indicated. Contractures are modified 
by warm baths and massage. Hot baths are dangerous. 

II. Acute Multiple Disseminated Myelitis. — This relatively infrequent 
affection is subacute in onset; foci develop irregularly, together or succes- 
sively in different parts of the cord or perhaps of the brain (disseminated 
encephalomyelitis) , with acute ataxia, scanning speech, dysarthria, tremor, 
nystagmus, optic neuritis, spasticity or weakness of the limbs. Sensation 
and the sphincters are usually not affected. The clinical picture is 
necessarily irregular, because the inflammation may occur anywhere; 
von Leyden distinguishes the atactic and the paraplegic forms. Myelitis 
which spreads after the first two or three days is of the disseminated 
type; once thought very fatal, numbers of recoveries have been reported. 
Treatment is as in the acute transverse variety. 

III. Chronic Myelitis. — This may be the stationary stage of acute 
myelitis or in very rare cases myelitis may be chronic from the beginning, 
i. e., a gradual onset and slow progression. Many deny the existence of 
this form and classify it under the paraplegic stage, multiple sclerosis or 
chronic system disease. 

IV. Subacute and Chronic Poliomyelitis. —Etiology. — Metallic poisons 
and syphilis are important factors. Pathologically, two main types are 
distinguished ; in the larger group there is no inflammation but a primary 
atrophy of the ganglionic cells, which heightens its resemblance to spinal 
progressive muscular atrophy; in a smaller group of cases there is early 
perivascular exudation in the anterior horn and later sclerosis, wherein 
it resembles acute poliomyelitis. The anterior roots are involved and in 
most cases there is degeneration in both pyramidal tracts, possibly also 
in the posterior columns or roots, in Clarke's columns or rarely in the 
medulla. The course is gradual; one extremity becomes slowly affected 
(in one to three years), sometimes with extension to others after months 
or years. There are paresis with atrophy, fibrillary tremors, partial or 
complete reaction of degeneration, decrease or absence of the reflexes 
and normal sensation. The ultimate outcome is unfavorable; if recovery 
occurs, neuritis, not poliomyelitis, is the actual lesion. Differentiation: 
(a) Multiple neuritis (see page 872) ; (b) from progressive spinal muscular 
atrophy, even an anatomical differentiation is not easily made. As a 
rule, in progressive muscular atrophy, atrophy precedes and exceeds 
the muscular weakness, fiber after fiber of muscle very slowly wastes, 
the atrophy is especially marked in the distal parts, and the reaction 
of degeneration is less complete. In chronic poliomyelitis, an outright 
atrophy (atrophie en masse) rapidly follows paralysis; it occurs more often 
in the proximal parts, as in the shoulder, and the reaction of degeneration 
is marked, (c) In amyotrophic lateral sclerosis the paralysis is spastic 
with increased reflexes, contractures and often with bulbar symptoms. 
Treatment is that of the chronic stage of acute poliomyelitis. 



842 DISEASES OF THE SPINAL CORD 

V. Landry's Paralysis. — Acute ascending paralysis was described by 
Landry and Kussmaul in 1859. Cuvier died of this disease in 1832. 
Acute ascending paralysis is a symptom-complex rather than a disease 
and may be conveniently classified under inflammatory affections of the 
cord. The etiology is vague. The affection occurs mostly between twenty 
and forty years of age and three times more frequently in males. It 
has followed acute infections, as diphtheria, typhoid or influenza and 
also chronic infections. 

Pathology. — In many cases no anatomical findings existed, upon which 
Westphal (1876) founded his three criteria : (i) that the disease is a progres- 
sive, ascending fatal affection, (ii) with normal electrical reaction and (iii) 
negative findings at autopsy. Recent cases have given definite though 
varying postmortem results, as structureless exudation in the cord, dis- 
seminated foci of inflammation in the cord, medulla and pons, changes in 
the pyramidal tracts, anterior horns and in the spinal or cerebral peripheral 
nerves. Two forms are distinguished : (a) the bulbar or medullary form, 
in which sensation and electrical reactions are normal, and (6) the 
peripheral neuritic form, with sensory and electrical alterations. The 
parenchymatous swelling of the liver, spleen, kidneys and lymphatics 
indicates a general infection or toxemia. Bacteriologically, an anthrax- 
like bacillus, the pneumococcus, typhoid bacillus, bacilli in all the 
peripheral nerves and streptococci have been found. 

Symptoms. — The onset is acute with paralysis in one foot, then in the 
other, and in the legs, thighs, abdomen, back, arms, even in the face or 
the eyes, possibly with optic neuritis; the paralysis is progressive and 
ascending; when the medulla is invaded, dysarthria, dysphagia and 
paralysis of the tongue occur, finally with death from respiratory par- 
alysis. The proximal parts of the limbs are more involved than the distal 
and some muscles may escape. Fever is usually absent; the sensorium, 
sensation, sphincters and electrical reaction are usually normal. There 
are no tremors, no twitchings, no convulsions, no contractures, no trophic 
disturbance. The reflexes are usually decreased or absent. In rare 
cases there may be partial reaction of degeneration (which usually has 
no time to develop), atrophy and moderate disturbance of sensation or 
the sphincters. The paralysis may be of the descending type, in which 
event the bulbar development is fatal before the paralysis in the legs is 
well developed. 

Course and Prognosis. — The disease lasts two days to two weeks. 
Bulbar symptoms are ominous, but not necessarily fatal. The central form 
of paralysis is fatal and the peripheral form includes most of the recov- 
eries. In rare cases, death may occur in a few hours or only after months. 
In still rarer cases of recovery, some chronic paralysis may remain. If 
recovery ensue, the paralysis regresses in an order inverse to that of 
development. A diagnosis is easily made, because of the ascending motor 
paralysis with loss of reflexes and without marked mental, sensory, 
sphincter or electrical alteration. 

Treatment. — The treatment is that of myelitis or multiple neuritis. 
Strychnine and other stimulation are indicated if the bulbar symptoms 
are manifested. C. L. Greene reports a case which was kept alive by 
artificial respiration forty-one days after respiratory failure set in. 



MULTIPLE SCLEROSIS 843 



MULTIPLE SCLEROSIS. 

Insular or disseminated sclerosis, sclerose en plaques disseminees, was 
described pathologically by Cruveilhier and Carswell (1838) ; Frerichs, in 
1849, made the first diagnosis, and Charcot (and Vulpian) in 1863-64, 
gave a description of the typical case. 

Etiology. — In fully 50 per cent, of the cases no cause is found. It 
occurs equally in either sex and 90 per cent, occur under the fortieth 
year; pseudosclerosis occurs after the fortieth year and is considered 
arteriosclerotic. Three main factors are thought to exist: (a) Acute 
infections, as typhoid, pneumonia, measles, smallpox, etc. (b) Chronic 
intoxications with alcohol, lead, etc. (c) The developmental theory 
(Strumpell) . 

Pathology. — Macroscopically, the sclerotic foci are seen as irregular 
grayish-red areas as large as a pea or walnut; they are multiple (numbering 
even over 100), distributed at random and largely in the white substance 
but also in the gray matter. Their distribution is cerebrospinal, in rarer 
cases in the cord alone, and most rarely in the brain only; the cortex is 
less frequently involved than the centrum ovale, central ganglia, corpus 
callosum and the undersurface of the pons and crus. The medulla is 
quite often, and the cerebellum rarely, involved. The white matter in 
the cord is more frequently affected than in the brain. On section, 
the focus is sunken and transparent, well demarked, firm, save in the 
freshest foci, and on hardening in Muller's solution, appears light green 
while the normal tissue is a darker green color. Microscopically, the 
medullary sheaths in the white substance are thinner or absent and though 
the axis-cylinders are somewhat wasted and at times varicose, their 
remarkable persistence, first noticed by Charcot, causes the incomplete 
character of the symptoms and the usual absence of ascending and descend- 
ing degenerations. The ganglion cells suffer some slight atrophy and 
pigmentation. The foci show corpora amylacea, granule-bearing cells, 
increase of the fine-meshed neuroglia fibrils and nuclear proliferation. 
In contrast with the system-degenerations, the primary change is inter- 
stitial with secondary changes in the nervous tissue. The cerebral 
nerves suffer often, especially the optic nerve, in which proliferation of 
connective tissue is followed by loss of the medullary sheaths, while the 
axis-cylinders are unaffected. The nuclei, roots and nerve trunks of 
the other cranial nerves may suffer similar alteration. The spinal roots 
are not infrequently involved. 

Symptoms. — The clinical picture is so variable that a definite descrip- 
tion cannot be made to cover all cases. Charcot's description included 
the intention tremor, the nystagmus, scanning speech, motor weakness 
and rigidity and apoplectic insults. 

1. Motor Symptoms. — These are the most important, (a) Muscular 
weakness is very common. Paresis is more frequent than paralysis, 
since some axis-cylinders remain intact. The movements are slow 
and fatigue rapidly follows their repetition, more so in isolated than 
synergistic movements. The paresis is most apparent in the legs, usual 



844 DISEASES OF THE SPINAL CORD 

in the arms and frequent in the eyes, head and speech. It sometimes 
does not develop until late, and is associated with increased reflexes 
and spasticity. The gait is spastic, scuffling and the feet stick to the 
ground; to this is sometimes added a cerebellar, atactic or paretic ele- 
ment. Muscular atrophy is rare. The electrical reactions are practically 
normal, (b) Muscular rigidity, the most frequent finding, is referred to 
disease of the lateral columns and is most developed in the legs. It 
increases with successive movements, each step becoming more stiff in 
walking. The spasticity may be so extreme and the muscles so hard that 
the limb cannot be moved. Contractures develop, which usually affect 
the adductors and extensors first and the flexors later and draw the heels 
up to the buttocks. Contractures often affect the muscles of the neck, 
(c) Tremor is one of the most striking phases of the disease, being present 
in 75 per cent, of cases. It is caused, as is the paresis, by the loss of 
the medullary sheaths which allows diffusion of nerve impulses, by foci 
in the pons or thalamus or by lack of coordination between antagonistic 
muscles. There is no tremor during rest, but it appears when voluntary 
efforts are attempted (intention tremor). The hand carrying a glass of 
water to the mouth shakes so much that all the water may be spilled by 
the rhythmic tremor, which possesses a wide range, and occurs five or 
six times to the second. It is apparent in the head when the patient 
sits, because the muscles of the neck are in constant action to support the 
head; it disappears in the recumbent posture. Tremor occurs in the 
face, larynx, trunk or legs on changing posture, as rising; in the fingers 
it produces handwriting which becomes more erratic with each word 
written; and in the thoracic muscles it causes a species of cog-wheel 
respiration, (d) Nystagmus occurs in 50 per cent, of cases. These short, 
jerking lateral movements of the eyes are most common on lateral or 
vertical movements. It is considered a tremor or an incoordination. 
(e) The speech is scanning (54 per cent.), syllabic or staccato; it is slow, 
monotonous, unmodulated and sometimes explosive, especially for the 
letters c, p, g and d. The speech muscles fatigue easily and the end 
of a sentence is often elided; the sounds are often nasal, interrupted by 
yawning inspiration or expiration. The cause of the peculiar speech 
may be tremor or ataxia from foci in the pons or medulla. (/) Paresis 
of the eye muscles (in 17 per cent.) affects the third or sixth nerve, con- 
vergence or associated movements. About 50 per cent, are nuclear. 
Transient diplopia, unequal pupils, hippus and strabismus are less 
common, (g) Apoplectiform seizures (in 1 per cent.) are marked by 
partial coma, increased pulse, high fever, aphasia and hemiplegia, which 
is usually fugitive and flaccid. In most cases negative pathological 
findings exist, but Leube and Leyden refer them to acute encephalo- 
myelitis. Though usually hemiplegic, they may exceptionally produce 
paraplegia, hemianesthesia or ataxia, or monoplegia. 

2. Sensory Symptoms. — Marked aberrations are less frequent (30 per 
cent.) because the sensory fibers are more resistant to disease. Sub- 
jectively, dull pains, formication and paroxysmal headache are frequent; 
lightning pains, crises, girdle sensation, trigeminal neuralgia, palpitation 
and dyspnea are very uncommon. Objectively, any species of sensation 



MULTIPLE SCLEROSIS 845 

may be involved. Ataxia referable to disease of the posterior columns 
or higher sensory tracts is marked in 50 per cent, and may produce a 
typical tumbling cerebellar gait. 

3. Special Senses. — The optic nerve is affected in 45 per cent., 
usually as a pallid partial atrophy involving its temporal side, and less 
often as neuritis or atrophy with total blindness. The change is more 
conspicuous pathologically than clinically. It may be the first sign 
of "the disease. In 60 per cent, of cases there is central scotoma, and at 
times narrowing of the field of vision. 

4. Psychical Symptoms. — Mental impairment is common;, the patient 
is complacent and the memory is weak. Compulsory laughing and 
weeping, partly without motive and partly emotional, probably should 
be referred to lesions in the medulla, pons or crus. 

5. Bulbar Symptoms. — These may, in rare cases, resemble the symp- 
toms of bulbar palsy, as dysphagia, anarthria and tongue atrophy. 

6. Reflexes. — The patellars are exaggerated, there are ankle-clonus 
and Babinski's sign, showing disease of the pyramidal tracts. The 
abdominal reflexes are absent in 70 per cent, of cases. 

7. Sphincters. — Lasting or severe symptoms in the bladder or 
rectum are uncommon; the bladder is often hypertonic and irritation 
is frequent. 

8. Trophic Symptoms. — These are rare; they consist of skin eruptions, 
edema, sweating, chronic arthritis and erythromelalgia. 

Course and Prognosis. — The onset is usually gradual; in most cases 
weakness in the legs appears first and for a long time is hard to interpret ; 
it occurs without pronounced sensory symptoms, bladder disorder or 
atrophy. Sometimes the onset is acute, with loss of consciousness, trans- 
ient hemiplegia, vertigo, headache, eye symptoms, vomiting and optic 
neuritis. Leg paralysis is followed by scanning speech, nystagmus and 
tremor. The symptoms remit and recur. Bramwell found that death 
occurred in less than five years in 29 per cent., in less than ten years in 
66 per cent., and in less than fifteen years in 89 per cent. The terminal 
stage presents dementia, decubitus, sphincter paralysis, cystitis and 
septicopyemia. 

Diagnosis. — The typical case is unmistakable, because of the cardinal 
symptoms: intention tremor; spastic paresis; nystagmus; scanning 
speech; ataxia; increased reflexes; optic atrophy; the slow, uneven 
course with remissions and recurrences; the variability of the symp- 
toms; apoplectic insults; and moderate involvement of the mentality, 
sensation, bladder and rectum. 

Differentiation. — Transient hemiplegia may suggest hemorrhage, 
syphilitic thrombosis, embolism, paretic dementia or tumor (q. v.). 
In paralysis agitans the fine tremor of the hands and fingers (not of the 
large joints, and much less of the head) which is not increased by move- 
ment, its persistence during rest, the mask-like facies, festinating speech, 
peculiar attitude, gait, propulsion, retropulsion, muscular rigidity with- 
out increased reflexes and the advanced age are clear and characteristic 
points. 



846 DISEASES OF THE SPINAL CORL 

Multiple Sclerosis. vs. Syphilis. 

Occurs in the medullary substance. Meningomyelitis and root symptoms. 

A focal disease. Diffuse. 

Nystagmus, scanning speech, tremor. More frequent insults, hemiplegia, etc. ; 

speech may be slow in pons lesions but is 

not scanning. 
Partial optic atrophy occurs. Amaurosis, choked disk or neuritis frequent. 

Mydriasis 1 per cent., myosis 4 per cent. Mydriasis is very common. 
Argyll- Robertson pupil very rare. Argyll- Robertson pupil frequent. 

Hysteria more than any other disease simulates early multiple sclerosis ; 
the two affections often occur together and in both the symptoms are 
changeable. In hysteria sensory symptoms are much more prominent, 
there are often limitation of the visual fields, monocular diplopia, con- 
tractures and convulsions, but there is no optic atrophy, nystagmus, 
scanning speech, or intention tremor. The movements in hysteria are 
often accompanied by contraction of the antagonist muscles, a most 
valuable diagnostic aid. In extremely rare cases, described first by 
Westphal as pseudosclerosis, the autopsy shows nothing; the tremor 
affects the arms chiefly; there is no ataxia or nystagmus; the fades is 
somewhat rigid and outbursts of anger are frequent; syphilis is a possible 
cause. Birth palsies accompanied by jerky movements, incoordination 
and even scanning speech are excluded by the history. 

Treatment. — Drugs, hydro- and electrotherapeutic measures are futile. 
The patient should live in a warm climate during the winter months. 

SYRINGOMYELIA. 

The term refers to cavities in the cord, and was first employed by 
Ollivier (1824). The affection was first described by Morgagni. 
Syringomyelia must be distinguished from hydromyelus, which is a 
dilatation of the central canal due to developmental anomalies; it is 
usually an accidental finding at necropsy, or if symptoms are present 
they are those of syringomyelia. 

Etiology. — Sixty-three per cent, of cases occur between the tenth and 
thirtieth years and 70 per cent, in males. 

Pathology. — 1. Gross Pathology. — The cord is often lax, sometimes 
fluctuating or flat. The cavity is usually localized but may extend from 
the medulla to the filum terminale; it is most often found in the lower 
cervical or upper dorsal region; in size it ranges from a narrow slit to a 
cavity as wide as the cord itself; it may communicate with the central 
canal, may be multilocular and diverticula may be found. Its wall 
is smooth, sometimes pigmented from rupture of the new-formed blood- 
vessels. The cord usually suffers sclerosis in the form of tumor-like, 
asymmetrical neurogliar proliferations, which later break down and form 
secondary cavities. The posterior horns and columns are often affected, 
the anterior horns and columns less frequently and the lateral columns 
very rarely. 

2. Minute Pathology. — The essential finding is the neurogliar hyper- 
plasia, probably due to some congenital anomaly, which also explains 
its frequent association with hydromyelus; the overgrowth is rich in 



SYRINGOMYELIA 847 

fibers, whereas the ordinary glioma (gliomatosis) especially abounds 
in cells; syringomyelia and gliomatosis may coexist. This proliferation 
contains large, sharply nucleated cells, and a few epithelial cells, is firm as 
a whole, but somewhat softer toward the posterior horns, is often hyaline 
nearest the cavity from compression and abounds in bloodvessels. The 
cavity is usually lined with cylindrical epithelium like that of the central 
canal; its contents resemble cerebrospinal fluid, but is occasionally 
blood tinged or less often gelatinous, mucoid or milky. The nerve fibers 
are not much involved. Secondary degeneration may occur in the 
posterior and less frequently in the lateral columns. 
Symptoms. — There are three cardinal symptoms. 

1. Anesthesia. — Partial or dissociated anesthesia occurs in the typical 
case, in which the sensation of touch, pressure and locality is preserved 
while heat, cold and pain are not recognized. Thermo-anesthesia usually 
concerns perception of both heat and cold, sometimes of only one of them, 
or one in one place and the other in another; analgesia is frequently 
preceded by hyperalgesia; it usually corresponds with the thermo- 
anesthesia. Thermo-anesthesia and analgesia begin in the hands and 
fingers and are later found on the upper trunk; sometimes the entire 
trunk, legs, mucous membranes and face may be affected, depending 
on the location of the cavity. The patient may suffer burns or injuries 
in these parts without pain. Dissociated anesthesia is most probably 
caused by disturbed conduction in the gray substance due to neurogliar 
proliferation and cavity formation. Anesthesia may involve all varieties 
of sensation. Subjective sensory disturbances include paresthesia and 
burning, tabes-like pain in the neck, arms or trunk and sometimes in the 
joints, spine or legs. 

2. Muscular Atrophy. — Muscular atrophy is due to involvement 
of the anterior horn and affects the arms mostly, because the disease 
is largely in the lower cervical and upper dorsal cord. It is slow in 
onset, more marked than the attendant flaccid paresis, degenerative 
and often observed • with fibrillary muscular contractions and increased 
myotatic irritability. It usually involves the small muscles of the hand, 
as the interossei, produces flattening of the thenar and hypothenar 
eminences and the claw-like hand, as seen in the Duchenne-Aran type. 
The radial supply is first affected, then the ulnar and median. Some- 
times the scapulohumeral type is observed, especially with bulbar symp- 
toms. The muscles of the trunk, and much less often of the legs, may be 
affected. From cervical compression of the pyramidal tracts, paraplegia 
results, with increased reflexes and spasticity, in 12 per cent, of cases. 
Other motor symptoms occasionally occur, as tremor, contractures, 
spasms, opisthotonos or choreiform movements. The gait is normal, 
spastic or paretic. 

3. Trophic Symptoms; — (a) Phlegmons said felons develop, particularly 
on the fingers. They are painless, chronic, often recurrent and lead to 
necrosis of the bone, ankylosis, deformity or mutilation, (b) The joints 
suffer in over 10 per cent., especially in males (75 per cent.), probably 
due to loss of articular sensation (whereby the joints are used inappro- 
priately) or to lack of the nutritional reflex. These arthropathies are of 



848 DISEASES OF THE SPINAL CORD 

the hypertrophic form, with thickening and bony formation, like arthritis 
deformans, or of the atrophic form with relaxation of ligaments or flail 
joint. There is little exudation, no fever, no pain. They are similar to 
the tabetic joints but are more chronic and more often involve the upper 
extremities (shoulder 32 per cent., elbow 28, hand 16, hip 8, ankle 8, 
knee 6 per cent.), (c) Painless bone necroses and spontaneous fractures 
may occur late in the disease. Moderate scoliosis, usually confined to 
the dorsal spine, sometimes with kyphosis, is due to trophic vertebral 
changes or atrophy of the back muscles; perforating ulcer, thick, friable 
nails and clubbed fingers are less common. Morvan (1883) described 
a paresie analgesique avec panaris, endemic in Brittany, which is clearly 
syringomyelia. "Morvan's disease" is marked by trophic disorders, 
excessive or deficient secretion of sweat, edema on the dorsum of the 
hands, erythema, urticaria, local asphyxia and herpes zoster. 

4. Other Symptoms. — (a). The skin reflexes are usually normal; the 
abdominal, cremasteric and plantar reflexes are sometimes increased; 
the tendon jerks are often decreased in the upper and increased in the 
lower extremities, (b) The sphincters are involved late in the disease. 
Retention of urine and constipation are more frequent than incontinence, 
(c) Bulbar or pontine symptoms are not infrequent, are usually unilateral 
and appear in the later stages. They include facial hemiatrophy or 
paresis, paresis of the tongue with atrophy, dysphagia, paresis of the 
palate (nasal speech), paralysis of the vocal cords, spinal accessory nerve 
(trapezius paralysis) and trigeminus (sensory symptoms), eye paralyses 
(abducens), unequal pupils, nystagmus, tinnitus, salivation, apoplecti- 
form attacks, polyuria, glycosuria and vagus symptoms (disturbed pulse 
or respiration, vomiting, and singultus). 

Diagnosis. — A positive diagnosis can be made from the three cardinal 
symptoms: (1) the dissociated anesthesia (thermo-anesthesia and anal- 
gesia with practically normal tactile sensation) is the earliest and most 
constant sign. Grasset collected cases of twenty or more nervous dis- 
eases (functional, traumatic, neoplastic, specific) in. which this sensory 
dissociation has been found; but it remains highly distinctive in con- 
junction with (2) muscular atrophy of the upper extremities with paresis 
and (3) trophic disorders, e. g., felons, arthropathies and scoliosis; to which 
may be added the spastic paresis of the legs and bladder symptoms. 

Differentiation. — Progressive spinal muscular atrophy and amyotrophic 
lateral sclerosis present no anesthesia, no trophic disturbance and bulbar 
symptoms are bilateral. Juvenile muscular dystrophy may be simulated 
in the scapulohumeral type of syringomyelia. In peripheral neuritis all 
varieties of sensation are disturbed; the paralysis is peripheral, not 
spinal or segmental, and there is the reaction of degeneration; neuritis 
of the upper brachial plexus produces paralysis of the shoulder, arm and 
supinator longus, a combination not found in syringomyelia. Focal 
disease of the anterior and posterior gray substance, as multiple sclerosis, 
hemorrhage or myelitis may simulate syringomyelia, but their course 
is less chronic and there is less trophic disorder. The root irritation 
of tumor of the cord is lacking. Located in the dorsolumbar region, 
syringomyelia may closely simulate tabes, from the lancinating pains, 



SYSTEM DISEASES 849 

crises and ataxia, but the Argyll-Robertson pupil is lacking and the 
sensory impairment is typical. In leprosy, anesthesia is peripheral, not 
spinal, in type; the Henssen bacillus is often found. 

Course and Prognosis. — The course is progressive for years or decades. 
When recognized, the affection is hopelessly advanced. Death occurs 
from cystitis, septicemia and bulbar complications. 

Treatment. — Treatment is unavailing. The danger of self-injury, as a 
result of the peculiar anesthesia, should be borne in mind. 



SYSTEM DISEASES. 

This small group of very important diseases involves structures or 
systems having a common function, thus differing from haphazard disease, 
as myelitis or multiple sclerosis. A primary slow degeneration of the 
nerve elements is followed by secondary proliferation of connective tissue. 
In the obscure pathogenesis of these degenerations hereditary weakness 
causing nutritional failure at a certain age (familial form) and the 
selective action of toxemia on certain nervous structures have been 
thought causative. 

I. System Disease of the Sensory Tract. 

The sensory type is locomotor ataxia in which the peripheral sensory 
neurone is affected, in the posterior roots and columns, while the motor 
types are spastic paraplegia, involving the upper motor neurone (pyram- 
idal tracts) and muscular atrophy due to lesions in the lower neurone 
(anterior horns and roots). 

Tabes Dorsalis, Locomotor Ataxia. — Definition.— A disease character- 
ized (a) etiologically by syphilis; (6) pathologically by lesions in the 
posterior spinal roots, posterior columns and nerves; and (c) clinically 
by ataxia, Argyll-Robertson pupil, pains, defective sensation, loss of the 
tendon reflexes and trophic disturbances. 

It is the best known and most frequent chronic disease of the cord. 
Todd, in 1847, gave the first accurate account, eliminated paralysis, 
and found the posterior columns diseased at autopsy. Stanley first 
(1840) referred the affection to the posterior columns and peripheral 
sensory nerves. Tiirck first examined the tissues microscopically and 
Romberg (1851), and Duchenne (1858), popularized the disease; it 
is still known in France as Duchenne's disease. 

Etiology. — Syphilis is the sole cause. The following etiological data 
are those of syphilis; age: 50 per cent, in the thirtieth to fortieth year; 
25 per cent, in the fortieth to fiftieth year; less than 25 per cent, in 
the twentieth to thirtieth year (Gowers); of 47 juvenile cases collected 
by Hirtz, the parents in 13 instances had syphilis, tabes or dementia. 
Sex: as in syphilis and paretic dementia, 10 cases occur in males to 1 
in females. Like syphilis, tabes is sometimes familial. It prevails largely 
in cities and among the higher classes (" syphilization and civilization"). 
It is uncommon in the negro. 
54 



850 DISEASES OF THE SPINAL CORD 

Pathology. — The gross changes are visible to the unaided eye; the 
posterior columns are smaller, outwardly flattened, gray from loss of the 
medullary sheaths and translucent from secondary increase of connective 
tissue. The pia may be secondarily opaque and thickened. The degener- 
ated areas are sunken on section. The posterior horns and roots are 
atrophied and grayish-red. As to minute changes, there is a very slow 
degeneration of the peripheral sensory neurone, its fibers and processes of 
the spinal ganglia cells. These processes run in two directions: to the 
periphery and to the posterior roots, (a) The peripheral spinal sensory 
nerves are often degenerated, less in large trunks (sciatic or crural nerves) 
than in the peripheral filaments of the skin, joints and muscles which 
are important in the sensory, trophic and atactic symptoms of tabes; 
their white substance wastes and then their axis-cylinders. The trophic 
centres for these fibers are largely in the root ganglion, (b) The fibers 
running from the ganglia to the posterior roots are more early, regularly 
and obviously changed. The posterior root fibers run (i) to the posterior 
columns, whence there occurs, low down in the cord, degeneration in 
Burdach's and then higher up in Goll's columns, into which the root 
fibers are pushed as higher root fibers enter the cord. The location of 
the degenerated fibers therefore differs at successive levels (ascending 
degeneration). In the lumbar cord the posterior columns are most inten- 
sively and extensively diseased, especially in their middle and posterior 
parts, nearest the posterior roots and surface of the cord. Early and 
marked degeneration is found in Lissauer's zone just back of the posterior 
horn. The anterior part of the post. ext. column and the central part of 
the post. int. column are slightly, if at all, diseased as they are not derived 
from the post, ganglia. In the dorsal cord the post, columns are degener- 
ated save in the post. ext. part and in the ant. part. In the cervical cord 
the post. int. columns are diseased (representing the root fibers of the 
lumbodorsal cord) and also some areas in the post. ext. column where 
degenerated root fibers have just entered, (ii) From the post, roots a 
series of fibers to Clarke's column is degenerated but the cells of Clarke's 
column and their ascending fibers to the cerebellum usually remain intact. 
(iii) The post, horns degenerate, because they contain fine root fibers. 
(iv) The reflex collaterals to the ant. horns also degenerate. 

Degenerative changes may involve analogous neurones, as the auditory, 
optic, visceral, sympathetic or ocular nerves, or the peripheral motor 
nerves, pyramidal tracts, muscles, medulla and brain. 

The exact pathogenesis is disputed: (i) Obersteiner conceives the 
initial changes are in the pia through which the dorsal nerve roots pass; 
(ii) Marie contends there is a lymphangitis of the post, columns; (iii) 
Edinger believes that toxins attack those nervous structures most in use 
and therefore most easily fatigued (the sensory tracts of the lumbar cord, 
pupil, bladder and intestine). 

Symptoms. — Symptoms vary chiefly as to their intensity, duration 
and succession. Three stages are described: (1) The initial, neuralgic 
or pre-atactic stage, lasting sometimes for years (usually 6 to 8, or even 
10 to 20). The earliest symptoms are pains which are lancinating or 
"rheumatic," perhaps neuralgic or like migraine or paresthesia. The 



TABES 851 

knee-jerk is lost, usually very early and the pupil reacts to accommodation 
but not to light. Much less often optic atrophy, sexual, sphincter, ocular, 
articular or visceral symptoms first attract attention. (2) The atactic 
stage may last many years; muscular movements become incoordinate, 
especially in the legs, sometimes, though later, in the arms. The tabetic 
gait develops, the patient sways when his eyes are closed, sensation is 
obtunded, especially the muscular sense, urinary and sexual disorders 
develop and in some cases diplopia. The gross muscular power is un- 
impaired. Trophic, joint, bone and skin lesions and visceral crises occur. 
(3) In the terminal stage the patient is bed-ridden, helpless from extreme 
ataxia, and bed-sores, lesions in the medulla and cystitis determine the 
fatal issue. 

Special Symptoms in Detail. — 1. Motor Symptoms. — (a) Ataxia 
(incoordination) is of such importance that the disease is named locomotor 
ataxia. It is present in 80 per cent, of cases, but may develop slowly 
or perhaps not at all; it occurred in barely 10 per cent, of Babinski's 
cases, who explains this low figure by his use of mercury. Ataxia is a 
disturbance of harmonic efficient muscular contraction and is probably a 
disease of the afferent muscular fibers (muscular anesthesia, Reynolds 
1855), intensified by sensory impairment, disturbance in the reflex 
collaterals and sometimes by optic atrophy. Duchenne first made the 
valuable distinction between ataxia and loss of muscular power which is 
preserved until late in the disease. Ataxia is frequently first observed 
by the patient when he walks in the dark or closes his eyes, as in washing 
the face. When he looks upward or brings the heels and toes together 
he sways {Romberg's sign) and perhaps falls, because vision is a sensory 
factor in equilibration. Later, incoordination occurs with the eyes 
open, and the patient can walk only with a cane. It is often increased 
by removing the shoes, which support the feet. The ataxia is marked 
when the patient attempts to "about face," to walk backward, stand on 
tiptoe or stand with the knees half-flexed. Ataxia is elicited also when the 
patient, with the eyes closed, attempts to place his heel on the opposite 
knee or perform with one limb those movements made by the physician 
in another limb. The gait is atactic, the feet are lifted too high, thrown 
too far forward and outward {wide-legged gait) and brought down sud- 
denly and forcibly — " stamping" or " rooster gait." A tumbling cerebellar 
gait is less frequent, observed later in the disease and referable to in- 
volvement of the trunk or hips. Movement in tabetics is characterized 
by excessive excursion, rapidity, irregularity and uncertainty of execution. 
The patient cannot execute finer movements, such as writing or buttoning 
the clothes. Ataxia is rare in the head, eyes, face, jaw and tongue. 
In women marked ataxia is less frequent than simple awkwardness. 
(b) Muscular power may be normal even with extreme ataxia. The 
muscles are hypotonic, which allows hyperextension and hyperflexion of 
the joints; it is due to loss of centripetal sensory conduction. There is 
a feeling of weakness in the legs in two-thirds of the cases. Transient 
muscular weakness is frequent (75 per cent.), as in the eye muscles. 
Paralysis, though usually transient, may be permanent from disease of 
the pyramidal tracts, ant. horns or peripheral nerves, (c) Atrophy is not 



852 DISEASES OF THE SPINAL CORD 

common, but may affect the arm (type of Duchenne-Aran), the leg 
(the tabetic club-foot, usually due to neuritis), or most rarely the face 
(hemiatrophy), (d) The electrical reactions are usually normal. Some- 
times muscular contractures, due to abnormal sensation, associated 
movements, in which one leg moves when its fellow moves, and spon- 
taneous movements, taking place without volition or consciousness 
of them and due to slight unnoticed reflexes, may occur. 

2. Sensory Symptoms. — In the majority of cases the disease begins 
with irritative sensory phenomena, (a) Spontaneous pains occur in 85 per 
cent., are sudden, paroxysmal, lightning-like, lancinating and often noc- 
turnal. They are usually severe, but may be agonizing, dull, burning or like 
those of muscular rheumatism, increased by dampness and cold. They 
last from a few hours to a day or two. The legs are the most common seat 
of pain, then the back, trunk, arms especially in the ulnar distribution 
and sometimes the head (occipital nerves) and face (trigeminus, whose 
ascending branch represents the sensory parts of most of the other 
cranial nerves); Collet found migraine-like attacks in 40 per. cent.; their 
bilateral occurrence is very suggestive. The pains are more often deep 
than superficial and more often irregular than exactly conforming to a 
nerve's course. The pain in the trunk may assume the "girdle form" 
over a narrow or broad zone (31 per cent.). Sometimes the area affected 
shows local trophic changes, as herpes, ecchymoses or friable hair, (b) 
Paresthesias are common, as creeping sensations, "pins and needles" 
sensations, a sense of heat or cold. They occur in the legs in 66 per cent, 
of cases. If in the arms, the ulnar distribution is especially involved 
(17 per cent.). The ulnars at the elbows are often insensitive to pressure 
(Biernacki's sign), pain, temperature and tactile impressions. In the 
face a perverted feeling may be noted ("Hutchinson's mask"), (c) 
In the early stages hyperesthesia may be noted from nerve irritation. 
In 86 per cent, of developed cases sensation is reduced; it is most often 
of the spinal or segmental type, though sometimes peripheral. Tactile 
sensation is often disturbed, especially in the legs and soles. Hypesthesia 
may be observed on the buttocks, scrotum, perineum, penis (the cause of 
early decreased sexual power) or on the trunk as a zone (80 per cent.), 
especially to light touch. It is not usually found higher than the third 
rib, although there may be occasional occipital or trigeminal anes- 
thesia. If the arms are affected it is mostly in the hands and palms. 
Sometimes a touch to one member is referred to another (allocheiria) 
or a single contact feels like several (polyesthesia). Perception of pain 
is lessened in 50 per cent, of cases, occurring alone or with hypesthesia; 
a short stab with a pin is often felt merely as a touch. Pain con- 
duction is often retarded (60 per cent.); the sharp stick of a pin is 
felt at once as a touch, but the pain is perceived only after 7 to 15, 
even 35 seconds; the patient says " now" when stuck and "ouch" as 
he feels the pain. Analgesia may be the cause of severe injuries, as in 
syringomyelia. Sometimes the testicles are insensitive to pressure, and 
inflammations such as pleurisy may run a painless course. The tempera- 
ture sense is rarely affected alone or completely. The muscle sense is dis- 
turbed; a change of angle of one or two degrees in the joints and tendons 



TABES 853 

is noted by normal individuals, while in tabetics much wider movements 
are not perceived, especially in the small distal joints; the toes may be 
moved unnoticed by the patient, perhaps in the later stages the fingers 
also. 

3. Reflexes. — (a) The skin reflexes may be increased early in the 
disease. Later the plantar and gluteal reflexes are somewhat decreased. 
The abdominal and cremasteric may long remain normal. (6) Of the 
tendon reflexes the knee-jerk is lost early (WestphaFs sign); this most 
constant finding in tabes (98 to 100 per cent.) is due to disease of the 
afferent nerves and reflex paths in the cord. These reflexes should be 
examined with the patient sitting on the edge of a table with his eyes 
closed and excluding cerebral inhibition of the reflexes by having him pull, 
in an outward direction, the locked fingers (Jendrassik's reinforcement). 
The patellar reflexes are rarely present save in exceptional cases of 
cervical tabes. The knee-jerk has been known to return after a cerebral 
hemiplegia. The Achilles reflex is lost equally frequently. 

4. The Eyes and Special Senses.- — (a) The pupils contract to accom- 
modation but not to light in 97 per cent. (Argyll-Robertson, 1869). The 
patient must look to a distance in the dark room and one eye tested at a 
time lest accommodation be confused with contraction to light. The 
Argyll-Robertson pupil may depend upon a degeneration of fibers con- 
necting the optic nerve with the oculomotor muscles (see page 805). 
The tabetic pupil rarely dilates on pinching the skin of the neck. In 
about 50 per cent, it is small (spinal myosis) ; the pupils are often unequal 
in size and irregular in contour, (b) The eye muscles are affected in 50 
per cent. Mobius holds that ocular paralyses are as important as the 
pupillary changes, especially when painless, wherein they differ from 
the rheumatic and syphilitic forms; he holds that the majority of all 
eye paralyses in the adult are tabetic. Diplopia is common and usually 
unilateral. The order of frequency of involvement is the sixth, third 
and fourth nerves. When one muscle is paralyzed the others are usually 
weak. The early form of paralysis is usually transitory; the late form is 
often permanent from nuclear degeneration, (c) Optic atrophy (10 per 
cent.) is generally an early symptom. The disk is pale and shrunken, 
especially on its temporal side and at the edges, which are sharp. The 
process is always bilateral; central scotoma and actual neuritis are 
rare. The process usually progresses to blindness. When optic atrophy 
occurs early, ataxia may not appear, "tabes arrested by blindness." 
When it develops later it has no effect on the ataxia, (d) Deafness may 
develop gradually or suddenly, sometimes with vertigo or Meniere's 
complex. It may be permanent or transient. Auditory defects are present 
in 80 per cent, of cases. Atrophy of the auditory and olfactory nerves 
has been found. 

5. The Sphincters and Genital Sphere. — (a) The bladder is frequently 
affected (60 per cent.), possibly as the first symptom of the disease. 
The bladder is slowly or imperfectly evacuated, because its centripetal 
sensory fibers are diseased. There may be overflow, incontinence and 
in the later stages cystitis frequently results from decomposition of the 
residual urine, followed in turn by pyelitis, nephritis and septicemia. 



854 DISEASES OF THE SPINAL CORD 

(b) The sphincter ani is weak but rarely incontinent, (c) The sexual 
appetite and power are reduced (66 per cent.), often early. Labor is 
sometimes painless. 

6. Trophic Disorders. — Local trophic changes are more common than 
general malnutrition, (a) Trophic alterations in the bones and joints 
were first thoroughly studied by Charcot — Charcot's disease. They 
usually appear late and develop in 2 per cent, of cases. The onset is 
usually gradual, sometimes acute with marked swelling or seemingly 
traumatic. Two forms are observed: first the more frequent atrophic 
form, especially in the hip and shoulder, in which the cartilages are 
eroded, the articular surfaces waste and crepitate, foreign bodies develop 
and the joint becomes so lax that dislocation of the hip or knee (genu 
recurvatum) results; second, the hypertrophic form with bony formation, 
ossification of the ligaments, and rigidity resembling arthritis deformans 
but painless, more acute, extreme and effusive. The £-ray plates are 
characteristic. The adjacent muscles atrophy — the arthropathic mus- 
cular atrophy. The large joints are usually involved, as the knee (45 
per cent.), hip (20 per cent.), shoulder (11 per cent.), elbow (5 per cent.) 
or ankle (4 per cent.), but smaller articulations may be affected, as the 
tarsus, jaw, spine, thumb, etc. The cause is the same as in syringomyelia. 
The tabetic foot is characterized by thickness and roundness of its inner 
border and arch, flattening of the sole, decreased motility, and patho- 
logically by erosion and atrophy of its bones. It must be distinguished 
from the tabetic club-foot due to muscular atrophy of the calf muscles 
with contractures. The bones may break easily but painlessly (Weir 
Mitchell), due to rarefying osteitis, which renders the medullary sub- 
stance more porous, the cortex thinner and the inorganic base less in 
amount. If a callus develops it is often exuberant. The tendons some- 
times rupture, probably from trophic changes. (6) The perforating ulcer 
of the foot (mal perforant du pied) is more frequent. It is "punched 
out" in appearance, painless, secretes but little pus and is due to nerve 
degeneration or centric changes. Similar ulcerations resembling syphilis 
may occur in the nose, ear, buccal mucosa, palate or uvula, (c) In the 
skin, local sweating, ecchymoses, herpes, blebs, alteration of the hair or 
nails, gangrene and ichthyosis may occur. Decubitus is not common 
save in the last stages, and it may not develop even after years in bed. 
There may be dental caries or painless falling out of the sound teeth 
with analgesia of the gums. 

7. Visceral Symptoms. — The most important are the painful crises 
first correctly interpreted by Charcot, (a) Gastric crises occur in 5 per 
cent, of cases. There is severe, sometimes excruciating epigastric pain, 
which often radiates into the back, vomiting of food, then fluid, finally 
bile or even blood; this is often attended by restlessness, epigastric 
retraction, hiccough, fever and a slow, rapid or irregular pulse; hyper- 
acidity is less frequent than hypacidity. The alkaline urine contains 
indican and decreased chlorides. The crisis lasts several hours to days 
and may greatly reduce the general nutrition; it is sometimes the first 
evidence of tabes. The cause is usually considered nervous, but Pal 
thinks it is due to increased arterial tension, (b) Laryngeal crises are next 



TABES 855 

in frequency but are shorter in duration. They are due to spasm of the 
laryngeal muscles, and are often dangerous. In some instances only a 
hoarse cough like pertussis is noted; in others there is collapse or death 
(ictus laryngis). Anatomically, the ascending branch of the fifth nerve 
and the glossopharyngovagus nucleus or its branches are degenerated. 
(c) Other crises are far less common, as intestinal crises, which are char- 
acterized by colic, diarrhea and sometimes rectal tenesmus; the author 
saw obstruction and abdominal retraction lasting twelve days, imme- 
diately relieved by morphine gr. § ; renal crises with scant urine, transient 
albuminuria or even hematuria, and less often nasal, pharyngeal, hepatic, 
cardiac, bronchial, vesical, urethral or vulvovaginal crises occur. 

8. Cerebral Symptoms. — Cerebral symptoms other than the eye changes 
noted above, are not frequent ; they are unilateral atrophy of the tongue ; 
paralysis of the vocal cords; vagus and accessorius symptoms other 
than those already noted, such as rapid pulse, palatal weakness or 
rarely paralysis affecting the trapezius and sternomastoid, which is 
probably neuritic; and very rarely facial or bulbar paralysis. Lachry- 
mation, salivation, polyuria or glycosuria is sometimes noted. 

Complications. — These include true cerebrospinal syphilis; aneurysm, 
aortic regurgitation (5 per cent.) and especially dementia paralytica, a 
closely correlated affection; myelitis; muscular atrophy, particularly the 
symmetrical form due to neuritis; cerebral thrombosis due to arterial 
disease; and apoplectiform seizures which occur as in paretic dementia. 

Course and Prognosis. — Pain is the first symptom in 68 per cent., while 
no other single early symptom is the first in more than 3 per cent. (Sarbo). 
Optic atrophy or insanity may arrest tabes. Leube instances a man 
who worked hard for forty years after the onset of tabes; tabetics may 
live for twenty years in the last stages of the disease. Crises, alcoholism, 
traumatism, acute onset, intercurrent affections unnoticed because of 
their painlessness, and affections of the bladder and kidney with sepsis 
are unfavorable prognostics. In 1960 well-observed cases (out of 4000) 
40 per cent, followed a long course with exacerbations, 30 per cent, were 
steadily progressive, 19 per cent, halted for three years or more, 6 per 
cent, ran a severe, rapid course and 5 per cent, almost recovered (Belugou 
and Faure). Tabes is incurable. 

Diagnosis. — The diagnosis is made by: (a) The Argyll- Robertson pupil, 
which is indicative of tabes, paretic dementia or rare lesions in the 
corp. quadrigemina. (b) The most common and early symptom, loss 
of the patellar reflex (which most rarely fails in health, marasmus, old 
individuals or as an hereditary lesion), (c) Lightning pains, "tabetic 
neuralgia," girdle sensation, gastric and other crises, (d) Sensory changes, 
subjective, objective and vesical, (e) Optic atrophy. (/) Painless ocular 
paralysis, (g) Ataxia, with Romberg's sign and the tabetic gait, is prac- 
tically pathognomonic after exclusion of peripheral neuritis. (/?) The 
Wassermann reaction is present in 70 to 96 per cent, of cases (see pages 
219 and 229) in the blood and spinal fluid, with globulin reactions and 
lymphocytosis. 

In cervical tabes (less than 1 per cent, of cases) the sensory changes, 
pains and ataxia are most manifest in the arms or even in the face. The 



856 DISEASES OF THE SPINAL CORD 

aim reflexes are sometimes abolished and the patellars rarely may be 
normal or increased. The characteristic pupils are present and gastric 
crises appear early and frequently. 

Differentiation. — In the earliest stage confusion with neurasthenia, 
hypochondriasis and nosophobia is possible, from common symptoms, 
as pains, paresthesia, girdle sensation and weakness of the legs, but close 
observation determines the diagnosis; the tabes of Hippocrates was prob- 
ably neurasthenia. One form of multiple neuritis (q. v.), viz., pseudo- 
tabes, may require differentiation. Cerebrospinal syphilis, especially of 
the roots and the membranes, may sometimes cause confusion. 

For differentiation from Friedreich's ataxia, see page 865. In cere- 
bellar tumor, usually the ataxia ceases when the eyes are closed and is not 
characterized by the excessive excursion or rapidity of tabes ; the patellar 
reflexes are increased, there is no anesthesia and signs of tumor are often 
present. In multiple sclerosis there exceptionally may be crises; pains 
and sensory disturbance, but the Argyll-Robertson pupil, ataxia, marked 
sensory and bladder disturbances are most rare. There are increased 
reflexes, nystagmus, scanning speech, intention tremor, central scotoma 
and functional oculomotor involvement. Paraplegias are not difficult 
to differentiate, since true motor disturbance is rare or late in tabes; 
the reflexes are increased and spastic rigidity is marked, even in atactic 
paraplegia. Tabetic pain is often misinterpreted; pain as a rule suggests 
disease of the vertebra? and membranes rather than of the cord itself, 
but in vertebral disease or cord tumor the pain is fixed, and often increased 
on pressure and movement. Tabes may be confused (on hasty or partial 
examinations) with rheumatism, intercostal or trigeminal neuralgia, and 
gastric, renal or other visceral disease. Bilateral sciatica always suggests 
tabes, diabetes or nephritis. Strumpell describes, among workers in 
tobacco, a nicotine tabes, in which pain, pupillary alteration, atactic gait 
and absence of knee-jerks are observed, but also a characteristic tremor 
and increased cutaneous reflexes in the legs obtain. 

Treatment. — 1. Etiological Treatment. — Antisyphilitic remedies 
(q. v.) are indicated. 

2. Hygienic Treatment. — Overwork, overexercise, worry, trauma, 
exposure and excess in tobacco, alcohol or sexual indulgence should be 
avoided. Tabetics should not marry. The diet should be regulated, 
since dyspepsia promotes pain. If possible, the patient should live in a 
warm climate and at a moderate altitude. 

3. Drug Treatment. — Silver, strychnine and nitroglycerin give 
uncertain results. Gowers considers arsenic beneficial. 

4. Balneotherapy. — Warm baths are injurious; lukewarm baths, 
electrotherapy and massage exert no specific influence on the disease. 

5. Symptomatic Therapy. — (a) If pain is superficial, sinapisms, chloro- 
form liniments or the galvanocautery should be tried; if moderate, 
acetanilide, cannabis indica or peripheral faradization is beneficial ; mor- 
phine should be avoided as long as possible, because the habit is readily 
acquired. Gowers described cases in which pain was a salient symptom 
and existed without ataxia or loss of the patellar reflexes; for this " tabetic 
neuralgia," differing from the ordinary pains of tabes, he recommends 



SPASTIC SPINAL PARAPLEGIA 857 

salicylates and aluminium chloride, gr. v-x, t. i. d. (b) Crises usually 
necessitate morphine hypodermics. Laryngeal crises often respond 
to nitroglycerin hypodermically, chloroform by inhalation or cocaine 
locally. Stretching the spine and cord probably relieves pain; the patient 
sits on the floor with the legs extended; without other movement, the 
body is carefully pushed forward (flexed) as far as possible. Section of 
the nerve roots (rhizotomy) and cocaine injections are recommended, (c) 
For vesical affections, catheterization for residual urine is indicated, but 
under most rigid antisepsis; belladonna and faradization are often helpful. 
Cystitis is treated by lavage, (d) Secondary infection should be avoided. 
Corns should never be cut but always rubbed off. 

6. Ataxia. — This may be relieved by H. G. Frenkel's systematic 
exercises, "a reeducation of the central nervous system by repeated 
exercises;" carefully and persistently executed muscular movements, 
not forceful movements, are desirable. Nerve stretching and suspension 
are useless. 

II. System Diseases of the Motor Tract. 

The motor paths may be diseased (1) in the upper neurone, as in 
spastic spinal paralysis; (2) in both neurones, as amyotrophic lateral 
sclerosis; (3) in the peripheral neurone, as spinal muscular atrophy 
or bulbar paralysis; (4) in the peripheral motor nerve, as the neuritic 
muscular atrophy and (5) in the muscles themselves, as the dystrophies. 
These types may blend; separate descriptions are necessary to bring 
out the classical symptoms. 

1. Spastic Spinal Paraplegia. — Lateral sclerosis described first by Erb, 
in 1875. concerns only the upper motor neurone. 

Etiology and Pathology. — The disease represents a symptom-complex 
rather than a pathological entity. The causal factors are uncertain, as 
syphilis or an hereditary tendency. In 75 per cent, it occurs between 
the twentieth and fortieth years. It was thought that there was a primary 
sclerosis of the lateral pyramidal tracts, especially their lower parts, for 
which confirmation is still lacking; there are some lesions in other 
neurones, as in the post, columns. 

Symptoms. — There are three cardinal findings, motor weakness, mus- 
cular rigidity and increased reflexes, (a) Motor weakness is usually the 
first sign; it begins slowly and is evidenced by weakness or stiffness 
in the flexors of the hips especially but also the knees and ankles. Every 
gradation from paresis to paralysis may be noted in different cases or in 
different stages. Strumpell attributes the loss of finer synergistic move- 
ments to involvement of the lateral pyramidal tracts; the coarser move- 
ments for groups of muscles are possible via the anterior pyramidal 
tracts. The muscles are large and well nourished, (b) Muscular rigidity 
results also from disease of the lat. pyram. tracts, which lessens the 
inhibition and is proportionate to the loss of power. The muscles resist 
quick, passive efforts at flexion, but yield to slow flexion and remain in 
the position given them, "lead-pipe contraction" The knees are rigidly 
extended, even when the patient sits on the edge of the bed; the great 
toe is strongly flexed dorsally; when one leg is lifted the other comes 



858 DISEASES OF THE SPINAL CORD 

with it; the specially tense adductors prevent abduction of the thighs. 
The muscles are stiff in the morning; painful spasms may occur during 
the night; hypertonicity may lead to active contractures and patients 
complain of the "tendons getting too short." In active movements 
rigidity is manifest ; the gait is paretic and spastic, the knees are extended 
and closely apposed, the steps are short, the balls of the feet cleave to the 
ground and the feet scuffle, (c) Increase of the reflexes is also due to lateral 
pyramidal sclerosis. The knee-jerks are most excessive; ankle-clonus 
and Babinski's reflex are present; a strong clonic contraction of the 
quadriceps follows depression of the patella and the gait may be 
hopping. The arms are often normal; there may be rigidity like 
that of a late hemiplegia; there may be clonic spasm of the fingers 
and increased tendon and periosteal reflexes. There sometimes are 
weakness in the back and painful contractions of the chest and back 
muscles with dull aching. The cranial nerves are rarely diseased, 
although the jaw-jerk may be increased. The electrical reactions, 
sensation, muscular nutrition and eyes are usually normal. The sphincters 
are usually affected late. 

Clinical Forms and Diagnosis.- — Diagnosis concerns the paresis, hyper- 
tonicity, increased reflexes and absence of sensory, trophic and other 
symptoms. Six types may be described: (1) There are rigidity and 
spasticity in the legs, arms and perhaps the face, sometimes with com- 
pulsory laughing or weeping, as in amyotrophic lateral sclerosis, but 
without muscular atrophy. 

2. The hereditary or familial form commences between twenty and 
thirty years of age; the paresis develops late; this form is characterized 
anatomically by sclerosis of the (congenitally w T eak) lateral pyramidal 
tracts and also by sclerosis of the cerebellar and GolFs columns (more 
properly classified under combined system disease). 

3. In infantile diplegia, the rigidity is less, foot-clonus less common 
and tonic spasms rare; athetoid movements, deficient mentality and 
epileptiform convulsions are common. 

4. In the syphilitic form of Erb there are paresis and slight spasticity, 
plus urinary incontinence, retention and impotence. 

5. There are forms symptomatic of brain disease (tumor, syphilis, 
paresis), cord disease (tumor, compression, syringomyelia, multiple 
sclerosis) and hysteria which has not the peculiar extensor spasm; loss 
of power is rarely complete and ankle-clonus is rare, although a spurious 
half -voluntary contraction of the calf muscles may be noted. 

6. Periodic familial paralysis affects the legs chiefly, is flaccid and 
results in decrease of the patellar and absence of the plantar reflexes, 
decreased faradic irritability, sleepiness, but without sensory symptoms; 
it lasts one to three days. The prognosis is good. 

Prognosis. — "It is perhaps the least dangerous to life of any chronic 
spinal lesion." Recovery or arrest is rare. 

Treatment. — Overexertion, fatigue, electrotherapy and strychnine are 
to be avoided. Massage, and warm baths relieve the spasticity. 

2. Amyotrophic Lateral Sclerosis. — This is often called the maladie 
de Charcot (Charcot and Joffroy, 1865). 



AMYOTROPHIC LATERAL SCLEROSIS 859 

Etiology. — It occurs mostly between the twenty-fifth and forty-fifth 
years, more frequently in males; its cause is not known. 

Pathology. — The name amyotrophic lateral sclerosis designates the 
leading changes, which are, amyotrophy, from atrophy of the anterior 
horns and sclerosis of the lateral columns, (a) The lateral pyramidal tracts, 
and to a lesser extent the anterior, show symmetrical primary degen- 
eration, followed by interstitial sclerosis which is most marked in the 
lower part of the upper neurone, but in some cases extends upward to 
the medulla, pons, cms or even the central convolutions, the ganglionic 
cells of which may be atrophied. In some cases unimportant changes 
may be found in the cerebellar tracts or posterior columns, (b) The 
ganglionic cells of the anterior horn are degenerated, so that the anterior 
motor part of the cord is distinctly smaller and natter. Likewise the 
nerve filaments from the pyramidal fibers, anastomosing with the pro- 
cesses of the ant. horn, are degenerated. These changes in the trophic 
centre of the second motor neurone explain the atrophy of the anterior 
roots, motor nerves and muscles, (c) The bulbar nuclei, analogues of the 
ant. horns, with their nerves and muscles, show identical changes. 

Symptoms. — The symptoms, like the lesions, are strictly motor. 

Stage 1. — The disease begins with weakness and atrophy of the 
muscles of one, then the other hand, most marked in the thenar, hypo- 
thenar and interosseal muscles, and followed by wasting and weakness 
in the forearm extensors, deltoid and triceps; other muscles of the arm 
and forearm escape or are involved later. Sensory symptoms are absent. 
Weakness is often manifest before the atrophy. Other symptoms of 
disease in the lower neurone appear, as fibrillary contractions and the 
reaction of degeneration; the nerve trunks respond normally. As evidences 
of involvement of the upper neurone, paralysis often precedes the wasting 
and accentuates the weakness from ant. horn involvement; there are 
increase of the reflexes (which never occurs in muscular atrophy due to 
disease of the ant. horns alone) and rigidity and contracture in which 
the arm hugs the chest, the forearm is flexed and pronated, and the 
wrist and fingers are flexed. Sometimes the neck is rigid and trismus 
is observed. 

Stage 2. — In less than a year the legs are involved; weakness, especially 
in the flexors of the hip, knee and dorsal flexors of the foot and spasticity 
prevail. The gait is spastic and paretic as in spastic spinal paralysis 
and walking becomes impossible because of the rigidity and the twitching 
tetanic movements of the extensors. The patellar reflexes are exaggerated; 
ankle-clonus is frequent; when the patient attempts to flex the thigh 
while the examiner holds the ankle, there is a visible contraction of the 
tibialis anticus (the tibialis phenomenon) ; Babinslri's reflex, is present — 
evidences, in short, of pyramidal disease, because symptoms referable to 
the lower neurone, as atrophy, are much less frequent, less marked and 
less early in the legs than in the arms. 

Stage 3. — This stage occurs in one or two years with dysphagia, 
atrophy of the lips and tongue with fibrillation, as in primary bulbar 
paralysis (q. v.). A marked jaw-jerk is elicited, tonic tension of the facial 
muscles may occur and spasmodic laughing or weeping from loss of in- 



860 DISEASES OF THE SPINAL CORD 

hibition. The mind is clear. Death results from respiratory failure, 
aspiration pneumonia, etc. 

Course and Prognosis. — In some cases the pyramidal or paretic, in others 
the atrophic, symptoms are dominant. The course covers one to four 
years and is fatal. 

Diagnosis. — The involvement of both motor neurones, muscle atrophy 
with increased. reflexes, rigidity and the final bulbar symptoms establish 
the diagnosis. 

3. Progressive Spinal Muscular Atrophy. — Duchenne and Aran (1849- 
50) gave the first full clinical description of this disease. 

Etiology. — The ultimate causes are not known. Seventy-five per cent, 
of cases occur in males, mostly between the twenty-fifth and forty- 
fifth years. Hereditary factors, often observed in the muscular dys- 
trophies (v. i.) are infrequent, although 28 familial infantile cases are 
reported. Hard work, mental distress, syphilis, trauma, infections and 
poliomyelitis are possible factors. 

Pathology. — In the cord, especially in the cervical region, (a) the 
anterior horns are small and flattened; their ganglion cells are deformed, 
wasted, their processes lost; interstitial changes are secondary, (b) The 
anterior roots, especially the cervical, are degenerated and often also the 
peripheral nerves, although changes in them are most difficult to dis- 
tinguish, (c) The muscles are small, stringy and pale and their individual 
fibers are small; their transverse striation persists remarkably, and 
waxy, fatty or granular degeneration and longitudinal splitting are not 
common; the muscle nuclei multiply, round cells may wander in, and 
there is usually increase of connective tissue. Amyotrophic lateral 
sclerosis, spinal muscular atrophy and bulbar paralysis. are one affection. 

Symptoms. — (a) The essential symptoms are motor. The earliest is 
muscular atrophy with weakness in the upper extremity (90 per cent.), 
especially the (right) thenar and hypothenar eminences. The abductor 
indicis and opponens pollicis are first involved, then the flexor brevis and 
adductor, the wasting of which brings closer together the metacarpi of 
the thumb and index-finger (the "ape-hand"). It is finally impossible- to 
appose the thumb to the fingers. The interossei on the dorsum waste 
and leave marked furrows, producing the "claw-hand," main en griff e, 
from contraction of the antagonist ext. digitorum communis, the tendons 
of which stand out prominently. The wasting lumbricales hollow the 
palm. In this Duchenne- Aran type, individual muscles are selectively 
involved. The muscles become lax, thin and flat. The atrophy long 
exceeds the paresis. The forearm may be next involved, first the extensors 
below the int. condyle, later the supinators and flexors. A deep depression 
between the ulna and radius eventually occurs. After years, the shoulder 
muscles, the posterior and middle thirds of the deltoid, the biceps and 
brachialis waste and much later the triceps. Sometimes the wasting of the 
muscles of the shoulder and arm immediately follows the involvement of 
the hand, or perhaps the disease begins in the shoulder. The bones of the 
shoulder stand out clearly, covered only by the skin, "the living skeletons" 
seen in museums. The trunk muscles are involved in this order : trapezius 
in its middle and lower parts (rarely in its upper third, which is the 



PROGRESSIVE SPINAL MUSCULAR ATROPHY .861 

ultimum moriens of Duchenne); pectoralis, latissimus dorsi, rhomboidei 
(causing the shoulder to droop) and extensors of the head (allowing 
the head to fall forward). Lordosis is common and the spine stands 
out distinctly. The platysma and face escape. The respiratory muscles, 
intercostals or diaphragm are involved, which latter imperils life. In the 
leg the muscles are affected late and to a lesser degree, as the glutei, 
quadriceps and the peronei. Very exceptionally the disease first develops 
in them. In the fully developed cases there is extreme helplessness; an 
added misery in the form of the sister-process, bulbar paralysis, may develop. 

(6) In the wasted muscles there are usually fibrillary contractions; 
they are involuntary twitchings, tremor- or even wave-like in character. 
They may appear in muscles not yet wasted, (c) The electrical reaction 
in the nerves is normal. In the muscles there is usually only quantitative 
reduction and the voltaic excitability remains long after the faradic is 
lost; in the last stages there is a partial reaction of degeneration, (d) 
The reflexes are weakened or abolished in proportion to the atrophy 
and due to disease in the motor side of the reflex arc. (e) Sensation shows 
no objective change; in some instances there are dull, aching pains in the 
muscles. (/) Vasomotor, secretory, sphincter and trophic symptoms 
are lacking. 

Diagnosis. — The diagnosis is based on the slow course; the involve- 
ment of the hand and its slow "individualization"; fibrillation; partial 
reaction of degeneration; and decreased reflexes. 

Differentiation is necessary (1) from disease in which muscular atrophy 
is but one among several symptoms, (a) Syringomyelia is marked by 
its trophic characteristics, its analgesia, thermo-anesthesia and less 
symmetrical wasting, (b) Meningitis, spondylitis and tumors are mani- 
fested by anesthesia, pain, tenderness and rigidity, (c) In multiple 
neuritis there is a clearer reaction of degeneration, more sensory signs 
and tenderness in the nerve trunks, (d) The occupation atrophies are 
distinguished by the history. 

2. Other muscular atrophies, (a) Chronic poliomyelitis causes paralysis 
first and atrophy afterward; it affects groups of muscles at once, its 
course is rapid and fibrillary contractions are infrequent, (b) The 
myopathic atrophies (see p. 864). (c) Amyotrophic lateral sclerosis is an 
allied, perhaps identical affection; the atrophy is not "individualized," 
but occurs en masse; the distinguishing features are the increase of the 
reflexes, spasticity and a much more rapid course, (d) Arthritic muscular 
atrophy, probably due to reflex influences, or direct extension of inflam- 
mation to the muscles or nerves, involves chiefly the extensors in a 
moderate wasting; diffuse wasting suggests a nervous cause. There is 
usually increased myotatic irritability and reflex action. 

Course and Prognosis. — The onset between the twenty-fifth and forty- 
fifth years is gradual, the course is slowly progressive, remissions in- 
frequent, and death usually results from intercurrent disease, respiratory 
affections (tuberculosis) or bulbar palsy. Arrest is rare and chiefly in 
cases marked by symmetry and synchronous involvement of both hands. 

Treatment. — Gowers gives strychnine hypodermically ; he has seen 
7 consecutive cases of arrest of which 6 were permanent; it has little 



862 



DISEASES OF THE SPINAL CORD 



effect by mouth. Massage, active and passive gymnastics and elec- 
tricity do not stay the disease. 

4. Neural Muscular Atrophy. — Charcot-Marie type. Peroneal family 
type (Tooth). Neurotic type (Hoffmann). 

Etiology. — It is often hereditary, even 
through five generations; it is usually 
familial. It occurs in the second half of 
childhood and rarely after the twentieth 
year. Sixty-six per cent, of cases are in 
males. 

Pathology and Symptoms. — The patho- 
logical characteristic is neuritis; secondary 
sclerosis has been seen in the posterior and 
lateral pyramidal columns. Early atrophy 
occurs in the small muscles of the feet, with 
bilateral, symmetrical peroneal paralysis and 
club-feet (pes equinus or varo-eguinus) . The 
calf muscles suffer next and the thigh still 
later. After years, paralysis and atrophy 
of the hands, as in progressive spinal atro- 
phy, develop, with the " claw-hand"; in 
the forearm, the extensors suffer more than 
the flexors. The shoulder, neck, trunk and 
face are seldom diseased. Fibrillation is 
infrequent; the reaction of degeneration is 
generally present, paresthesia and anes- 
thesia (especially plantar) are common; 
the patellar reflexes may long persist. 

5. Muscular Dystrophy. — The dystro- 
phies or myopathies are often classed 
with diseases of the muscles, which indeed 
show the sole constant pathological lesions. 
They are so closely related clinically -to 
the less frequent spinal atrophies that they 
are here considered. Changes in the cord, 
nerve trunks and nerve filaments have 
been found in some cases of each type. 
(a) Heredity is an obvious cause in 56 per 
cent, or a familial incidence is often ob- 
served ; the muscular system seems deficient 
in development or vitality, (b) It occurs in 
childhood or pubescence, (c) The muscles 
waste, with or without hypertrophy or 
with increase of fat or interstitial growth. 
Pseudohypertrophic Muscular Paralysis. — Lipomatous muscular atrophy 
is the least frequent, but is the oldest and best known type (Bell, 1830; 
Partridge, 1837; Meyron, 1852; Duchenne, 1861). It occurs in males 
(80 per cent.) and is less marked, less early in life and less fatal in women. 
It is often transmitted by healthy mothers, the males being impotent, 




Fig. 74. 
pertrophic 
(Dercum.) 



- Typical 
muscular 



pseudohy- 
paralysis. 



MUSCULAR DYSTROPHY 863 

and may be seen in five generations. It begins early (75 per cent, under 
ten years). 

1. Impaired motility is the earliest symptom. The weakest muscles 
are the invisible hip flexors and the knee extensors which make climbing 
of stairs difficult, cause the waddling gait (paresis of glutei) and interfere 
with rising from the floor, so that the child must rise by resting on all 
fours and by "climbing his own legs with his hands." Paresis of the back 
muscles and hip extensors causes lumbar lordosis and abdominal pro- 
trusion. The ankle extensors also weaken. The child stands with legs 
far apart. The depressors of the shoulders are weakened early in the 
disease, later the shoulder muscles, biceps and triceps, but the hand 
remains normal for a long time, or escapes. The weak muscles show 
nuclear increase, atrophy and division of their fibers, which are usually 
undersized, pale and narrow; fatty degeneration and loss of striation are 
rare. Increase of connective tissue is a later but most characteristic 
change. 

2. Certain muscles show apparent increase in size (pseudohypertrophy ) , 
due largely to early adipose deposit or rarely to actual muscular hyper- 
trophy. The calf muscles are especially enlarged, then the glutei, knee 
extensors, or infraspinatus which contrasts strongly with the wasted 
latissimus and deltoid. 

3. The electrical irritability is lowered, but there is no reaction of 
degeneration. The deep reflexes disappear, from the muscular lesion. 
Mentality, sensation and the sphincters are normal. Cardiac hyper- 
trophy was observed in 60 per cent, of Glotz's cases. The patient becomes 
bed-ridden, arrest is rare and death occurs after years from intercurrent 
disease or respiratory inflammation. 

Infantile Atrophic Form with or without Facial Involvement. — Wasting 
occurs from the beginning. It may be combined with the first form, and 
the legs then show pseudohypertrophy and the arms simple atrophy. 
The pathology is that of the first form, but there is no hypertrophy, 
true or false; increased connective tissue characterizes this type of 
atrophy and also that of the juvenile form (v. i.). 

The face may be involved. The lids droop and cannot be wholly closed, 
the forehead is smooth, the cheeks are flaccid and droop, the lips part 
and functionate poorly, the lower lip protrudes, the nasolabial fold disap- 
pears, the face becomes expressionless (fades myopathica) . The masseters, 
tongue, palate, larynx, pharynx and eye-balls are implicated rarely. 
Simultaneously or more often later, the shoulder girdle wastes as in the 
first type — the facioscapulohumeral form of Landouzy and Dejerine; the 
latissimus and lower part of the pectoralis are usually first affected, but 
in the biceps, triceps and often in the supinator longus, the symmetrical 
wasting and paresis are more conspicuous. The forearm, save for the 
supinator longus, and the hand usually escape. The neck is seemingly 
lengthened (Brissaud), because of the drooping of the shoulders and 
clavicles. The leg muscles then waste, especially the hip flexors, knee 
extensors and less often the glutei; lordosis, the waddling gait and 
symptoms observed in the next type {v. i.) may develop. The facial 
wasting may follow that of the arms. The course is progressive, very 



864 



DISEASES OF THE SPINAL CORD 



chronic (ten to fifty years) and death results from intercurrent infections, 
respiratory catarrh, tuberculosis, etc. In the second and third types the 
prognosis is more favorable than in the first form and the outlook is 
better when the face is unaffected. 

The Juvenile Form of Erb. — This type begins after puberty, possibly 
later (twentieth to fortieth year) and is more frequent in girls than the 
above forms. It begins more often in the shoulders and arms than in 
the legs. The pectoralis, latissimus, trapezius, serratus mag., rhomboidei, 
sacrolumbalis, longiss. dorsi, supinator longus and later the triceps 
are wasted, while the sternomastoid, supra- and infraspinatus, lev. 
anguli scapulae, coracobrachialis, teretes, deltoid and the hand and 
forearm (except the supin. long.) are almost always exempt. If we lift 
the patient with our hands beneath His shoulders he tends to " slip 
through"; this is due to "loose shoulders" (Erb). The scapulae stand 
out prominently from weakness of the serrati. The glutei, quadriceps 
and less often tibialis ant. and peronei become atrophied. The lordosis 
and gait are as above described. 

Diagnosis of Myopathic Atrophies. — (a) Atrophy from cerebral lesions is 
less marked and follows the marked loss of power, (b) Spinal muscular 
atrophy: 



Spinal Atrophy. vs- 

Begins in small hand muscles. 

Extends upward (face free). 

Muscular atrophy. 

Fibrillation the rule. 

Tendon reflexes increased in amyotrophic 

lat. sclerosis. 
Partial reaction of degeneration. 
Age; usually begins after thirtieth year. 
Heredity — rare. 
Bulbar symptoms not uncommon. 



Myopathic Dystrophy. 

In trunk, shoulder or pelvic girdle, leg and 

upper arm. 
Downward (face sometimes affected). 
Frequently with hypertrophy. 
Very exceptional. 
Never increased; decreased. 

Practically never present. 

In childhood, rarely after twentieth year. 

Frequent. 

Never present. 



(c) In congenital spastic paraplegia, increased reflexes and a regressive 
rather than a progressive tendency are characteristic, (d) Peripheral 
neuritis (q. v.) is toxic, acute and shows sensory symptoms and local 
tenderness over the nerves and muscles, (e) In congenital defects in the 
pectoral muscles and trapezius, progression is absent. 

Treatment. — Electricity causes too much pain. Reasonable exercise 
is advisable, because the patients begin to fail when they cannot walk. 
The respiratory tract must be watched, since catarrh predisposes to 
tuberculosis. 

Under diseases of the motor neurones, ophthalmoplegia, Landry's 
paralysis, bulbar palsy, myasthenia, poliomyelitis, etc., might also be 
described, but are treated elsewhere for differential reasons. 



III. Combined System Diseases. 

Kahler and Peck, in 1877. directed attention to cases with simultaneous 
disease in several systems of neurones. Von Leyden, Goldscheider and 
Nonne consider them diffuse, vascular or even myelitic affections rather 



HEREDITARY ATAXIA 865 

than true system diseases, of which, in their opinion, there are but two 
examples, tabes and progressive muscular atrophy. 

1. Hereditary Ataxia, Friedreich's Ataxia (Friedreich, 1861). — Etiology. 
— This affection is hereditary in 33 per cent., and in 80 per cent, 
familial. Most cases occur in boys. It is generally considered a con- 
genital abiotrophy of the pyramidal and other tracts (Freidreich, 
Schultze, Strumpell). 

Pathology. — -The cord, medulla and pons are small. The earliest and 
dominant change is atrophy with secondary sclerosis of the post, roots 
and post, columns, and in GolFs more than in Burdach's columns. Lis- 
sauer's "root zone" is less affected than in tabes, but more than in 
ataxic paraplegia. The direct cerebellar tract, lat. ascending tract of 
Gowers and Clarke's gray columns share in the atrophy. The lat. pyram- 
idal tract suffers in most cases, its inner portion being usually normal. 
Chronic leptomeningitis, with annular sclerosis of the cord, is occa- 
sional. 

Symptoms. — (a) The cardinal sign is ataxia, which is less rapid, ex- 
cessive and stamping than tabetic ataxia, and more closely resembles 
cerebellar ataxia in its tumbling character and involvement of the trunk. 
Static ataxia appears later, the head oscillates or the arms show jerky 
movements (51 per cent.). Romberg's sign is usually present and the 
subject leans over to watch his feet; this leads to some kyphosis. Testing 
the sense of location elicits ataxia, as in the knee-ankle test. The arms 
become atactic after a few years. Nystagmus develops as a late symptom; 
it is elicited chiefly on lateral (or upward) movements and is atactic, 
as is also the disturbance of speech, which is monotonous, irregular, 
unclear, slightly scanning, slow and strained; syllables are often 
elided. 

(b) The knee-jerks are early decreased or abolished and Babinski's 
sign obtains. The skin, pupillary and sphincter reflexes are usually 
normal. In some (possibly syphilitic) cases the pupil reflex may disappear. 
(c) Club-foot (pes equino varus) is common; the foot is shortened and 
widened, the arch is exaggerated (pes cavus), the great toe is strongly 
extended dorsally. Scoliosis and kyphosis are common. Muscular 
paralysis or wasting is rare. Paresthesias, crises, lancinating pains and 
trophic, vasomotor and sensory disturbances are lacking. General or 
sexual development may be retarded. 

Course and Prognosis. — About 33 per cent, develop before the sixth 
year, 33 between the sixth and tenth and 33 after the tenth year. The 
atactic gait is the first sign, then speech is involved, possibly then the 
kyphosis and club-foot develop, and later the arms are affected; the 
course is progressive, possibly with remissions, and the patient becomes 
bed-ridden in twenty .to thirty years. Death follows from acute infection, 
cystitis and sepsis. 

Diagnosis.— The diagnosis is based on the hereditary or familial 
etiology, age, ataxia, absent knee-jerks and disturbance of speech. 

Differentiation. — 1. In tabes there are the syphilitic stigmata, 
immobile pupil, optic atrophy, pains, crises and vesical, trophic and 
marked sensory disturbances. 
55 



866 DISEASES OF THE SPINAL CORD 

2. Multiple sclerosis is differentiated by the spasticity, increased reflexes, 
optic atrophy, compulsory laughing, apoplectiform insults, intentional 
tremor and scanning speech. 

3. In cerebellar tumors there are optic neuritis, headache and vomiting. 
Marie, Londe and Nonne described an hereditary cerebellar ataxia, which 
is possibly due to congenital atrophy of the cerebellum (middle lobe), 
degeneration in Clarke's columns, cerebellar tracts and posterior columns, 
is also hereditary or familial, but develops later, between the twentieth 
and thirtieth years. The ataxia is cerebellar. The reflexes are increased 
(which Patrick thinks is the sole differentiating point), often with spas- 
ticity; quite frequently there are optic atrophy, limitation of the visual 
field, eye paralysis and sometimes an immobile pupil, nystagmus, chorei- 
form movements and moderate sensory and speech disturbances. Club- 
foot, scoliosis and Romberg's sign are absent. Sanger Brown reported 
25 and Neff 13 cases. 

4. Cerebral diplegia of children and ataxic paraplegia are distinguished 
by reflex increase and spasticity. 

5. " Amaurotic family idiocy" (Warren Tay, 1881, and B. Sachs, 1887) 
is characterized by paralysis, idiocy, optic atrophy, marasmus and death 
before the third year of life. Most cases are Jews. At autopsy hypoplasia, 
microgyria, decreased pyramidal cells, tangential and other fibers are 
noted. Bing (1909) collected 106 cases. 

Treatment. — Treatment is symptomatic. 

2. Ataxic' Paraplegia. — Most cases occur in males between thirty and 
forty; syphilis is a rare cause. Pathologically, there is a lateroposterior 
sclerosis; in the lat. column the degeneration is not wholly symmetrical 
or pyramidal; it may invade the mixed zone; in the post, column the 
process is not more intense in the lumbar cord and is less intense in the 
root zone than in tabes. Sometimes the process is so diffuse that it 
suggests myelitis or arterial obstruction. 

Symptoms.- — The early symptoms are those of a gradual spastic para- 
plegia (weakness, exaggerated reflexes, rigidity), followed by ataxia 
(mostly in the legs, with Romberg's sign). The arms are involved later 
and to a less degree. In the last stages the ataxia is obscured by the 
spastic paraplegia; vesical or rectal tenesmus and muscle cramps are 
common. Cranial nerve involvement is sometimes suggested by slightly 
disturbed articulation, nystagmus, tremulous facial movements and 
increased jaw-jerk. The mind is usually clear. Dull sacral pain is 
sometimes observed. 

Differentiation. — (a) Certain tabetic symptoms are absent, as the high- 
stepping, stamping gait, immobile pupils, pains, crises, and absent knee- 
jerks, (b) Friedreich's ataxia is distinguished by the age, heredity, 
speech and absence of patellar reflexes. 

Prognosis and Treatment. — See Spastic Spinal Paraplegia. 

3. Other Combined System Diseases. — Combined sclerosis may also 
occur in pellagra, ergotism, lathyrism (q. v.), multiple neuritis, diabetes, 
pernicious anemia, icterus, leukemia, brain tumor, plumbism or diphtheria. 
It was found by Putnam in enfeebled, middle-aged persons, especially 
in women, 



MONONEURITIS 807 

Pathologically, there is posterolateral sclerosis with diffuse or discrete 
degenerative foci. The most diffuse changes are in the cervical and the 
least in the lumbar cord and sometimes changes exist in the ant. horns 
and Clarke's columns. There are sensory symptoms (lancinating pains, 
paresthesia, anesthesia, ataxia), motor symptoms (paresis, paraplegia, 
chloreiform movements) or reflex symptoms (the patellars being exag- 
gerated or lost). 



DISEASES OF THE PERIPHERAL NERVES. 

MONONEURITIS. 

Definition. — Inflammation of a single nerve trunk. 

Etiology. — (a) Wounds, fractures, dislocations, delivery, violent mus- 
cular contractions ; disturbed metabolism ; anesthesia paralyses, the arms 
being held over the head, the legs bound in holders or when Esmarch's 
bandage is applied too tightly; ether hypodermically, malpositions of 
the arm during sleep and the use of crutches are causes, (b) Contiguous 
disease (pleurisy, pelvic inflammation, tumors or aneurysm) may produce 
neuritis, (c) Cold (rheumatic paralysis) causes inflammation in the sheath 
with extension to the nerve, (d) Toxic causes and infections are factors 
(v. i. Multiple Neuritis). 

Pathology. — In acute cases the nerve is red, swollen and sometimes the 
seat of punctate hemorrhages or extravasation of white cells in the sheath 
or between it and the nerve fibrils. In some cases inflammation involves 
chiefly the sheath (perineuritis) and in others the interstitial tissue (inter- 
stitial neuritis), in which the enclosed nerve fibrils are compressed. The 
process is disseminated or focal (where the nerve divides or enters the 
fascia or bone). It is often difficult to distinguish between inflammation 
and degeneration (parenchymatous neuritis); in both processes there are 
nuclear multiplication and protoplasmic swelling in the neurilemma; 
this compresses the myelin sheath, which becomes varicose, granular, 
fragmented and finally emulsified. The axis-cylinder, composed of thirty 
to fifty primitive fibrils, becomes granular, divided and may largely 
or wholly disappear. Regeneration is accomplished from the spinal or 
cerebral centres and probably also from the periphery. 

Symptoms. -^-Constitutional and local symptoms vary with the intensity, 
extent and seat of the neuritis. 

1. Sensory Symptoms.— The chief local symptom is pain, experienced 
locally or eccentrically over the area of distribution of the sensory nerves, 
increased by tension or movement and usually intense. Tenderness 
indicates involvement of the nervi nervorum. Hyperesthesia, hypesthesia 
and paresthesia may be noted, but complete anesthesia is rare except for 
relatively small areas. Sometimes the swollen or nodular nerve may 
be felt. 

2. Motor Symptoms. — The muscles supplied are tender to touch, pain- 
ful on movement, paretic and atrophied (separation from their trophic 



868 



DISEASES OF THE PERIPHERAL NERVES 



centres). They are less clearly striated, granular and finally indurated. 
Muscular contractures may result reflexly, especially in traumatic and 
occupation neuritides. The reaction of degeneration is present. The 
normal nerve is stimulated by the faradic current which produces a 
continuous muscular contraction and by the voltaic which produces 
a contraction when the circuit is made or broken — the cathode closing 
contraction, which is first to appear and stronger than the anode closing 
contraction. In disease the following changes occur: (a) The muscle 
responds weakly and sluggishly to faradism, and tends to maintain 
contraction after the current is, withdrawn. This modal change is the 
essential element in the reaction, (b) The nerve trunk loses progressively 
its responsiveness to both galvanism and faradism — a quantitative change. 
(c) The muscle becomes more excitable by galvanism and less excitable 



DEGENERATION 
OF NERVE 



ATROPHY A.ND NUCLEAR 
PROLIFERATION OF MUSCLE 



VOLUNTARY 
MOTION 



REGENERATION 

9 




DEG „ E C N ™L 0N COMPLETE 

OF NERVE ATROPHY AND PROLIFERATION OF MUSCLE, CIRRHOSIS degeneration 




3 10 20 30 40 50 00 70 SO l J0 100 WEEK 



Fig. 75. — 1, Paralysis with early return of motion; 2, incurable paralysis with com- 
plete degeneration. 



by faradism; the latter reaction and the- responses in the nerve trunk 
are completely lost after two or three weeks — a qualitative change, (d) 
A polar change appears in the muscle about the second week when directly 
stimulated by galvanism; the muscle is more readily caused to contract 
by the constant current, but the normal mastering strength of the nega- 
tive closing contraction over the positive disappears and the positive 
closing contraction equals or exceeds the negative. 

3. Trophic Symptoms. — The skin is sometimes red, "glossy," edema- 
tous or more rarely thickened. Increased secretion of sweat, eruptions 
as herpes, erythema or pemphigus, inflammation or adhesions in the 
joints and perforating ulcers are less common. 

Neuritis may sometimes ascend to the cord, as in traumatic cases or 
in bladder disease. In the rare progressive hypertrophic interstitial neuritis 



MULTIPLE NEURITIS 869 

of childhood (Dejerine and Sottas, 1893), sclerosis and hypertrophy of the 
nerves, ant. and post, nerve roots, and sclerosis of the post, columns 
cause muscular atrophy, pains, anesthesia, nystagmus, immobile pupils 
and kyphoscoliosis. 

Diagnosis. — Diagnosis depends on localization of symptoms to a 
nerve trunk and its distribution; pain, tenderness and objective sensory 
alteration; muscular atrophy or paralysis; and trophic changes. The 
early diffuse pain may simulate disease of the bones or joints. Chronic 
sensory forms may resemble neuralgia, in which the pain is paroxysmal, 
the tender points more localized and objective sensory alteration absent. 
Disease of the cord or nerve roots usually paralyzes several muscles and 
affects sensation segmentally. 

Prognosis. — The prognosis depends on the cause and intensity of the 
process. Acute cases last for weeks; chronic cases, for months. The 
outlook is usually good in traumatic cases. 

Treatment. — The treatment is (a) that of the cause. (b) Absolute rest 
is indicated. Exertion increases as it may initiate neuritis, (c) Pain. 
The salicylates and iodides are of uncertain value. Local heat may 
cause burns and ulcerations in the anesthetic skin. Coal-tar products 
should be given in preference to morphine or cocaine because habits 
may be contracted; opiates are necessary in severe cases. The positive 
pole of the voltaic current, just strong enough to be felt, may relieve 
pain, (d) Paralysis should be treated only after the acute stage, by the 
weak interrupted voltaic current (not the faradic), massage and later 
passive motion (the veins from the nerves empty into the muscle veins). 



MULTIPLE NEURITIS. 

Polyneuritis, peripheral neuritis, described by James Jackson (1822) 
and Ladd (1854), was first accurately described pathologically by Dumeil 
(1864) andLeyden (1880). 

Definition. — Neuritis, due to the selective action of toxic substances 
on the less resistant peripheral nerves, causing (a) multiple, symmetrical, 
flaccid or atrophic paralysis with (6) the reaction of degeneration, (c) 
sensory and (d) trophic disturbances. ' 

Etiology. — The causes are (a) poisons; alcohol is the most important; 
lead, arsenic (in beer), mercury, phosphorus, carbon monoxide, silver, • 
aniline and ergot may also produce the disease, (b) The infections, acute, 
as diphtheria, typhoid, sepsis and, occasionally, almost every acute 
infection, and chronic, as beri-beri, leprosy, tuberculosis or syphilis, 
are etiological factors, (c) Intoxications, as diabetes, nephritis, digestive 
disorders, cachexias and pregnancy, may be causal, (d) Other causes 
include the seemingly primary cases. Our present knowledge cannot 
explain the action of cold and rheumatism; probably these cases should 
be classified as infectious. It may occur with tabes or arteriosclerosis 
of the nerve vessels. It is a disease of adults (twentieth to fiftieth year) ; 
Thomas and Greenbaum, 1907, collected 138 non-diphtheritic cases in 
children. 



870 DISEASES OF THE PERIPHERAL NERVES 

Pathology. — In acute cases the nerve may be red, swollen and the 
seat of punctate hemorrhage, exudation of leukocytes or albuminous 
exudation in the connective tissue, but usually parenchymatous de- 
generation predominates. It appears first and most markedly in the 
smaller nerves. As in mononeuritis, the axis-cylinders waste and the 
medullary sheaths disintegrate. The symmetry and multiplicity of 
degeneration in the nerve endings are caused by the blood condition 
or toxins. Acute polymyositis of similar origin may accompany neuritis 
multiplex. In cases which are chronic from the beginning there is slow 
degeneration of the nerves. The connective tissue is increased in certain 
forms, as gouty or leprous neuritis. The toxic cause may also produce 
degeneration of the cord or brain and changes in the liver (alcoholic 
cirrhosis), kidneys (alcohol and lead), etc. 

Symptoms. — Acute cases may begin with chills, fever, delirium, head- 
ache, diarrhea, icterus, splenic tumor, albuminuria or other toxemic 
symptoms; chronic cases develop slowly. 

1 . Sensory symptoms are usually first to appear, the last to disappear 
and throughout are the most vexing manifestations. Paresthesia precedes 
pain and pain precedes paralysis. The muscles, nerve trunks and skin 
are the seat of spontaneous pain, tenderness to pressure and pain on move- 
ment. The palms and soles are especially hyperesthetic in the tabetic, 
diabetic and diphtheritic forms. Sensation is often blunted, perverted 
or less often completely suspended, most markedly below the elbows and 
knees, although higher extension, even to the face, is possible. Some 
sensory disturbance is rarely absent. Delayed conduction may occur. 
The joints may be painful, swollen and thickened. 

2. Motor Symptoms occur chiefly in the peripheral distribution of the 
spinal nerves; they develop first and are most marked in the extensors 
of the leg and foot, forearm and hand, and produce the ankle- and wrist- 
drop (ext. popliteal and musculospiral nerves). The foot is also inverted. 
The paralysis is flaccid. If it is only moderately severe in the legs, the 
" steppage " gait is noted and the patient lifts the legs high to clear the 
pendant toes (" turkey-gobbler walk") . Paralysis later involves the flexors 
and the muscles of the arm and thigh. The reaction of degeneration 
sometimes appears before paralysis. The muscles rarely fail to respond 
to the galvanic current, even in the extreme cases. Then the muscles 
atrophy, chiefly in distal parts, i. e., where the sensory and motor changes 
predominate. Other motor manifestations are cramps, tremor, fibrilla- 
tion, ataxia and contractures. The patient lies on the back with the 
members extended or on the side with flexor contractures, which draw 
the heels to the buttocks and the thighs to the abdomen. The trunk 
muscles may be affected as well as those of the neck, eyes, face, tongue or 
indeed those supplied by any cranial nerve as in the neuritic form of 
Landry's paralysis; rapid pulse, palpitation, dyspnea and vocal disturb- 
ance indicate involvement of the vagus; optic neuritis and amblyopia 
may occur. The tendon and skin reflexes decrease or disappear. The 
organic reflexes are almost always preserved. Involvement of the 
sphincters is very rare and referable to the mental state or neuritis of 
the pudendal plexus. 



MULTIPLE NEURITIS 



871 



3. Trophic Symptoms. — The skin is cold, turgid, harsh, sometimes 
glossy; herpes, erythema, ulceration, bed-sores and trophic changes 
in the nails or hair are uncommon; edema over the wrists and ankles, 
especially in alcoholics, is trophic or vascular in origin. 

4. General Symptoms. — Mental symptoms and malnutrition may 
result from the antecedent toxemia or pain; Korsakow's "neuritic 
psychosis" is marked by amnesia for the recent past, confabulation, 
delirium and hallucinations; recovery is the rule. 

Course and Prognosis. — The common order of symptoms is paresthesia, 
pain, paralysis, amyotrophy, trophic and mental symptoms. The distal 
parts are involved more early and intensely than the proximal. The 
prognosis depends in part on the cause. It is good in sensory types and 
in forms of slow evolution, when the sensorium, arms and trunk, cranial 
nerves (vagus) and sphincters escape involvement, and when visceral 
disease, as liver cirrhosis, cord or brain complications, and edema, are 
absent. The prognosis must cover the possibility of recurrence and the 
progress of the disease, inevitably slow, requiring a year, despite treat- 
ment. 

Diagnosis. — The cardinal signs are (a) the motor and sensory symptoms, 
which correspond in function, peripheral distribution and symmetry; 
(b) the reaction of degeneration; (c) tenderness of the nerves and muscles; 
(d) loss of reflexes and (e) the etiology. 

Diagnosis of Type. — (a) The alcoholic form is the most frequent; 
70 per cent, of cases occur in women; the legs are often involved; there 
is the "steppage" gait; atactic, sensory and mental symptoms are 
marked. (6) In lead poisoning the occupation, lead line, colic and 
constipation are characteristic; the arms alone are involved as a rule; 
there is little sensory participation; the involvement rarely extends; 
the wasting is conspicuous, (c) Diphtheritic form (q. v.). (d) In the 
toxemic form with fever and constitutional reaction, it begins in the 
legs or all members simultaneously, involves equally the flexors and is 
attended by slight sensory symptoms, (e) Beri-beri, leprous neuritis, 
erythromelalgia and Dercum's disease are considered elsewhere. 

Differentiation. — Atactic polyneuritis (pseudotabes, Dejerine) with 
little motor disturbance, may resemble locomotor ataxia: 



Locomotor Ataxia. 

History or stigmata of syphilis. 

Argyll-Robertson pupil 

Optic atrophy, 10 per cent. 

Eye paralysis frequent. 

Girdle sensation and lightning pains. 

Gait ataxic, stamping, striking heel first. 

Sensory symptoms predominate. 

Paralysis, reaction of degeneration and 

amyotrophy rare. 
Nerve trunks often insensitive. 
Arthropathies, osteopathies. 
Crises. 

Sphincters frequently involved. 
Clinical evolution very slow. 
Disease incurable. 



-Multiple Neuritis. 



Rare; infection or intoxication. 

Loss of accommodation in diphtheria. 

Rare, but toxic amaurosis is frequent. 

Much more rare. 

Very rare. 

Disturbance motor. Striking toe first. 

Motor predominate. 

In nearly all cases; rapid in development 

and symmetrical. 
Tender, as are muscles. 
Unknown; glossy skin more common. 
Almost unknown; toxemic vomiting, etc. 
Very rarely, and from delirium. 
Rapid. 
Recovery usual, if not early death. 



872 DISEASES OF THE PERIPHERAL NERVES 

Poliomyelitis. vs.— — ■ — Multiple Neuritis., 

Usually in children. In adults. 

More sudden onset. Gradual. 

Embraces whole limb, at random. Strictly peripheral and symmetrical. 

Muscles functionating together. Reaction Dissimilar muscles involved, 
of degeneration in both, but strong gal- 
vanic current not required to produce Muscles respond only to strong galvanic 
muscular contraction. current. 

Pain and tenderness rare. Common in nerves and muscles. 

Sensory disturbance rare. Usually (but not invariably) present. 

Immediate tendency to regress, but usually Tendency to progress, 

some deformity. Total recovery the rule. 

In acute myelitis the onset is acute, there are girdle pains, paraplegia, 
with corresponding anesthesia, bed-sores, disturbance of the bladder 
and rectum; there is no tenderness of the nerves or muscles, little or no 
ataxia and recovery is unusual. Landry's paralysis often cannot be 
distinguished (one form of Landry's disease is neuritic). 

Treatment. — Alcohol must always be considered and deception guarded 
against; it should be withdrawn at once. For pain see Neuritis. Ab- 
solute rest should be enforced. A full diet, rich in fats, should be given 
if the stomach is tolerant; tonics, as iron, maintain nutrition, but arsenic 
should be avoided. When the lower cranial nerves are affected, feeding by 
the nasal tube or by rectum, measures to avoid hypostasis, as in typhoid, 
and cardiac stimulants are indicated. To overcome contractures from 
ankle- or wrist-drop, splints or sand-bags are employed when they do not 
cause excessive pain, and frames to lift the bedclothes from the feet. 
Gentle massage and voltaism may be tolerated after the acute stage, may 
prevent contractures and aid the return venous flow. Bromides and 
chloral are the most certain somnifacients, but chloral requires care in 
chronic alcoholism. 

• NEUROMA. 

Two varieties exist, the true and the false. The true neuroma may be 
medullated or non-medullated, though ganglion cells are exceptional; 
they are usually multiple, sometimes very numerous (3020 in one case) 
and have been found on every cranial, spinal and sympathetic nerve 
(von Recklinghausen's disease, of which Adrian assembled 447 cases). 
They may undergo sarcomatous degeneration. The tuber cula dolorosa 
(Virchow) are small, painful, subcutaneous nodes on the trunk or ex- 
tremities, the anatomy of which is obscure. The congenital neuroma 
plexiforme consists of twisted cords with nodes and occurs largely in the 
distribution of the fifth nerve. The false neuroma is usually fibrous; 
glioma is rare; sarcoma or carcinoma may by contiguity invade adjacent 
trunks; neuromata have been found in the cerebral nerves in syphilis and 
in the peripheral nerves in leprosy. The nerve trunks suffer more in the false 
than in the true form. Neuromata in amputation stumps are frequent. 

Symptoms and Treatment. — There may be no symptoms; local tender- 
ness and local or projected pain are frequent. Reflex muscular spasm 
is common from nerve irritation. Mentality, sensation or motility may 
be affected. Pigmentation is usual. Treatment is symptomatic for the 
exhausting pain or radical in localized growths. 



OPTIC NERVE 873 

DISEASES OF THE CRANIAL NERVES. 

OLFACTORY NERVE. 

The end nerves located on the two upper turbinate bodies and the 
upper septum, run to the olfactory bulbs, which are part of the brain, 
thence to the centre in the uncinate gyrus and hippocampus, with re- 
lations to the optic thalamus, opposite internal capsule and cerebral 
cortex. The anterior nares perceive odors, the posterior flavors. 

Anosmia is loss of smell. Tests are made not with pungent sub- 
stances, as ammonia, which irritate the fifth nerve, but with musk, 
asafetida, cologne-water and the essential oils, (a) Disease in the nasal 
mucosa is the most frequent cause — from paralysis of the fifth nerve, 
arrest of secretion or atrophy. (6) Disease may result from congenital 
absence of the bulb, basal fracture or meningitis, tabes, foci in the opposite 
internal capsule, etc. (c) Central disease, as softening, may develop 
in the hippocampus and uncinate convolution. The prognosis is unfavor- 
able and treatment ineffectual. Hyperosmia, over sensitiveness of smell, 
occurs in insane and neurotic subjects; it may be cultivated, so that 
individuals are recognized by their odor. Parosmia, perverted sensation, 
is rare and arises from irritation of the nerves or centres. Hallucinations 
of smell may occur, as of burning flesh in the epileptic aura. 

OPTIC NERVE. 

1. The Retina. — Retinitis occurs in general diseases, as nephritis, 
especially late in interstitial forms. The degenerative form is most 
common, next the hemorrhagic form, with "flame-like" hemorrhages 
along the vessels, and finally the inflammatory type, with marked 
swelling of the retina, serum exudation, cloudiness and disk blurring; 
the white foci are due to exudation, fatty change or sclerosis. Similar 
findings may occur in syphilis, anemia, malaria, leukemia, plumbism, dia- 
betes, etc. (see Plates IV and VI). There are apparently primary cases. 

2. Optic Nerve. — Optic neuritis (papillitis, choked disk) has been 
described (see Brain Tumor and Plates IV and VI). Tumors or in- 
flammation in or back of the orbit or errors in refraction may be causal. 
In the primary form there is no initial inflammation. The edges of the 
disk are distinct, its arteries nearly normal and its color grayish; it may 
develop hereditarily in males at puberty; it occurs in tabes, paretic 
dementia, multiple sclerosis, syphilis and less often from diabetes, 
alcoholism, plumbism, specific fevers, amaurotic family idiocy and 
familial cerebellar ataxia. The form secondary to inflammation commonly 
follows choked disk and has the same significance; the disk has an 
irregular contour, small arteries and is translucent. The symptoms 
are diminution in acuity of vision, field of vision, color perception and 
the pupillary reaction. 

3. Chiasm. — Each half of the retina contains fibers from the corre- 
sponding occipital lobe (see Plates XXIII), that is, each right half receives 
fibers from the right and each left half from the left occipital lobe. The 



874 DISEASES OF THE CRANIAL NERVES 

outer temporal portion of the field of vision is more limited than the inner 
nasal portion, because the nose cuts off light and it receives fewer nerve 
fibers. The larger number of fibers from each eye, i. e., those from the 
nasal retinal half, decussate at the chiasm and lie in its centre. Those 
from the temporal half are direct and lie at the side of the chiasm. While 
disease of one optic nerve causes blindness in the corresponding eye, 
lesions affecting the centre of the chiasm (decussating fibers to the 
nasal half of each retina) cause half-blindness in the opposite (tem- 
poral) visual fields, bitemporal hemianopsia, since oblique rays passing 
the pupil fall on the opposite half of the retina. The macula, the point 
of sharpest vision, receives fibers from both sides of the brain and escapes 
involvement. Temporal hemianopsia may result from tumors of the 
pituitary gland, pressure from the third ventricle, gummata and hemor- 
rhage. The "oscillating" or varying bitemporal hemianopsia often 
indicates syphilis. The diagram illustrates effects of lesions of the lateral 
part of the chiasm (3), lesions affecting both sides of the chiasm (3 and 
3 A), as calcareous or aneurysmatic carotids; binasal hemianopsia is 
most exceptional; a large lesion might produce temporal hemianopsia 
in one eye and total blindness in the other; still more extensive disease 
might produce total blindness. 

4. Optic Tract. — Just back of the chiasm the temporal fibers of the 
right and the nasal fibers of the left side form the right optic tract; 
i. e., the right tract contains all fibers from the right half of each retina. 
The tract runs over the crus cerebri, where a lesion very often causes 
hemiplegia on the same side as the blind field. The fibers enter the 
geniculate bodies (in which 80 per cent, of the optic fibers end), opt. 
thalamus and ant. quadrigeminate body, from which gray ganglia the 
fibers pass by way of the posterior limb of the internal capsule and, 
by the optic radiation, to the visual centre in the occipital lobe, the 
cuneus. A lesion in the optic tract anywhere between the chiasm and 
cuneus produces homonymous hemianopsia (at 5, in diagram); for in- 
stance, if it occurs in the right optic tract it produces loss of function in the 
temporal half of the right and nasal half of the left retina, so that the 
left half of each field of vision is lacking. Hemianopsia may be partial, 
or only a quadrant may remain after partial recovery. Heteronymous 
hemianopsia designates blindness of the right half of one field and the 
left half of the other or the converse. Disease in the gray ganglia or 
internal capsule may produce contralateral hemiplegia; in 50 per cent, 
of cases of hemianopsia this association is observed, and less frequently 
hemianesthesia. The optic tract is injured in tumors, "multiple sclerosis, 
trauma, hemorrhage or softening. 

5. Optic Centre (See page 753). — A lesion in the cuneus produces (a) 
homonymous hemianopsia. Sometimes only an upper or lower quadrant 
is blind. Purely cortical hemianopsia is impossible, Monakow holding 
that the optic radiation must be involved; (b) hemichromatopsia, or 
homonymous color-blindness or confusion, in which all colors seem gray, 
is probably due to lesion of the anterior superficial cuneal cortex. Other 
results are (c) mind-blindness; (d) alexia; (e) optic aphasia; and (/) 
crossed amblyopia, concentric blurring or limitation of the visual fields 



PLATE XXIII 




V/SUAV, 



r WSUAL ^ 



Visual Paths. (After Vialet.) 

OP.N., optic nerve. OP.C, optic chiasm; OP.T., optic tract; OP.R., optic radiation; 
F.S., visual speech centre. A lesion at (1) causes total blindness in that eye; lesion 
at (2), bitemporal hemianopsia; at (3), unilateral nasal, and lesions at (3) and (3A), 
bilateral nasal hemianopsia; at (4), hemianopsia of both eyes and the hemianopsic pupillary 
reaction; at (5) or (6), hemianopsia of both eyes (pupillary reflexes being normal; at (7), 
amblyopia, especially of the opposite eye; at (8), word-blindness. 



OCULAR PARALYSIS; THIRD, FOURTH AND SIXTH NERVES 875 

for form and color; this is usually referred, however, to disease of the 
gyrus angularis, in which there is thought to be a higher centre in which 
the half-fields are combined and the whole opposite field and part of the 
field of the same side are represented. 

Diagnosis. — The eyes should be tested separately. Disease of an 
optic nerve causes loss of sight and pupillary reaction in the corresponding 
eye. Central scotoma (blindness in the centre of the visual field) indicates 
inflammation or hemorrhage in the central (axial) fibers of the nerve, 
usually back of the orbit; it is common in poisoning from tobacco and 
alcohol. Peripheral limitation of the visual fields indicates damage to 
fibers coursing in the periphery of the optic nerve and some damage 
to all the nerve fibers. Sectorial blindness indicates a pronounced but 
circumscribed affection of the nerve. Bitemporal hemianopsia always 
results from chiasm disease; unilateral temporal hemianopsia in one eye 
with complete blindness in the other has the same significance, but also 
implies that the process has extended laterally, possibly even to the optic 
tract. Homonymous hemianopsia indicates disease of the optic tract 
between the chiasm and cuneus. If the geniculate (or quadrigeminate) 
bodies are the seat of the lesion, Wernicke's hemianopsic pupillary re- 
action is obtained ; a small beam of light in a dark room should be thrown 
on the hemianopsic half of the retina and the patient should look at a 
distance to eliminate accommodation; if the pupil does not react to light 
on the blind half (Wernicke's reaction) the disease focus lies at or to 
one side of the geniculate or quadrigeminate bodies. If the lesion lies 
between these ganglia and the cortex, the reaction of Wernicke is absent. 
Transient hemianopsia is common in vascular lesions; if it lasts for 
weeks it will probably remain. In Sequin's case it was present for twenty- 
three years. It may occur in migraine and very rarely in hysteria. Its 
association with the crus, internal capsule or cortex symptoms already 
considered is of localizing importance. Amblyopia and concentric limita- 
tion in the fields, marked in one eye and less in the other, may result 
from (a) optic atrophy, with the absent pupillary reaction, and seen 
with the ophthalmoscope; or (6) disease of one hemisphere, the ophthal- 
moscopic finding and pupillary reflex being normal. 

Functional and Toxic Blindness. — (a) Hysterical blindness is transi- 
tory and rarely complete; the eye functionates normally, though the 
visual centre neglects the impression; it is often associated with loss 
or inversion of the color perception and with hemianesthesia, (b) In 
amblyopia from tobacco, vision is gradually impaired in both eyes, 
largely as central scotoma with invariable loss of perception for red 
and green colors; the fundus is usually normal, sometimes congested; 
recovery is usual, but atrophy may result, (c) Toxic amaurosis, usually 
transitory, may occur from uremia, poisoning by lead, alcohol or quinine, 
syphilis, acute anemia, etc. 

OCULAR PARALYSIS; THIRD, FOURTH AND SIXTH NERVES. 

General Etiology. — (a) Trauma to the eye, orbit or base may cause 
ocular paralysis, characterized by a slow course and often imperfect 



876 DISEASES OF THE CRANIAL NERVES 

recovery, (b) Compression by tumors in the orbit which often produce 
exophthalmos; tumors at the base, aneurysm and rarely hemorrhage into 
the nerve sheath may produce it. (c) Neuritis produced by the above 
factors, orbital cellulitis, meningitis, syphilis, cavernous thrombosis, 
alcoholism and acute infections, as diphtheria may be etiological factors ; 
exophthalmic goitre, plumbism, and diabetes are rarer causes, (d) 
Nuclear disease is usually due to chronic wasting disease, as in tabes, 
multiple sclerosis or bulbar palsy, but sometimes to acute lesions, polio- 
encephalitic or vascular, (e) Supranuclear disease (v. i.) or (J) in rare 
cases muscular dystrophy may be a cause. 

Anatomy and Physiology. — The nerve supply is by the sympathetic 
(which through the ciliary ganglion dilates the pupil) and by the third, 
fourth and sixth cranial pairs, which arise from the middle ventricle, 
Sylvian aqueduct and fourth ventricle and are arranged as follows from 
before backward : (a) the third nerve nucleus with the ciliary and behind 
it the pupillary centre, then its muscles in this order : the internal rectus, 
levator palpeb. superior, inferior rectus and inferior oblique; (6) fourth 
nerve nucleus for the superior oblique and (c) nucleus of the sixth nerve 
for the ext. rectus. Their connection with the motor cortex is through 
the internal capsule and corona radiata. The third nucleus is connected 
with the seventh; winking and movements of the eyelid are thus asso- 
ciated with the pupil reaction and accommodation. The action of the 
muscles is indicated by their names but convergence is supplemented by 
the sup. and inf. recti and the two oblique muscles. The inf. oblique 
turns the eye upward, the sup. oblique downward. The upper lid is 
raised by the levator palp. sup. (acting usually with the sup. rectus) 
and by Miiller's muscle. 

Paralysis of the Third Nerve. — This nerve emerging from the crus 
follows the cavernous sinus, and therefore may be involved in disease 
of these structures. A complete paralysis results in drooping of the lid 
(ptosis), which the patient attempts to overcome by overaction of the 
frontalis; the eye can be moved only outward and a little down and 
inward (ext. rectus and sup. oblique). Accommodation is lost, the pupil 
is wide from the unopposed action of the sympathetic nerve and does not 
react to light. There is double vision from divergent strabismus, due to 
action of the unrestrained ext. rectus muscle. Paralysis is often partial; 
the levator palp. sup. may escape involvement or be affected alone or 
with its associate (the sup. rectus), especially in bilateral nuclear disease. 
Ptosis may be (a) part of an ordinary oculomotor palsy; (b) part of a 
chronic ophthalmoplegia (v. i.); (c) reflex in rare cases of trigeminal 
irritation, as from disease of the teeth; (d) myopathic, as in muscular 
dystrophy; (e) a result of sympathetic paralysis, false or pseudoptosis 
(with a red, edematous skin, slight recession of the eye-ball and con- 
tracted pupil); (/) an incurable congenital form, usually partial and 
bilateral; (g) a transient form, observed in the morning in women, 
usually with a good prognosis; (h) an hysterical form, usually bilateral, 
in various associations with the sup. rectus, inf. or int. rectus, the eye- 
brow being frequently lower. 



OCULAR PARALYSIS; THIRD, FOURTH AND SIXTH NERVES 877 

Internal Oculomotor Palsy. — Internal oculomotor palsy includes 
c5 T cloplegia and iridoplegia. (a) Cycloplegia (paralysis of the ciliary 
muscle) results in loss of accommodation. Near vision is poor, distant 
vision is good; extreme myopia or presbyopia make its detection difficult. 
Isolated cycloplegia in one eye may indicate disease of the lenticular 
ganglion; in both eyes it is nuclear, as in diphtheria or tabes, (b) Irido- 
plegia may assume three forms: The first is loss of associated action, 
accommodation iridoplegia, in which there is no pupillary narrowing in 
the act of accommodation. It is due to the same causes as cycloplegia 
and is usually associated with it. The second is loss of the light reflex, 
reflex iridoplegia^ the Argyll-Robertson pupil, seen especially in tabes 
and paretic dementia (very seldom in softening, tumors, senile atrophy, 
hydrocephalus or congenitally). The reflex occurs through the optic 
nerve, optic tracts, corp. quadrigemina or corp. geniculata, anterior 
part of the oculomotor nucleus, probably the second branch of origin of 
the third nerve, its trunk, the ciliary ganglion and its nerves. The pupils 
are often equally affected and small (spinal myosis) but may be unequal 
(anisocoria, also observed in some normal persons). If the pupils are 
not too small, cutaneous iridoplegia is not present. The third form is 
loss of the skin reflex, cutaneous iridoplegia, in which the normal dilatation 
of the pupil upon pinching, sticking or faradizing the skin of the neck 
is lost. It indicates, in general terms, disease in the cervical sympathetic 
nerve, in the fibers between it and the cervical cord, diseases of the cord 
affecting sensation, or of the centre (probably in the corp. quadrigemina 
outside the light reflex centre in the trunks of the first and third nerves). 
The seat of lesion is probably nuclear, unless special localizing symptoms 
indicate otherwise. Specifically it is characteristic of tabes, paretic 
dementia or syphilis. 

Recurrent Palsy. — Periodic palsy, to which Gubler (1860) and Mobius 
drew attention, is a rare form, involving most of the third, and rarely the 
sixth nerve. It occurs chiefly in women. At intervals of months to years, 
possibly throughout life, a recurrent paralysis develops for a few days 
or weeks and disappears. Forms which begin with headache, pain and 
vomiting were called ophthalmoplegic migraine by Charcot. Its nature 
is unknown (peripheral or nuclear) ; von Monakow holds that its cause 
is tumor, meningitis or tubercle; the lesion affects the eye nerves (or 
centres) and the descending branch of the fifth; few cases are seemingly 
hysterical. 

Paralysis of the Fourth (Trochlear) Nerve. — Paralysis of the superior 
oblique is of little importance. In attempts to converge downward the 
normal inward rotation of the eye-ball is lacking. 

Paralysis of the Sixth Nerve. — The eye cannot be moved outward, 
and is rotated inward by the unopposed- internal rectus, marked diplopia 
resulting. This nerve is frequently involved, because of its long and 
exposed course. The muscles of the eye are involved in the following 
order of frequency: 1, ext. rectus; 2, sup. oblique; 3, inf. rectus; 4, 
sup. rectus; 5, int. rectus; 6, inf. oblique (von Grafe). 

Combined Eye Paralysis. — Convergence and accommodation are asso- 
ciated functionally and their centres lie adjacent, whence they are often 



878 DISEASES OF THE CRANIAL NERVES 

lost together. The internal recti may fail to contract together but may 
move separately in lateral eye movements. Conjugate deviation may occur 
(see pages 761, 769); if a lesion occur above the sixth nucleus, the eyes 
cannot be directed toward the side of lesion and are directed toward 
the paralyzed side; if the lesion is at the sixth nucleus the sixth nerve 
on that side is paralyzed, often also the seventh, and the opposite third 
nerve is paralyzed, not from lesion in the third nucleus but from the fact 
that each third nucleus receives afferent impulses from the contralateral 
sixth nucleus for associated eye movements. 

Symptoms. — The symptoms of paralysis are five: 

1. Limitation of movement in the paralyzed muscle, followed by 
secondary contraction of the unresisted opponent. The habitual position 
of the head corresponds in every way to the physiological action of the 
paralyzed muscle (Landholt). 

2. Strabismus (squint), causing lack of parallelism in the visual axes, 
which are divergent when the int. rectus and convergent when the ext. 
rectus is affected; this constitutes the primary deviation. 

3. Secondary deviation is the extra movement of the sound eye in 
its efforts to see, due to its increased innervation, detected by testing 
with the diseased eye closed or by testing with ground-glass over the 
sound one. 

4. Erroneous projection in the paralyzed eye. Distance is normally 
judged by the position of the eye-balls and muscles and therefore when 
secondary deviation from excessive innervation of the sound muscles 
occurs, it increases the impression of distance. 

5. Diplopia (double vision) results from failure of the visual axes 
to correspond. The sound eye sees the true image, while the paralyzed 
eye sees the false one, which is less clear, since the image falls on a less 
sensitive retinal area. When the images are either near together or 
else widely separated the false one may be "neglected." Erroneous 
projection and diplopia always produce vertigo at first. If the false 
image is on the same side of the true image as the eye by which it is seen, 
the diplopia is simple or homonymous; if on the other side, it is crossed 
or heteronymous. The eyes are tested by holding red glass before one 
eye and testing vision with a strip of white paper. If the red image and 
covered eye are on the same side the diplopia is simple; if on opposite 
sides it is crossed. When the eyes converge it is simple, when they diverge 
it is crossed; i. e., "when the prolonged visual axes cross, the diplopia 
is not crossed." Holding the test object stationary and the head being 
turned in one way or another, in some directions the images converge 
or perhaps blend, while in the opposite direction they separate. "The 
affected eye is that one in the direction of whose image the diplopia 
increases; the paralyzed muscle is the one which would give to the eye 
the direction of the false image" (Landholt). Monocular diplopia is 
hysterical (unless there is disease of the eye media or error in curvature). 

Treatment. — Treatment is often unsatisfactory from the etiological 
standpoint. Surgical interference or specific treatment is sometimes 
indicated, but syphilitic forms (q. v.) often recur or become permanent. 
In acute forms counter-irritation back of the ear bv blisters, leeches or 



OCULAR PARALYSIS; THIRD, FOURTH AND SIXTH NERVES 879 

hot fomentations is indicated. Some find mercury useful in peripheral 
forms. Galvanism is the best form of electrotherapy, but is seldom 
beneficial. Prisms and tenotomy are sometimes helpful. 

Progressive Nuclear Ophthalmoplegia. — Nuclear palsy was first de- 
scribed clinically by von Grafe (1856) and pathologically by Hutchinson 
and Gowers. The etiology is not clear; syphilis (in 17 per cent.), lead, 
alcohol and toxemia, as from diabetes, grippe or diphtheria, are possible 
causes. A few cases are hereditary or congenital. Most cases develop 
in males under thirty years of age. The pathology usually consists of 
degenerative nuclear atrophy resembling bulbar paralysis; sometimes 
compression or meningitis is found or rarely no anatomical alteration is 
detected, the functional form. 

Symptoms. — The symptoms are those of a slowly progressive paralysis 
of the eye muscles; ophthalmoplegia is called external when it involves 
the extrinsic muscles, internal when it involves the pupil, or total when 
both are concerned. The eye muscles are successively affected, but in no 
given order. The fades of Hutchinson is peculiar, staring, from immobility 
of the eye-balls, or sleepy from partial bilateral ptosis. Diplopia is un- 
common, or only an early symptom, because of the chronicity of the 
process. Associated muscles are often affected by groups, because of their 
successive nuclear involvement, as the pupil and convergence, one internal 
and the opposite external rectus, the two internal recti and the sup. 
rectus and levator. Chronic ophthalmoplegia may be associated with the 
analogous bulbar paralysis or progressive spinal muscular atrophy; with 
optic atrophy or with double facial paralysis (the rare and obscure infantile 
or congenital oculofacial paralysis, without pupillary involvement, of 
which Mobius collected 44 cases) ; it may be a part or a precursor of tabes, 
paralytic dementia or multiple sclerosis. 

Diagnosis. — Nuclear involvement is probable when there is partial 
and bilateral ptosis, escape of the pupil, or involvement of one or more 
conjugate groups. The lesion may be supranuclear, when the head and 
limbs are involved, exceptionally when there is isolated convergence 
paralysis or paralysis of up-and-down movements with ptosis. Apoplecti- 
form nuclear palsy from basilar thrombosis is usually asymmetrical, 
acute and associated with hemiplegia. Wernicke's superior poliencephal- 
itis is distinguished by its acuity and toxemia. Ophthalmoplegia from 
syphilitic meningitis, polyneuritis, tumors (corp. quadrigem.) and orbital 
disease, is generally distinguished by the relatively acute course and 
concomitant symptoms. 

Prognosis. — The disease is very chronic, possibly lasting twenty to 
forty years and is progressive. Arrest is possible, but can never be 
predicted. The disease itself causes little risk to life, but its associates 
are dangerous, as tabes or psychoses, which develop in 18 per cent. 

Treatment. — Treatment is generally ineffectual. Iodides and mercury 
are useless in nuclear disease, but may be given if the localization is not 
definitely known. 

Sympathetic Paralysis. — This disease was first described by Horner; it 
produces myosis, due to paralysis of the dilator iridis, and slight ptosis, 
due to paresis of Miiller's muscle. The ocular tension is decreased, 



880 DISEASES OF THE CRANIAL NERVES 

the cheek wasted and the skin reddened and warmer than normal. Irri- 
tation of the sympathetic is characterized by wide pupils, widening of the 
interpalpebral space and exophthalmos. 

Ocular Muscular Spasms. — Spasms occur in conjugate deviation, irri- 
tation of the nerve trunks when compressed by tumor, and rarely in 
chorea, facial tic and spasmodic torticollis. In hysteria the eyes may be 
rolled upward and to one side, concealing the iris, or they are often fixed 
in convergence; they never diverge; what appears to be ptosis is really 
spasm of the orbicularis. Convergent spasm may also occur in hyper- 
metropia and divergent spasm in myopia. Isolated spasm of the levator 
palpebral may occur in irritation of the cervical sympathetic or fifth 
nerve, in advanced years or Graves's disease. Secondary deviation (v. s.) 
is spasmodic, as is also nystagmus, which latter consists of rapid, rhythmic, 
clonic, involuntary oscillations, due to muscular spasm with alternating 
contraction of the opposing muscles. It is continuous, as distinguished 
from the "tremor of weakness" which occurs in paretic muscles on move- 
ment. It is usually horizontal, less often rotatory and rarely vertical. 
Its mechanism is probably centric. The causes are (a) disease of the eye, 
as opacities and choroiditis; (b) it occurs frequently in albinos, and (c) 
in miners, from working with the head down and eyes strained to one 
side; (d) it occurs as a cardinal sign in multiple sclerosis and Friedreich's 
ataxia, as a common sign in tumor of the cerebellum, corp. quadrigem. 
and opt. thalamus, occasionally in meningeal disease, sinus thrombosis, 
hemorrhage or softening and very rarely in hysteria. 

FIFTH NERVE (TRIGEMINUS; TRIFACIAL NERVE). 

The nerve originates from its motor nucleus in the pons, from motor 
fibers descending from the corpora quadrigemina, and from sensory 
fibers ascending from the medulla. It is connected with the motor 
cortex and cerebellum. The motor and sensory fibers leave the pons 
separately and join after the sensory trunk has passed through the Gas- 
serian ganglion, which has three branches; (1) which passes to the orbit 
by the sphenoidal fissure, supplying the skin of the forehead, anterior 
scalp, upper lid, bridge and top of the nose; it is connected with the 
cervical sympathetic nerve; (2) which passes by the foramen ovale to the 
sphenomaxillary fossa to supply the upper and lower lids, cheek, fore- 
part of the temples, side of the nose, upper teeth, gums, pharynx, tonsils, 
soft palate, uvula and roof of the mouth; it has connections with the 
sympathetic nerve and the facial nerve by the Vidian; (3) which passes 
by the foramen rotundum and sphenomaxillary fossa supplying the rest 
of the temples, anterior and upper parts of the ear, meatus, lower cheek, 
lower lip, lower teeth, gums, chin, tongue, oral mucosa, salivary glands, 
and as a motor nerve to the muscles of the lower jaw, temporals, masseters, 
pterygoids, mylohyoids and post, belly of the digastric. The lingual 
branch gives off the chorda tympani which joins the facial nerve. From 
the otic ganglion arises the small superficial petrosal nerve which connects 
with the facial nerve and ends in the tympanic branches of the glosso- 
pharyngeal nerve. 



FIFTH NERVE 881 

Causes of Paralysis. — (a) Lesions of the cortex in very rare cases. 
(b) Focal disease in the pons, as hemorrhage, tumors and less often 
tabes or bulbar paralysis, (c) Diseases of the base, as syphilis, meningitis, 
tumors, caries or aneurysms, (d) Affections involving the first branch 
by cavernous thrombosis, pituitary tumor, aneurysm or orbital disease, 
or the second and third branches by lesions in the sphenomaxillary fossa. 
(e) Trauma, puncture or bullet wounds, but (/) rarely fractures, or 
neuritis, unless it is secondary. 

Symptoms. — 1. Sensory Portion. — Anesthesia, generally unilateral, 
is found in one or all branches, and tactile sensation is more involved 
than the sense of pain. It is often preceded by tenderness along the 
nerves, irritation or neuralgia. In complete cases the skin and mucosa 
of the mouth, nose and conjunctiva are anesthetic. The tongue is furred 
on its anesthetic half, because the food is not chewed on that side. The 
conjunctival reflex is abolished. The secretions are increased by irrita- 
tion or decreased by paralysis. Smell is blunted and taste is lost (v. %.). 
Sometimes there is redness, cyanosis or swelling of the face or the teeth 
may be loosened. Two trophic manifestations are important. The first 
is neuroparalytic ophthalmia, which may lead to ulceration of the eye 
or loss of the bulb; it is due not simply to conjunctival anesthesia, 
which predisposes to inflammation because of foreign particles remaining 
unnoticed in the eye, but is rather due to irritation of the fifth nerve or 
Gasserian ganglion. It has not occurred in many cases in which the 
ganglion has been surgically removed. The second is herpes zoster, which 
is most common in disease of the first branch, results from irritation of the 
Gasserian ganglion or the nerves just anterior to it, is often preceded 
by pain and sometimes leads to iritis or ophthalmitis. 

2. Motor Portion. — Placing the fingers on the temporal and masseter 
muscles, when the patient attempts to close the teeth, reveals their 
failure to contract. Paralysis of the ext. pterygoid is shown by failure 
to move the jaw toward the sound side and by deviation toward the 
paralyzed side, when the jaw is depressed. The wasted muscles are too 
deep to elicit distinctly the reaction of degeneration. 

3. Gustatory Portion. — The sense of taste covers only bitter, sweet, 
sour, salty and metallic substances, while flavors are recognized by 
the olfactory nerve. The tip and edges of the tongue detect saltiness 
or sourness; its base, bitterness and sweetness. It is often stated that 
the fifth nerve supplies the anterior two-thirds of the tongue and the 
glossopharyngeal nerve the posterior third and the palate; but glosso- 
pharyngeal disease alone does not destroy the sense of taste. In a study 
of cases of Gasserian extirpation, Gushing decides that taste is only 
temporarily lost and that it does not travel by the fifth nerve. Disease 
of the lingual nerve (from the fifth), after the chorda tympani joins it, 
produces loss of taste {ageusia); disease of the lingual above the juncture 
or disease of the central part of the fifth does not result in loss of taste. 
It is thought that the gustatory fibers of the fifth run with the chorda 
to the seventh nerve which they leave by the petrosal nerve to again 
reach the fifth through Meckel's ganglion. Anesthesia of the tongue 
may result from facial neuritis and middle-ear disease. 

56 



882 DISEASES OF THE CRANIAL NERVES 

Diagnosis. — Organic irritation characterized by pain alone may be 
difficult to differentiate from trifacial neuralgia, although there is less 
radiation and more hyperesthesia in organic irritation. When all branches 
are anesthetic the disease probably lies at the base of the brain or in the 
Gasserian ganglion. In disease of the mid-pons the first division alone 
may be affected; in disease at its side all divisions are involved, often 
with implication of the third, sixth or less often seventh and eighth 
nerves. 

Treatment. — Counter-irritation may induce ulceration. Galvanization 
is said to be beneficial. Gelsemium, cocaine and morphine must be used 
at times because of severe pain, but the acquisition of drug habits must 
always be borne in mind. Boric acid and castor oil should be dropped in 
the eye several times daily. Antisyphilitic remedies are tried in doubtful 
cases. 

Masticatory Spasm. — Romberg's spasm is not common. In the tonic 
type (trismus) the spasm is usually bilateral and the tense muscles are 
hard and may be tender. The cause may be tetanus, hysteria, epilepsy, 
tetany, tumor in the pons, cortical hemorrhage, or it may be reflex from 
trigeminal irritation, as from temporomaxillary disease or dental caries. 
The rare clonic type may be serial or intermittent; chattering of the teeth 
is an example. It may occur in chorea, epilepsy or hysteria. Grinding 
of the teeth occurs in paretic dementia, meningitis or typhoidal states. 
Treatment consists of tonics, galvanization, blisters and morphine and 
cocaine locally. 

Progressive Facial Hemiatrophy. — Of this affection, first described by 
Parry (1825), about 200 cases are reported. Its pathogenesis is obscure, 
but it is described here because the only autopsy on record showed 
neuritis of the ascending root of the fifth nerve. Mobius holds that acute 
infections, as measles or scarlatina, are causal, some virus entering through 
the skin or tonsils and resulting in atrophy. The essential change is a 
facial hemiatrophy, which develops most often in persons between ten 
and fifteen years of age, in girls (66 per cent.) and in 60 per cent, affects 
the left half of the face. In some half-dozen cases the atrophy was 
bilateral. The cardinal sign is atrophy of the skin, which is blanched and 
shrunken ; its fat disappears and later the muscles waste and the rough 
skin lies directly on the bone. The hair, eyebrows and beard on the 
affected side lose pigment and may fall out, sweat secretion is lessened 
and the mouth is drawn toward the side of lesion. The bones waste, 
especially in young subjects, most notably the maxillae, but even the 
smaller bones and nasal cartilages. On the wasted side there may be 
no vasomotor reaction; sensation is usually normal, although pain or 
paresthesia may be noted. The tongue, tonsils and palate are rarely 
involved. The course is very chronic and practically always progressive, 
possibly with remissions. The outlook is hopeless. There is no treatment 
other than thyroid extract; the injection of paraffin to lessen the facial 
deformity is dangerous. 

Facial Hemihypertrophy. — Facial hemihypertrophy, of which only 13 
cases are on record, affects largely the cheek; Werner collected 9 con- 
genital cases. Irritative neuritis is its suspected cause. 



SEVENTH OR FACIAL NERVE 883 



SEVENTH OR FACIAL NERVE. 



The face is represented in the lower Rolandic cortex, whence the 
fibers run through the corona, internal capsule, crus and pons (q. v.), 
where they decussate and enter the nucleus of the opposite side. The 
nucleus lies in the floor of the fourth ventricle inside of the ascending 
branch of the fifth nerve and receives fibers from the third nucleus above 
for the orbicularis of the eye (whereby ocular movements, winking and 
accommodation are coordinated) and fibers from the hypoglossus below 
for the orbicularis oris (whereby correlation of lingual and labial move- 
ments is effected). It curves around the sixth nucleus, emerging near 
the juncture of the pons and medulla, and enters the auditory meatus 
with the eighth nerve, bends sharply, and presents a ganglionic swelling 
which receives the large superficial petrosal from the Vidian nerve, 
containing fibers of taste from the fifth nerve. These latter again leave 
the facial nerve by the chorda tampani. In the Fallopian canal the facial 
nerve gives off branches as follows: (a) a motor branch to the tympanic 
plexus; (b) a motor twig to the stapedius muscle; (c) the chorda tympani 
nerve with secretory branches to the salivary glands. Passing through 
the stylomastoid foramen, it supplies (i) a few sensory branches to the 
external ear; (ii) motor fibers to the external auricular muscles; (iii) 
motor fibers to the posterior part of the occipitofrontalis; and (iv) in 
the parotid gland breaks up into branches which supply all the muscles 
of the face, the platysma, stylohyoid and post, belly of the digastric. 

Peripheral Facial Paralysis. — Prosoplegia, Bell's paralysis (Bell, 1830), 
is the most frequent peripheral palsy. 

Etiology. — 1. Neuritis is the usual cause. Exposure to cold ("rheu- 
matism") produces 73 per cent, of cases, especially in men between the 
twentieth and fortieth years. Angina, gout, diabetes, diphtheria, typhoid, 
erysipelas, mumps, sepsis, etc., are occasional causes. 

2. Disease of the petrous portion of the temporal bone (7 per cent.), 
especially caries and otitis media in childhood, is dangerous in proportion 
to the extent of the bone disease; 88 per cent, of cases of labyrinth 
disease cause facial paralysis. 

3. Trauma causes 6 per cent, of cases, as basal fracture by tearing, 
hemorrhage, inflammation or undue formation of callus; much more 
rarely meningeal or cerebellar hemorrhage at birth; the use of obstetrical 
forceps and trauma to the jaw or surgical operations on the parotid 
gland. Facial paralysis may occur in "head tetanus." 

4. In intracranial lesions at the base, syphilis (3 per cent.) should 
always be considered; syphilis rarely causes peripheral facial paralysis. 

'Aneurysm, tumor, meningitis and hemorrhage usually involve the closely 
contiguous eighth nerve. 

5. In the pons the root fibers or nucleus may be affected, usually 
with the sixth nerve of the same, or the arm and leg of the opposite 
side. Degenerative affections, as tabes, bulbar paralysis, multiple 
sclerosis, progressive muscular atrophy or acute poliencephalitis rarely 
invade the seventh nucleus. 



884 



DISEASES OF THE CRANIAL NERVES 



6. Rarer factors are hemorrhage into the Fallopian canal, disease of 
the parotid or lymphatic glands and leukemic infiltration. 

Pathology. — Few autopsies have been made. The nerve has been found 
severed, its sheath and axis-cylinders destroyed, the nuclei in Schwann's 
sheath increased, the connective tissue increased and the muscles the 
seat of fatty change. The essential and usual change is perineuritis, 
exudation in the sheath compressing the nerve fibers, which undergo 
parenchymatous degeneration. In some cases degeneration only is 
seen; it is probable that slight swelling interferes with conduction. 
Facial neuritis differs from multiple neuritis in that alcoholism is a sub- 
ordinate factor and the chief change is not in its peripheral twigs but 
in the trunk, usually within the Fallopian canal. 



TRSGEMI 



SUPER. MAJOR 



ROOT FACIALIS 

ROOT ACOUSTICUS 

LATE GANGLION 



STYLO-MASTOIO 
FORAMEN 




6PHENO-PALATINE 
GANGLION 



POSTERIOR AURICULAP 
NERVE 



DIACASTRIC NERVE 
STYLOHYOID 



2' QS TO FACE 
AND PLATYSMA. 

Fig. 76. — Relations of the fifth and seventh nerves and branches of the seventh. 



Symptoms. — The affection sometimes begins with headache, pain, 
twitchings in the face, even fever or albuminuria, or without prodromes, 
when one half of the face is suddenly paralyzed and completely immobile 
and toneless within two days. The forehead is smooth, the lids cannot 
close (lagophthalmos), the tears run over the cheek and when a strong 
effort is made to close the eyes the eye on the affected side is turned 
upward by the inf. oblique muscle (Bell's sign). The orbicularis at times 
escapes involvement, since it receives some fibers from the third nerve. 
Smell is impaired because of absence of tears, the nasal aperture is smaller 
and cannot be dilated, sniffing on the affected side is impossible and the 
nasolabial furrow is lost. The mouth is lower from paralysis of the levator 
anguli oris, it cannot be closed and the saliva runs out, although its total 
secretion is often lessened. Labial enunciation is imperfect, puckering 
the lips, as for whistling, is impossible and expectoration is impaired. 
The loss of wrinkles and expression on the affected side is less marked in 
young subjects, especially about the eye, since years lessen the elasticity 
of the skin and the subcutaneous fat. Chewing is impaired by weak- 



SEVENTH OR FACIAL NERVE 885 

ness of the buccinator and food accumulates between the teeth and the 
cheek. The unused half of the tongue becomes furred. The tongue does 
not deviate on protrusion but may seem to, on account of asymmetry 
of the mouth. The tongue is sometimes slightly depressed from weak- 
ness of the stylohyoid and digastric muscles. The platysma paralysis is 
elicited by asking the patient to depress the lower lip. The palate is 
sometimes described as sagging, the speech as nasal, the uvula as deviat- 
ing toward the sound side, but the uvula and palate are often asym- 
metrical in health and there is a tendency to regard the spinal accessory 
as the motor nerve for these structures. 

Taste is lost in disease of the nerve between the geniculate ganglion 
and the offset of the chorda; it is lost in half the cases of "exposure" 
neuritis; it is not impaired in disease of the pons or in disease outside 
the skull. The chorda supplies the anterior two-thirds of the tongue 
and the glossopharyngeal the posterior third. Perverted taste (para- 
geusia) results from irritation of Jacobson's nerve or the tympanic plexus. 
Deafness and tinnitus result mostly from coincident disease of the ear. 
When the stapedius is paralyzed the unopposed tensor tympani (fifth 
nerve) overacts and results in aural oversensitiveness, especially to low 
notes (hyperakusis or oxyokoia). 

All facial reflexes are abolished, with wasting in thin subjects and the 
reaction of degeneration in a week or two in severe cases. In cases of 
moderate severity the excitability may be first increased and then grad- 
ually decreased in seven to ten days. Pain, even anesthesia in the ear 
and tenderness over the nerve trunk are sometimes observed, caused by 
involvement of the fifth nerve or possibly because the facial carries some 
sensory filaments. Sympathetic edema and sweating have been observed. 
Herpes indicates trifacial involvement. The saliva is decreased (the 
fibers for its secretion run with the chorda) and secretion of tears is 
lessened (the fibers from the facial nerve run to the fifth by the large 
petrosal nerve). 

Diagnosis. — The diagnosis is made at a glance in fresh cases; in older 
cases secondary spasm on the paralyzed side may cause confusion. The 
etiological and topographical diagnosis is important. 

1. Supranuclear paralysis, paralysis in the upper neurone, from the 
cortex to the nucleus, is differentiated as follows: 

SUPRANUCLEAR PALSY. VS. PERIPHERAL PALSY. 

Etiology; vascular disease, tumor, etc. Neuritis, ear disease, etc. 

Distribution of paralysis; partial, lower facial Complete; orbicularis and occipitofrontal is 

involved or only slight weakness of orbi- involved. When eyes cannot be closed, 

cularis palpebrarum. probably peripheral or nuclear. 

Reflexes persist and increased. Lost. Paralysis flaccid. 

Taste, auditory, salivary and sensory symp- Often present. 

toms lacking. 

Pilocarpin increases salivary flow. Does not increase it. 

Voluntary motion lost, while emotional Both lost. 

movement very often persists. 

Degenerative reaction and wasting absent. Present. 
Cerebral symptoms present, general as ' Absent. 

headache, or focal as cortical epilepsy, 

alternating paralysis (see cms and pons 

localization). 



886 DISEASES OF THE CRANIAL NERVES 

In lesions of the pons all parts of the facial nerve are affected, wherein 
it differs from facial nerve disease in the internal capsule. In nuclear 
disease the orbicularis oris is less involved or escapes affection, its centre 
being in the hypoglossus nucleus. 

2. Localization in the peripheral type (see Fig. 76) may be (a) in the 
pons (q. v.). General disease of the posterior pons also affects the sixth 
nerve about whose nucleus the seventh nerve curves. (6) In localization 
at the base, taste is not involved and deafness results from coincident 
disease of the eighth nerve, (c) If in the Fallopian canal taste is impaired, 
the salivary flow decreased and hearing often abnormally acute, (d) 
If external to the skull there is no involvement of taste, salivary flow or 
the stapedius. 

Double facial paralysis is rare and usually indicates disease within 
the skull, bulbar paralysis, disease of both sides of the pons or one focus 
in its centre, double otitis, especiallv syphilis, multiple neuritis, tetanus 
or in a form observed in childhood with ocular paralysis (g. v.). Organic 
facial paralysis may exist on one side and an hysterical paralysis on 
the other. 

Prognosis. — Its duration varies from two to three months for moderate, 
and six to eight months for severe cases. Even in cases which seemingly 
recover and in those lasting over a month, some vestige of paralysis 
usually remains. The prognosis depends (1) on the cause; it is favorable 
in syphilis, birth trauma and polyneuritis; in ear disease it is better if 
the drum has not ruptured; it is unfavorable in tumor or nuclear disease; 
(2) on the electrical reaction. If after ten days the irritability is not 
reduced recovery may be expected in about three weeks; if after fourteen 
days it is lowered but not lost, recovery occurs within two months; 
if after fourteen days the irritability is lost, the prognosis is doubtful 
and the course is likely to cover months. Recurrence is infrequent, 
although five attacks are recorded. Contracture (secondary overaction) 
usually occurs in four to six months and progresses for eight to twelve 
months, when it lessens and disappears in mild but remains in severe 
cases. In old subjects it balances up the facial contour; in young subjects 
it produces deformity. It depends on functional alteration of the nucleus. 

Treatment. — (a) The cause should be reached, if possible; antisyphilitic 
remedies and ear-drainage have cured cases even of twenty-three years' 
duration, (b) Antirheumatic drugs do not shorten the course. A mer- 
curial purge, hot fomentations, which must be carefully maintained for 
two or three days, keeping the patient indoors, and a blister over the 
mastoid and one over the side of the neck are beneficial, (c) Correction 
of deformity: The eye should be douched with boric acid, bandaged 
closed during sleep and the lids massaged, the cheek and mouth should 
be massaged upward and a hook in the angle of the mouth (sustained 
by tape over the ear or by adhesive plaster) prevents deformity to some 
extent, (d) Electricity should not be used for two or three weeks, and 
then the galvanic current should be given, for fifteen minutes each 
day, in strength just sufficient to produce muscular contraction; the 
application of the anode over the muscles is the least painful method. 
The faradic current causes pain, (e) For contracture little can be done 






Me eighth or auditory nerve 887 

excepting massage and steaming the face. (/) In irreparable cases, 
surgical transplantation of the facial trunk into the spinal accessory or 
hypoglossus has been successfully performed. 

Facial or Mimetic Spasm (Tic Convulsif).— Etiology. — The causes 
are (a) organic disease in the cortex, pons or nerve trunk, which irritates 
(perhaps later paralyzes) the centre, nucleus or paths. Irritation of the 
fifth nerve is considered causal, (b) There is an idiopathic form, which 
occurs in persons between the fortieth and sixtieth years, most often in 
women with neuropathic or emotional tendencies (see Habit Spasm 
under Chorea) . "(c) There is also a reflex form which results from worms 
or uterine disease. 

Symptoms. — The spasm begins paroxysmally on one side and is more 
often clonic than tonic. The clonic form affects the orbicularis palpe- 
brarum (blepharospasm) and zygomatici most frequently, although the 
frontalis, chin depressors or all the facial muscles may be concerned 
in severe cases. Pain and paresis are absent save in progressive organic 
disease. The spasm is lessened by rest and increased by cold or emotion. 
It may spread to the opposite side or exceptionally to the muscles of 
mastication, tongue, pharynx, larynx, neck or arm. The tonic form is 
seen in photopbobic disease of the eye, paralysis agitans, tetanus, tetany 
or hysteria. 

Prognosis. — The prognosis is unfavorable after the first few months 
and the disease is then likely to last for years or for life. 

Treatment. — Treatment varies with the cause. Trigeminal irritation 
should be removed if possible. Arsenic is beneficial in some cases, but 
nervines and antispasmodics are useless. Some cases are cured by 
galvanization, if tender points are found, freezing of the cheek with 
ethyl chloride, stretching of the facial nerve usually with but temporary 
relief and alcohol injections. 

THE EIGHTH OR AUDITORY NERVE. 

The eighth nerve in the old nomenclature was the portio mollis of the 
seventh pair, the facial nerve being the portio dura; as the names imply, 
the auditory is softer than the facial nerve and therefore less resistant to 
pressure. It is purely sensory and consists of two distinct roots, the 
cochlear and vestibular. At the point where the roots separate is found 
a group of cells, analogous to the spinal ganglia, from which arises 
Wrisberg's nerve, an accessory structure with vasomotor and salivary 
secreting fibers. 

The cochlear nerve is the true auditory nerve and its nuclei are found 
in the floor of the fourth ventricle. It is connected through the teg- 
mentum of the crus and internal capsule with the contralateral and to a 
less degree the homolateral temporosphenoidal lobe. It is distributed 
to the cochlea and ganglionic cells of the organ of Corti. (a) Cortical 
disease (see Bkain Localization) may in rare cases cause word-deafness, 
as may (b) disease of the auditory tracts by lesions of the lateral lemniscus, 
the post. corp. quadrigemina, internal capsule or pons. Nuclear disease 
is almost unknown. Neuromata are rare, but occur on the auditory 



888 DISEASES OF THE CRANIAL NERVES 

trunk oftener than on any other cranial nerve. The nerve trunk may 
degenerate in tabes, (c) Lesions at the base may follow trauma, menin- 
gitis, hemorrhage or syphilis, (d) Most auditory nerve disease results 
from disease of the internal ear, either primary or secondary to disease 
of the middle ear (inflammation, syphilis, degeneration or hemorrhage 
in the labyrinth). There are three prominent symptoms: (a) Nervous 
deafness may result. Deaf-mutism is congenital in 80 per cent, and 
acquired in early life in 20 per cent, of cases. Deafness from occlusion 
of the meatus or from disease of the middle ear is excluded by Rhine's 
test; a vibrating tuning-fork or watch, if held over the meatus, is not 
heard in these affections, but is heard when its base is placed on the 
mastoid which conducts vibrations to the internal ear. In disease of the 
internal ear, bone-conduction is lacking. Differentiation between deafness 
due to disease of the internal ear and that due to bone disease is only made 
by means of the associated symptoms. The treatment of nervous deafness 
is etiological. Iodides are sometimes beneficial, as are full doses of pilo- 
carpine. Electricity is useless, (b) Auditory hyperesthesia may result 
from central or peripheral disease. In genuine hyperesthesia (hyperacusis) 
sounds are heard by the patient which other individuals may not hear, 
as in hysteria, epilepsy, migraine, meningitis, acute mania and at times 
after use of caffeine, alcohol or opium. Spurious hyperacusis results 
from paralysis of the stapedius. In dysacusis ordinary sounds cause 
disproportionate sensations or discomfort; this is common in headache 
and cerebral disorders, (c) Tinnitus aurium designates subjective dis- 
tressing and intractable sensations, as ringing, roaring or whistling in 
the ears. In 80 per cent, of cases it is caused by disease of the internal 
ear. It may also occur in any disease of the middle ear, when there is 
cerumen or foreign bodies in the external meatus, or occlusion of the 
Eustachian tube, when the individual is subject to long exposure to loud 
sounds, as in boiler factories, and in the neuroses (hysteria, neurasthenia, 
migraine, epilepsy), aneurysm, anemia, gout or cinchonism. Sounds of 
centric origin are usually continuous and sometimes elaborate. Wax 
or bilateral labyrinthine disease may also cause continuous tinnitus, 
while in anemia or aneurysm, these sensations are intermittent. Hearing 
may be hyperacute, deranged or lost. Spasm of the palate or musculature 
of the Eustachian tube may produce a most annoying snapping sound, 
at times audible to bystanders. Treatment depends on the cause. 
Bromides are most useful, combined with a few drops of the tr. bella- 
donna or cannabis indica. Quinine and salicylates seldom give relief. 
Full doses of nitroglycerin relieve certain cases and counter-irritation 
over the mastoid sometimes mitigates tinnitus. 

The vestibular nerve arises from the medulla, supplies the vestibule 
and semicircular canals, subserves sensation of space and equilibration 
and has cerebral and cerebellar connections. 

Meniere's Disease, Auditory Vertigo (Vertigo ab aure laesa). — Paul 
Meniere, in 1861, described a syndrome consisting of vertigo, tinnitus, 
vomiting and sometimes deafness, developing with apoplectiform sudden- 
ness and due to acute labyrinthine disease. The lesion is usually a slightly 
irritative disease of the vestibular nerve, which supplies the organs of 



THE EIGHTH OR AUDITORY NERVE 889 

equilibration, the semicircular canals. According to Gowers, 80 per cent, 
occur in persons between the thirtieth and sixtieth years, 66 per cent, 
in males, and 90 per cent, of all cases of vertigo not due to epilepsy or 
organic brain disease are caused by lesions of the labyrinth. Frankl- 
Hochwart classifies Meniere's complex as follows: (a) Apoplectiform 
cases, which occur in healthy ears, of which few more than 30 cases 
are recorded, due to labyrinthine hemorrhage or to trauma; leukemia 
and arteriosclerosis are promoting factors and it is thought that acute 
angioneurotic transudation of lymph may occur in the canals, (6) 
Cases developing in ears already acutely or chronically diseased; the 
internal ear is the usual seat of disease, but the external or middle ear 
may be affected or the branches of the eighth nerve, perhaps by tumors, 
syphilis, tabes, paretic dementia, gout, cold, facial paralysis or quinine 
and salicylates, (c) External influences, are pressure on the drum by 
violent douching of the ear; (d) pseudo-Meniere's disease, which occurs 
in epilepsy, hysteria, neurasthenia, migraine or sea-sickness. 

Symptoms.— The symptoms begin gradually or suddenly, with occa- 
sionally momentary loss of consciousness; the paroxysms may be sepa- 
rated by weeks or months or perhaps occur daily, (a) The vertigo is 
subjective or objective, perhaps combined; the patient cannot stand; 
he is likely to fall backward or if standing is possible is ataxic. These 
symptoms indicate lesion in the vestibular nerve; slight vertigo may 
persist between paroxysms. (b) Nausea and vomiting are usual, save 
in the lighter forms and are often attended by headache, sometimes 
collapse, pallor and clammy skin and rarely by death, (c) The tinnitus 
of a roaring throbbing character and (d) nervous deafness, which is usually 
not absolute, indicate disease of the cochlear nerve. Nystagmus, double 
vision and ataxia are occasional symptoms and result from the relations 
between the labyrinth, cerebellum and cerebrum. Acute or progressive 
disease is unfavorable. The vertigo may cease when complete destruction 
of the nerve results in deafness. Some cases recover. 

Diagnosis. — Aural vertigo constitutes 90 per cent, of vertigo. Differ- 
entiation is as follows : (a) Gastric disease may cause vomiting and vertigo 
(a stomacho l&so) but does not produce tinnitus or deafness. Gastric 
vertigo was once thought to cause 80 per cent, of cases of vertigo; now, 
but 5 per cent, are attributed to it (Gowers). Many of these cases are 
neurotic. (6) Epilepsy, especially petit mat, may produce vertigo, very 
rarely tinnitus or deafness and much oftener loss of consciousness, (c) 
Cardiac disease, as aortic regurgitation or arteriosclerosis, may cause 
vertigo but not the other symptoms, (d) Organic brain affections, as 
tumor, have other distinctive signs, as headache or focal lesions. Con- 
fusion is possible with arteriosclerotic vertigo, and especially with coinci- 
dent accidental deafness, (e) Ocular vertigo ceases on closing the eyes. 
Gerlier (1887) described a form endemic in France, Switzerland and 
Japan, and characterized by vertigo, great depression, paretic weakness 
of the neck and limbs, ptosis, strabismus, diplopia and retinal hyperemia, 
hemorrhage or edema. Recovery occurs in one to four months. 

Treatment. — Labyrinthine disease is little influenced by drugs, except 
when syphilis and gout are its causes. Quinine, salicylates and nitro- 



890 DISEASES OF THE CRANIAL NERVES 

glycerin should be given (see Tinnitus). Bromides are most useful 
in daily doses of one dram. Galvanization with the anode over the ear 
and cathode to the neck seemingly has helped some cases, as have blis- 
ters over the mastoid. Disease of the pharynx, Eustachian tube and 
accumulation of wax must be treated. Removal of the malleus and 
incus with mobilization of the stapes relieves a few cases. 

NINTH OR GLOSSOPHARYNGEAL NERVE. 

This nerve is almost inseparably connected in its origin, course and 
functions with the vagus and the internal part of the spinal accessory 
nerve. Compared with disease of the first eight cranial nerves, affections 
of these visceral nerves are infrequent. Of all the cranial nerves, the 
ninth is least understood and is never alone diseased. The causes of 
its disease are the same as those of the vagus (v. i.). 

It is distributed as follows: (a) its sensory fibers supply the back of 
the tongue, pharynx, soft palate, tonsil, upper pharynx, Eustachian 
tube and tympanic cavity. It is probably the nerve of nausea, (b) 
Its motor fibers supply the upper pharynx and possibly the palate. 
(c) Taste fibers are usually thought to be distributed to the posterior 
third of the tongue and palate, but they are not found in the nerve 
root and are considered to pass through the fifth nerve to the brain. 
Increased flow of saliva and loss of taste on the root of the tongue may 
result from disease of the middle ear due to relations between the nerve 
of Jacobson (ninth) and the branches of the fifth nerve. The nerve is 
thought to regulate contractions of the pharynx, which become frequent 
(spasms) in disease or on section of the nerve. 

TENTH OR VAGUS NERVE. 

Arising in the medulla, it has with the internal part of the spinal 
accessory nerve an enormously diffuse and important visceral distribu- 
tion. It is a mixed nerve, the motor fibers originating from the nuclei 
and the sensory fibers from the jugular and plexiform ganglia; the vagiis 
carries the sensory and the accessorius, motor fibers. 

Etiology. — Affections of the vagus result from: (a) Nuclear disease, 
as degenerative bulbar palsy or acute vascular lesions, which usually 
also involve other nuclei; (b) involvement of the root and trunk by 
meningitis, syphilis, caries, trauma, aneurysm of the arch or its branches, 
carcinoma, esophageal growths, tuberculous or other adenopathies, 
pleural (right-sided) or pericardial effusions or adhesions, mediastinitis, 
goitres, operations on the neck or rarely neuroma and neuritis from 
diphtheria or other infections, tabes or plumbism. Cortical, especially 
functional, causes may occasion symptoms. 

Pharyngeal Branches. — The pharyngeal plexus consists of branches 
from the ninth and tenth nerves. In paralysis, sensation and the pharyn- 
geal reflex are lost; bilateral disease causes dysphagia. The stomach- 
tube can be introduced without sensation or spasm. Pulpy foods are 
better swallowed than dry foods or fluids. Food is likely to enter the 



TENTH OR VAGUS NERVE 



891 



larynx and when the palate is involved there is regurgitation into the 
nose and nasal speech results. The palate is probably supplied by the 
accessory nerve. Spasm is always functional, transient 6v recurrent, 













Fig. 77. — The laryngeal paralyses: 1, normal phonation; 2, normal deep inspiration; 
S, normal cadaveric position; A, bilateral adductor palsy; attempted phonation; B, left 
adductor palsy; attempted phonation; C, bilateral abductor paralysis; deep inspiration; 
D, left abductor paralysis; deep inspiration; affected cord in cadaveric position; E, left 
abductor paralysis; phonation; affected cord in cadaveric position; right cord crossing 
median line; F, bilateral thyro-arytenoid paralysis; G, bilateral thyro-arytenoid paralysis 
and paralysis of arytenoideus, giving an hour-glass opening. (From Church's Nervous 
Diseases.) 



does not allow of introduction of the stomach-tube and includes the 
globus hystericus, esophagismus, pharyngismus, false and genuine hydro- 
phobia and the pharyngeal crises of tabes. The esophagus is rarely 
affected except in diseases of the centres or trunk. 



892 DISEASES OF THE CRANIAL NERVES 

Laryngeal Branches. — The superior laryngeal is (a) the sensory nerve 
for the larynx above the vocal cords, (b) the motor nerve for but one 
larynx muscle, the cricothyroid, which modulates the voice by regulating 
tension in the cords, and (c) the motor nerve for the depressors of the 
epiglottis, the thyro-epiglottic and aryepiglottic muscles, paralysis of 
which causes the epiglottis to stand upright, thereby risking aspiration 
of food and pneumonia. 

The recurrent laryngeal curves around the aorta on the left and the 
subclavian artery on the right side; (a) it is the sensory nerve to the 
larynx below the cords and the trachea and (b) is the motor nerve to 
every intrinsic larynx muscle except the cricothyroid. 

Treatment. — Paralysis is usually peripheral (v. i. table). In nuclear 
tvpes there is no therapy. Suggestion is valuable in hysterical forms. 
The faradic current may be used with the positive pole to the forehead 
and the negative to the larynx externally or internally. Other measures 
include laryngeal gymnastics, in which the patient repeatedly attempts to 
speak, intralaryngeal insufflations of alum, the administration of strychnine 
hypodermically and Ollivier's procedure, in which the thyroid cartilage 
is compressed between the index-finger and thumb during inspiration and 
expiration, while the subject attempts to phonate. Tracheotomy and 
nasal feeding are sometimes indicated. 

Anesthesia and Hyperesthesia of the Larynx. — Anesthesia of the larynx 
is rare, but may occur uni- or bilaterally in disease of the sup. laryngeal 
nerve, the vagus roots, its nucleus or in the hemianesthesia of hysteria 
or organic brain disease. In nuclear disease it is partial; in affections 
of the nucleus, root and trunk the reflexes are lost, but they are present 
in supranuclear and functional affections. Hyperesthesia is rarer, being 
observed in neurotics as a tickling, tendency' to cough or spasm; neuralgia 
and crises also occur. 

Laryngeal Spasm. — The most common form of laryngeal spasm is 
spasm of the adductors, which are concerned in reflexes inimical to 
entrance of foreign bodies into the larynx; it may result from centric, 
local (laryngitis with croup-like cough at night) or reflex irritation 
from distant or neighboring foci, as elongated uvula, goitre or hyper- 
trophy of the pharyngeal tonsil. It includes laryngismus stridulus, 
which occurs in children under three years of age and is due to rickets 
in 66 per cent, of cases, tetany, and reflexly to alimentary disorders; 
it comes on at night or on awakening in the morning, with croup-like 
cough, and presents all the symptoms of acute suffocation, as stridor, 
pallor, cyanosis, wide pupils, protruding eyes, low diaphragm, involuntary 
evacuations, centric vasomotor and cardiac disturbances and convulsions 
either generalized or of the infantile carpopedal type. The attacks last 
from a few seconds to one-half or one minute and are sometimes at- 
tributed to loss of temper when they follow a reproof. In the adult, 
laryngeal spasm occurs in tabes, hysteria, tetany, hydrophobia, epilepsy 
(the initial cry), asthma or migraine. The attacks are recognized by 
the negative larvngoscopic findings, paroxysmal occurrence and the stridor 
being manifest in both inspiration and expiration. Partial spasm occurs 
in some types of stuttering, clergymen's sore throat and explosive, 
unmodulated speech. 



TENTH OR VAGUS NERVE 



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894 DISEASES OF THE CRANIAL NERVES 

Nervous cough is present in the explosive hysterical type, in the metallic 
ovarian form in young girls and in the barking variety in young mas- 
turbators. 

Treatment. — Treatment of spasm includes removal of local irritation, 
as affections of the ear (which has branches from the vagus) or pharynx, 
hygiene, tonics, as cod-liver oil in children, and such immediate measures 
as thrusting a finger into the throat, dashing water in the face, hydro- 
therapy and for the attack chloral and bromides by enema, local applica- 
tion of cocaine, inhalation of chloroform and in adults nitrite of amyl 
and morphine. 

Pulmonary Branches. — The vagus and the sympathetic form the pul- 
monary plexus. Afferent fibers convey sensory impressions to the 
respiratory centre; these include accelerating fibers which predominate, 
and inhibitory fibers, stimulation of which (sup. laryngeal nerve) arrests 
breathing. Afferent impulses are also carried to the vasomotor centre. 
Efferent motor impulses are conveyed to the bronchi. Division of the 
vagus causes rapid congestion of the lungs with hemorrhage (also observed 
in acute lesion of the pons) and slower but deeper breathing; stimulation 
of the divided end of the nerve accelerates breathing even to its tetanic 
arrest. Bronchopneumonic foci are not trophic but aspiration pneumonia 
from paralysis of the palate and larynx. The pulmonary twigs are 
probably concerned in Cheyne-Stokes's breathing, bronchial asthma and 
hiccough. 

Cardiac Branches. — The vagus and sympathetic nerves constitute the 
cardiac plexus, (a) Motor fibers from the spinal accessory nerve inhibit 
and coordinate cardiac action, which is sometimes under the control 
of the will; the heart may at times be slowed by pressure on the neck; 
marked irritation of the vagus slows or even arrests the heart. Bilateral 
division may cause sudden death. Paralysis of these fibers allows the 
sympathetic accelerator fibers to dominate, producing arrhythmia and 
tachycardia. Digitalis is ineffective in vagus paralysis, (b) The sensory 
fibers are concerned in the cardiac neuroses (q. v.). (c) These fibers 
are probably trophic, as Eichhorst's experiments show fatty myocardial 
degeneration on division of the vagi. 

Gastric Branches. — (a) Motor branches supply part of the stomach; 
they cause nausea and are concerned in reflex, direct or centric vomiting, 
as in brain lesions, Avherein the vomiting usually occurs without nausea. 
(6) Sensory branches; the vagus is the nerve of hunger and thirst, and 
its disease often causes anorexia and loss of thirst. Centric disease 
causes the gastric crises of tabes and cortical functional disease produces 
the epigastric aura of epilepsy and perhaps gastralgia in the neuroses. 
Vertigo probably causes vomiting through the vagus. Intestinal and 
splenic symptoms are lacking. 



ELEVENTH OR SPINAL ACCESSORY NERVE (EXTERNAL PORTION). 

The internal, minor part runs with the vagus, while the major, external 
segment is a spinal motor nerve, arising from the lateral portion and 



ELEVENTH OR SPINAL ACCESSORY NERVE 895 

ant. horns of the cord between the sixth cervical segment and the medulla. 
It courses upward through the foramen magnum into the cranium. 
It is the chief supply of the sternomastoid muscle and the upper part 
of the trapezius, the lower two parts of which are usually supplied by 
the cervical and upper dorsal nerves. 

Paralysis. — Paralysis is rarely caused by cortical disease, because the 
muscles have bilateral representation. The usual causes are bulbar 
paralysis, lesions near the foramen magnum, meningitis (usually with 
involvement of the inner accessory branches and the twelfth nerve), 
syphilis, trauma, tabes, syringomyelia, progressive muscular atrophy, 
caries or tumor of the spine, or neuritis. The symptoms are paralysis of 
(a) the sternomastoid, in which there is impaired rotation of the face to 
the side opposite the lesion; in old cases contracture turns the face 
toward the paralyzed side, (b) That part of the trapezius from the occi- 
put to the acromion is paralyzed, showing a concave instead of a straight 
line, best seen in deep inspiration or shrugging the shoulders. (Paralysis 
of the second portion causes imperfect elevation of the arm, some droop- 
ing and winging out of the scapula, the lower part of which is drawn 
toward the spine by the rhomboids and lev. anguli scapulae; paralysis of 
the third portion results in weakness in the adduction of the scapula 
to the spine.) If it is bilateral, the head falls forward or backward as 
the sternomastoids or trapezii, respectively, are affected. In peripheral 
disease there are wasting and the reaction of degeneration. 

Accessory Spasm, Spasmodic Torticollis or Wryneck. — Etiology. — It 
occurs in women in 66 per cent, of cases (Gowers). A neurotic tendency, 
trauma, overexertion, infections, alcoholism, plumbism, cervical caries, 
brain tumor and diseases of the eye and ear (torticollis ab oculo la?so, 
ab aure lsesa) are among its uncertain causes. 

Symptoms. — The symptoms vary as the affection is clonic or tonic, 
unilateral or bilateral, and with the number of muscles involved. One 
sternomastoid is generally involved, especially in tonic spasm, in which 
the occiput is turned to the diseased side, the face to the opposite side 
and the ear nearer the clavicle. The upper part of the trapezius comes 
next in frequency of involvement and is affected equally by clonic and 
tonic spasm. The affected shoulder is raised and slightly rotated, the 
scapula drawn toward the spine and the head backward. The spine is 
often convex toward the diseased side. The splenius is half as frequently 
affected, the head being drawn backward, the face a little to the affected 
side and upward. Less often the scalenus, platysma, rectus and obliquus 
capitis are affected. The muscles in tonic spasm are hard, prominent 
and sometimes hypertrophied. Clonic spasm disappears during sleep, 
is increased by fatigue and may also invade the face, neck, eye-balls, 
vocal cords or the arm. There may be pain, fatigue and rarely tender 
spots from compression of the brachial plexus by the scaleni. Bilateral 
clonic or tonic spasm of the trapezius draws the head backward (retro- 
collic spasm) and always involves the frontalis muscle. 

Course and Prognosis. — The onset is gradual, the disease is usually 
stationary or progressive in its course, rarely recurrent; recovery is 
infrequent. The outlook is generally grave in well-developed types. 



896 DISEASES OF THE CRANIAL NERVES 

Diagnosis. — (a) In congenital or fixed wryneck there is no active spasm. 
One sternomastoid (but rarely the trapezius) shows atrophy, induration 
and cicatrization, due to traction on the neck during delivery or perhaps 
from a central lesion; 70 per cent, occur in left occipito-anterior pre- 
sentations. The disease escapes notice for years because of the shortness 
of the child's neck. Wilks always found facial asymmetry. Tenotomy 
cures it. (b) Hysterical torticollis occurs in subjects under thirty years 
of age; other stigmata usually develop. Bompaire and Brissaud describe 
a mental torticollis, clearly a psychical phenomenon, (c) In children 
clonic spasms, especially in the deep muscles, lead to nodding, salaam 
movements, spasmus nutans, nictitatio spastica. The affection may 
develop from reflex dental or digestive disorders or from organic cerebral 
disease. It is sometimes habit spasm, hysteria, epilepsy or idiocy. 

Treatment. — Treatment is etiological. Nervines, sedatives and electric- 
ity seldom produce permanent results. Morphine is a dangerous agent, 
although its local hypodermic use has led to recovery. Massage and 
deep compression are occasionally helpful. In chronic cases resection 
of the accessory nerve is indicated. If many muscles are involved the 
third and fourth cervical nerves are also resected. 

THE TWELFTH NERVE. 

The hypoglossal is purely motor. Paralysis of the tongue is (a) 
rarely cortical; supranuclear glossoplegia from lesions between its centre 
and the frontal convolutions, almost always occurs with hemiplegia and 
paralysis of the lower facial fibers; there is no wasting or reaction of 
degeneration. The root of the tongue is higher (hyoglossus paralysis) 
and on protrusion the tongue deviates to the paralyzed side, being pushed 
over by the sound genioglossus. (b) Nuclear paralysis occurs in bulbar 
paralysis, sometimes in tabes or paretic dementia, and much less fre- 
quently in acute inflammation or softening in the medulla. Nuclear 
lesions are bilateral since the nuclei are closely contiguous, and cause 
the reaction of degeneration and wasting, the mucosa being wrinkled 
over the atrophic half. Fibrillation is frequent, as in paretic dementia, 
from cortical and nuclear changes. In bilateral glossoplegia the tongue 
cannot be protruded, there is impairment of the first act of swallowing, 
in chewing and articulation, all of which are but slightly marked in 
unilateral paralysis, (c) Intranuclear paralysis results from lesions near 
the surface of the medulla, which may produce unilateral paralysis of 
the tongue, palate and vocal cord. Contralateral hemiplegia may occur. 
Syphilis, trauma or tumors are causal; there are recorded only 40 cases 
• of peripheral, isolated hypoglossal paralysis (Panski, 1903). Wasting, 
the degenerative reaction and fibrillation are present. Treatment is that 
of other paralyses. 

Spasm. — The tonic or clonic form is rare. It occurs in chorea, facial 
spasm, certain types of stuttering, epilepsy (in which the tongue is 
bitten), hysteria (in which the tongue is rarely bitten), psychoses, 
meningitis, neurotic spasm in speakers (aphthongia) or musicians. The 
prognosis in general is favorable. 



THE PHRENIC NERVE 897 



DISEASES OF THE SPINAL NEKVES. 

The spinal nerves differ from the cerebral in that they contain sensory, 
motor and vasomotor fibers. Disease or injury therefore suspends 
motility and sensation, causes vasomotor paralysis, trophic changes, 
the reaction of degeneration, atrophy and contracture. 

THE PHRENIC NERVE. 

Paralysis. — (a) Disease or trauma of the vertebrae, cord, membranes 
or of the third, fourth and fifth cervical nerves of origin may cause it. 
In disease of the cord other paralysis is always present. (6) Its trunk 
may be injured in its course or damaged by aneurysm, tumors or pleurisy. 
Neuritis sometimes occurs in multiple neuritis or tabes, etc. 

Symptoms. — The diaphragm is paralyzed, usually on both sides. 
The abdomen retracts on inspiration and bulges on expiration, the 
converse of its normal movements. Litten's sign is absent and there is 
no inspiratory descent of the liver or spleen. Blowing, coughing and 
pressing at stool are impossible. Costal breathing is exaggerated, the 
accessory muscles are strongly in play, dyspnea and cyanosis are present, 
especially on exertion, and coincident bronchitis may cause most alarming 
symptoms from stagnation of mucus. The nerve may be tender in the 
neck. 

Diagnosis and Treatment. — Costal, hysterical breathing may at first 
cause confusion, as may inflammation from diaphragmatic pleurisy. The 
outlook is grave. It is more favorable in syphilis, lead or diphtheritic 
neuritis than in the alcoholic form. Treatment is that of the cause but 
is usually futile. Faradic, phrenic stimulation is sometimes beneficial, as 
in apparently asphyxiated newborn infants. 

Phrenic Spasm. — 1. In clonic spasm, singultus or hiccough, the dia- 
phragm spasmodically contracts with a sound due to sudden closure of 
the glottis, sometimes 50 to 100 times a minute. Probably the vagus 
and respiratory centres are involved, for dyspnea, dysphagia or dysarthria 
may occur. Clonic spasm occurs (a) in inflammation, either thoracic 
(pleurisy, pericarditis) or abdominal (peritonitis, appendicitis, obstruc- 
tion); (b) in irritation, esophageal, mediastinal, hepatic or gastric, 
directly or reflexly; (c) in nervous affections, as centric disease or the 
neuroses; and (d) in toxemia, uremia, etc. Treatment is that of the cause. 
Gastric lavage; apomorphine; circular constriction of the lower chest 
with the head bent forward; attempts to sneeze, cough, breathe deeply 
or press down with the glottis closed; faradization, blistering the neck 
and epigastrium; asafetida, chloral or bromides; and narcotics and 
inhalations of chloroform or amyl nitrite may be beneficial. 

2. Tonic phrenic spasm is rarer. The causes are tetany, epilepsy, 
tetanus and hysteria. The diagnosis is easy. The lower chest and upper 
abdomen are distended and often sensitive; the upper chest moves 
rapidly and forcibly, with the accessory respiratory muscles in full play; 
there is no respiratory excursion, the lungs are acutely distended, the 
57 



DISEASES OF THE SPINAL NERVES 

abdominal viscera are luxated downward, there is dyspnea and cyanosis, 
and death may result. Treatment consists of the application of heat, 
blisters and the faradic current to the lower chest and chloroform 
inhalations and morphine internally. Analogous spasm may occur in 
the respiratory muscles, as yawning, sneezing, coughing, laughing and 
weeping spasms, possibly from vagus disease or from the neuroses, 
psychoses, multiple sclerosis, bulbar paralysis or disease of the ear, nose 
or stomach. 

THE POSTERIOR THORACIC NERVE. 

This nerve is often affected in its long course, from trauma, muscular 
strains in overhead work (the nerve originates in the scalenus medius) 
and from carrying loads on the shoulder — whence its occurrence in men 
in 90 per cent, of cases; it is also involved in muscular atrophies and 
neuritis. The results are impaired fixation of the scapula, movement of 
the arm and inspiration. The scapula wings out when the arm is moved 
forward and stands less obliquely than normal, its outer part moving 
forward, while the lower angle is drawn in by the rhomboids and 
trapezius. The sole sensory change is pain in the neck and shoulder. 
The course is tedious and rest, especially of the scaleni, is the prime 
indication. 

SUPRASCAPULAR NERVE. 

It originates in the fourth, fifth and sixth cervical nerves and is affected 
in disease of the plexus or alone in trauma, shoulder dislocations or falls 
on the hands. The supraspinatus and infraspinatus are paralyzed, 
giving some weakness in fixation of the humerus, as uncertainty in writing, 
turning up and in of the lower scapular angle, some anesthesia over the 
scapula, frequently shoulder-girdle pain and often involving the circum- 
flex nerve, which arises from the fifth, sixth and seventh cervical nerves 
of the posterior cord of the brachial plexus. Deltoid paralysis (dislocation, 
crutch paralysis, plexus disease) produces inability to deviate laterally 
the arm, changes in the shoulder, which becomes angular, sometimes 
adhesions in the joint, probably trophic from its articular branch and 
anesthesia over the lower part of the deltoid. It may be confused with 
primary joint disease, in which, however, the scapula follows the arm 
movements. 

THE MUSCULOSPIRAL NERVE. 

Arising from all the roots in the plexus except the first dorsal and 
curving around the humerus, it is the most exposed and most fre- 
quently injured nerve in the arm or body; injuries result from fract- 
ure, callus, blows, muscular exertion, carrying heavy weights, tying the 
arm to the side or behind the back, sleeping with the arm over the back 
of a chair, especially in alcoholics, lifting the arms during surgical anesthesia 
and from a tight Esmarch's constrictor; less often injury results from cold 
or lead palsy. Musculospiral (radial) paralysis involves (a) the extensors 
of the upper extremity; i. e., the triceps, so that the elbow cannot be 
extended, and the supinators; the triceps sometimes escapes affection; 



THE ULNAR NERVE 899 

the supinator longus is not involved in lead palsy or traumatism below 
the lower third of the humerus and in centric disease it escapes because 
its centre is with the flexors. The extensors of the wrist are involved, 
producing marked atrophy of the back of the forearm and the char- 
acteristic wrist-drop; the extensors of the thumb and fingers are affected; 
they become semiflexed and can only be extended by the interossei (ulnar 
nerve) after the first phalanges are passively extended. Changes in the 
synovial sac or bones of the dorsal w r rist produce the painless carpal 
tumor of Gubler, from involvement of branches to the wrist or the mere 
mechanical action of flexion (see Lead Intoxication), (b) Sensory 
disturbance, slight compared with the palsy, may rarely cause anesthesia 
over the deltoid and back of the forearm or more often over the radial 
side of the dorsum of the hand, thumb, index and half of the middle 
finger. Most cases recover with rest and immobilization. Flexor con- 
tracture can be avoided by splints. 

THE MEDIAN NERVE. 

The median nerve originates from the outer and inner cords of the 
plexus and contains fibers from all its cervical roots. Isolated paralysis 
is not common. It results from trauma, fractures, stabs, carrying weights 
in the bend of the elbow and sleeping on the arm. (a) Motor symptoms 
are conspicuous. Both pronators are involved, besides all flexors of the 
forearm, wrist and fingers except the flexor carpi ulnaris and the ulnar 
part of the deep flexor of the third and fourth fingers. In the hand, the 
palmaris longus, the abductor, opponens and short flexor of the thumb 
(resulting in flattening of the thenar prominence and the "ape-hand" 
from the index-finger and thumb lying parallel) and the two radial 
lumbricales are affected. The second phalanges cannot be flexed on the 
first (save in the two ulnar fingers); flexion of the first phalanges by 
the interossei is possible; metacarpophalangeal subluxation may result 
from the unopposed extensor action of the interossei on the second and 
third phalanges. The paralyzed muscles may waste and trophic mani- 
festations are common, (b) Sensory symptoms are often slight. Anes- 
thesia, if present, is greatest in the palm, front of the thumb, first two 
fingers and half of the third. 

THE ULNAR NERVE. 

Its origin is from the last cervical and first dorsal nerves; its superficial 
course at the inner condyle, forearm and wrist, exposes it to injury, as 
by dislocation of the elbow T , cuts and pressure on the elbow during sleep 
and work. Neuritis occasionally causes paralysis. It must be dis- 
tinguished from spinal disease, which ascends from the dorsal to the 
cervical region; this form is usually bilateral and is preceded by ulnar 
anesthesia in tabes and paretic dementia (Biernacki). The flexor carpi 
idnaris is paralyzed (the hand deviates to the radial side in attempts 
at flexion), and also the ulnar half of the deep flexors of the fingers, the 
muscles of the little finger, palmaris brevis, the interossei, the third and 



900 DISEASES OF THE SPINAL NERVES 

fourth lumbricals, the adductor and inner head of the short flexor of the 
thumb (the thumb being rotated toward the palm). The first phalanges 
cannot be flexed nor the others extended, although this is less marked 
in the first and second fingers, in which the lumbricals are supplied by 
the median nerve. The "claw-hand" results; the hypothenar eminence, 
palm and interosseous spaces become thin. Sensory loss is limited to the 
back and front of the ulnar side of the hand, the dorsum of two and a 
half fingers and the front of one and a half fingers on the ulnar side. 

Combined Paralysis of the Arm Nerves. — This common affection, 
described by Erb (1884), is due to affections of the vertebrae, cord or 
nerve roots, to tumors, trauma or cicatrices of the neck and wrenches 
or forcible delivery in obstetrics. Several nerves are involved, as the 
musculospiral and ulnar in fracture of the humerus, or in subcoracoid 
luxation. In Erb's case the circumflex, suprascapular and musculo- 
cutaneous nerves, fifth and sixth cervical roots, with some branches 
from the fourth, were imbedded in a cicatrix and paralyses of the deltoid, 
teres minor, spinati, biceps, brachialis and supinators, with few sensory 
signs resulted ; excision of the scar and nerve suture resulted in recovery ; 
in one spot between the scaleni all these nerves could be stimulated and 
therefore simultaneously affected. Obstetrical paralysis usually recovers, 
while adult forms are often protracted or permanent, depending on their 
etiology. Flaubert (1827) described a combined paralysis, which usually 
bears Klumpke's (1885) name, in which paralysis of the first dorsal 
and eighth cervical roots (ulnar and median paralysis) also causes 
narrowing of the pupil and the interpalpebral fissure. 

BRACHIAL NEURITIS. 

Gowers first clearly described a perineuritis of the plexus or nerve roots 
(radicular neuritis), occurring largely in gouty or rheumatic subjects over 
fifty years of age. Cervical rib may cause compression symptoms; 
Reisman collected 46 cases of which 24 were operated on with good 
results. But 5 per cent, cause symptoms and 85 per cent, are bilateral, 
as shown by radioscopy; (a) a tumor may be palpated; (b) nerve pressure 
or wasting may be manifest; or (c) the subclavian artery, compressed 
by the scalenus anticus, may be abnormally high or pulsate like an 
aneurysm; even gangrene may ensue. Neuritis is marked by great pain, 
the first, most severe and most enduring symptom. It is constant, with 
paroxysmal exacerbations, is increased by the least movement and is 
experienced over the plexus, nerves or referred to the wrist or scapula. 
Associated with it are tenderness over the trunks or plexus, hyper- 
esthesia of the skin, some muscular wasting, mostly in radicular forms, 
and somewhat less often anesthesia, anesthesia dolorosa, edema, glossy 
skin and trophic alterations in the joints. Neuralgia, angina pectoris 
and aneurysm may cause diagnostic difficulties. Remak holds that 
reported recoveries of acute poliomyelitis in children (Kennedy's tem- 
porary paralysis) are only plexus neuritis. A long course of from a month 
to more than a year, relapses and even wasting, and joint adhesions must 
be considered in framing the prognosis, despite early and careful treat- 



THE NERVES OF THE LOWER EXTREMITIES 901 

ment. Treatment, as in neuritis, consists of rest by immobilization, 
injection of cocaine in severe cases and treatment of the underlying 
trauma, gout or rheumatism. 

THE NERVES OF THE TRUNK. 

These are rarely involved except in lesions of the spine or cord. The 
neuritic pain in Pott's disease or cord tumor and the girdle pain of tabes 
are of great localizing value. Herpes zoster is due to inflammation in the 
spinal root ganglia. 

THE NERVES OF THE LOWER EXTREMITIES. 

These nerves, except in sciatica, are less frequently affected than those 
of the arm. 

The Lumbar Plexus. — The first three and a half lumbar roots may 
suffer in abdominal tumors, adenopathies, parturition, psoas abscess, 
pelvic inflammations, meningitis or vertebral disease. The symptoms 
are paralysis of the flexors and adductors of the hip and extensors of the 
knee; all the hip flexors are involved in plexus disease only; in neuritic 
forms great pain is noted in the ilio-inguinal, iliohypogastric and genito- 
crural areas. Anesthesia exists over the lower abdomen, front and sides 
of thigh and inner side of leg and foot and adjacent sides of first and 
second toes. 

Anterior Crural Nerve. — Lesions in the abdomen cause paralysis of 
the iliacus (not the psoas), the hip flexors and knee extensors, with 
wasting, loss of knee-jerk and anesthesia over the front and sides of the 
thigh and the inner side of the leg and foot. It may result from stab 
wounds of the thigh, in which case the iliacus escapes involvement, or 
after delivery. Neuritis of its external cutaneous branch (multiple neuritis, 
alcoholism, nicotinism or gout) may cause isolated anesthesia over the 
lower outer half of the thigh, paresthesia or marked hyperesthesia; the 
last condition, known as meralgia, is usually neuritis but may be due to 
pressure from varicose veins or corsets. It is noted, chiefly, on standing 
or walking. In 1900 Musser and Sailer collected 99 cases (74 per cent, 
in men). 

Pressure on the cord at the fourth lumbar roots produces the same 
result as a partial lesion of the ant. crural nerve, as paralysis of knee 
extensors, loss of knee-jerk and anesthesia of anterior part of thigh, but 
foot-clonus is present. Anterior horn disease may occur exceptionally, 
but its wider prevalence and sensory exemption are sufficiently distinctive. 
Caudal lesions are usually bilateral. 

Obturator Nerve. — This nerve is rarely alone involved save during 
parturition. Its paralysis affects the thigh adductors, so that the knees 
cannot be crossed, and the pectineus and ext. obturator, with impairment 
of outward rotation of the thigh. The hip and knee-joints sometimes 
show trophic disturbance. The pain of hip disease is referred to the knee 
by the obturator nerve. 



902 DISEASES OF THE SPINAL NERVES 

Superior Gluteal Nerve. — This arises from the lumbosacral cord, being 
intermediate between the lumbar and sacral plexuses. Its rare isolated 
involvement results in loss of thigh abduction and circumduction (gluteus 
medius and minimus). 

The Sacral Plexus. — Half of the fourth, the fifth lumbar and the first 
four sacral nerves supply motion to the extensors and rotators of the hip, 
flexors of the knee and all the foot muscles, and sensation to the gluteal 
region, the back of the thigh, outside and back of the leg and most of the 
foot by the gluteal nerves and the two sciatic nerves. The lesser sciatic 
is affected only in disease of the plexus; it is often involved in pelvic 
inflammation and tumors, parturition, traction in leg deliveries and 
diseases of the hip. 

Great Sciatic Nerve. — This is the largest, the most exposed through- 
out its course and hence the most frequently diseased nerve of the lower 
extremity. Paralysis of the gluteus maximus interferes with rising more 
than with walking. A lesion near the sciatic notch paralyzes the extensors 
of the hip, the flexors of the leg and all muscles below the knee. If the 
lesion lies below the upper third of the thigh the flexors of the leg may 
escape involvement and walking is still possible, even though all muscles 
below the knee are paralyzed, if the ant. crural nerve (hip flexors and 
knee extensors) is intact. Sensation is lessened over the outer half of the 
leg, most of the dorsum of the foot and all of the sole. Wasting is marked 
over the back of the thigh and perforating ulcer of the foot may develop. 
It has two branches: (a) the external popliteal or peroneal nerve, involve- 
ment of which causes paralysis of the tibialis anticus, peronei, long toe 
extensors, extensor brev. digitorum; the ankle cannot be flexed dorsally, 
the first phalanges of the toes cannot be extended, adduction and lifting 
the inner edge of the foot are difficult and abduction and lifting the outer 
edge are impossible. Foot-drop results and contracture assumes the 
equino varus type. This nerve is the analogue of the musculospiral in the 
arm. Wasting is often observed and the anesthesia covers the anterior 
outer half of the leg and the dorsum of the foot. (6) Internal popliteal 
nerve, involvement of which affects the popliteus, tibialis posticus, long 
flexors of toes and all the foot muscles except the extensors; plantar 
flexion, abduction of the foot, inability to stand on tiptoe, talipes cal- 
caneus and the claw-foot from overextension of the proximal and over- 
flexion of the second and third phalanges result. Sensory alterations 
are variable; anesthesia may be observed on the outer lower posterior 
part of the leg and on the sole of the foot. Its plantar branches are 
rarely affected alone; (i) paralysis of the internal plantar nerve, which is 
analogous to the median ; anesthesia on the inner part of the sole and the 
plantar surface of the three inner toes and one-half of the fourth; paralysis 
of the short toe flexors, plantar muscles of great toe (except the ab- 
ductor) and the two inner lumbricals; the big toe is overextended, 
"the hammer toe"; (ii) paralysis of the external plantar nerve, the ana- 
logue of the ulnar, produces anesthesia of the outer half of the sole, little 
toe and one-half the fourth, paralysis of the accessory flexor, small toe 
muscles, all the interossei, two outer lumbricals and great toe adductor; 
the results are serious, walking being impaired by flexion of the second 
and third and extension of the first phalanges. 



SCIATIC NEURITIS 903 

Caudal Lesions. — (See Spinal Localization.) 

Sciatic Neuritis. — Sciatica, Ischialgia, Malum Cotunnii (Cotugno, 
1764) is, after facial neuritis, the most frequent isolated neuritis. 

Etiology. — 1. General Causes. — (a) Sex and age; 88 per cent, of 
cases occur in men; 16 per cent, between twenty and thirty, 31 per cent, 
between thirty and forty, 25 per cent, between forty and fifty and 18 
per cent, between fifty and sixty years of age. It is very rare in children. 
(b) Acute infections, as rheumatism and grippe are causative, (c) In- 
toxications; gout, fascial rheumatism (sometimes by extension from 
lumbago) and diabetes are factors, (d) Anemias and neuroses are less 
significant than in neuralgia. 

2. Local causes include (a) spinal affections, tumor and caudal 
neuritis; (6) abdominal and pelvic diseases, as aneurysm, tumors or 
inflammation; (c) cold, exposure and dampness, favored by certain 
occupations; (d) trauma to the spine, pelvis, hip or peripheral course of 
the sciatic trunk or branches, as from the use of forceps or pressure of the 
head in labor, fractures, dislocations, falls, protracted sitting or riding, 
use of the sewing machine, marching, peripheral pressure by popliteal 
aneurysm, tumors, callus or varicosities. 

Pathology. — The infrequent autopsies or operations show perineuritis 
with edema and in some cases increase of connective tissue or varicosities 
of the sheath vessels, especially in the mid-thigh. Sometimes interstitial 
neuritis is found. 

Symptoms. — The symptoms are unilateral and chiefly sensory, as 
pain and tenderness over the sciatic roots, trunk and branches, (a) 
The onset of pain is usually gradual but is sudden and febrile in some 
rheumatic cases. It is usually constant, with exacerbations which may 
be agonizing. The pain descends more often than it ascends; it sometimes 
radiates to the buttocks, crural region, even into the other leg. The 
local pain is perineuritis and the distant pain interstitial neuritis. Any 
movement which increases sciatic tension increases or renews the pain 
(Lasegue's phenomenon), as flexing the hip, extending the knee, walking, 
stooping or defecation. The patient seeks positions which spare stretch- 
ing of the nerve and its compression by the muscles; he may lie on the 
opposite side with the thigh extended, knee flexed and foot extended, or 
on his back with hip and knee flexed and foot extended ; in standing, he rests 
on the sound leg and in protracted cases scoliosis develops (ischias scolio- 
tica), in which the lumbar convexity is toward the diseased side, heterol- 
ogous scoliosis, which, usually disappears with the disease; a homologous 
scoliosis (with the lumbar concavity toward the affected side) may result 
in case the muscles of that side become spasmodic, (b) Tenderness may 
be detected over the entire course of the nerve or in certain locations only: 
(i) over the lumbar region; (ii) near the sacrum and post. sup. iliac spine; 
(iii) at the lower gluteal fold where it leaves the sciatic notch; (iv) be- 
tween the tuber ischii and trochanter; (v) especially over the middle of 
the posterior surface of the thigh; and (vi) lower over the popliteal space, 
head of fibula, calf, malleoli and sole. The enlarged nerve may occasion- 
ally be felt. Pain is often experienced in the hip and sciatic notch when 
pressure is made in the popliteal space, (c) Other symptoms are less 
frequent, as vasomotor changes, herpes, muscular cramps, twitchings, 



904 DISEASES OF THE SPINAL NERVES 

fibrillation or myokymia; there is rarely a marked degenerative reaction; 
muscular atrophy from disuse or neuritic atrophy, sciatic paralysis, 
hypesthesia, paresthesia, or in severe cases anesthesia, may develop in 
the posterior part of the thigh, leg or foot. The patellar reflex is 
usually normal, the Achilles reflex is often decreased or absent and the 
cremasteric usually increased. 

Diagnosis. — (a) The etiological factor should be sought, (b) The 
pelvis must be examined in women and the rectum in both sexes, because 
compression produces more distant than local pain; the urine should 
always be examined for sugar and albumin; and free catharsis and bowel 
lavage given, (c) Bilateral sciatic pain suggests diabetes, or disease of 
the cord, especially tabes, or a lesion of the cauda, in both of which there 
is no sciatic tenderness, (d) Coxitis, sacro-iliac and psoas disease present 
appropriate local signs, without Lasegue's sign or sciatic tenderness, 
both of which are also absent in (e) hysteria. (/) Muscular rheumatism 
is chiefly confused with pain over the sciatic branches. 

Prognosis. — The prognosis, generally good, depends on (a) whether 
the affection is primary, as from cold, or secondary, as from disease of the 
cord or pelvic neoplasm; (6) the amount of rest which the patient accepts; 
(c) the intensity of the neuritis, which may extend to the lumbosacral plexus ; 
and (d) the chance of relapse (33 per cent.) . The average course is from two 
to eight weeks, but cases may last a year, indeed three to thirty years. 

Treatment. — (a) Treatment is that of the cause; the salicylates, in 
some, but unfortunately few, cases afford relief; gouty or syphilitic 
taints may be benefited by colchicum or antisyphilitic remedies, which 
are often given as a last resort in other cases, (b) Rest in bed is the most 
important indication. In this, extension or Weir Mitchell's long splint 
is often beneficial, (c) Counter-irritation by blisters over the nerve's 
course or by touching the tender or painful points with the hot iron, 
may give temporary, though rarely lasting, relief, (d) Analgesics and 
narcotics. Acetanilide has little effect. Gelsemium (flextr. Tfljj) at 
intervals of two to four hours, not infrequently gives relief, though it is 
necessary to watch for pulse weakness and cutaneous tingling. Codeine 
and atropine should be given before resorting to morphine; morphine 
is often inevitable, but chronic morphinism may be initiated by severe 
pain, the long course and tendency to relapse. Hypodermics of cocaine 
are very beneficial, though attended by the same danger. The author 
has seen good results from deep hypodermic use of Schleich's solution 
given in quite large amounts over sensitive points. 1 Injections of 
chloroform and ether should be avoided because of the possibility of 

1 Hecht found the sciatic at its point of exit from the great sacrosciatic foramen 
in the following manner: A line is drawn with tincture of iodine from the sacrococ- 
cygeal articulation to the postero-external border of the great trochanter; at the 
junction of the inner one-third with the outer two-thirds of this line is the spine of 
the ischium. Placing the needle a thumb's breadth to the outer side of this point and 
penetrating in a directly perpendicular line to a variable depth, one engages the sciatic 
nerve;. The needle with the stylet partly withdrawn is put through the skin, and when 
well in the subcutaneous tissue the stylet is returned to cover the point and the needle is 
directed perpendicularly to the necessary depth. The moment the nerve is touched the 
patient feels a sharp, lancinating pain at the heel or in the calf associated with a quick, 
jerky movement. Occasionally the pain is felt in the buttock, thigh, or at the knee. The 
filled syringe is now attached and the solution (60 c.c.) injected slowly with steady, firm 
pressure. 



HYSTERIA 905 

sloughing and accentuating the neuritis, (e) Acupuncture, the old 
Chinese treatment, is recommended; it resulted in complete relief in 56 
per cent, of Gibson's cases, improvement in 32 per cent., slight benefit 
in 10 per cent, and failure in but 2 per cent. (/) Massage. Negro obtained 
results from frequent and severe local rubbing and rolling, over the nerve 
trunk, (g) Electrotherapy may aggravate the pain and is at least of 
uncertain value, (h) Nerve stretching may be effected by extension by 
weights, although it is rarely tolerated by the patient in personal ex- 
perience. The direct exposure of the nerve has justly fallen into disuse, 
for the same results attend simple stretching, performed under anesthesia. 
The hip should be strongly flexed, the knee extended, the foot dorsally 
flexed and the pelvis firmly immobilized. Ordinary care prevents luxation 
of the hip. The results were excellent in half of 20 personal cases and 
were seemingly curative in 7. 



THE NEUROSES. 



HYSTERIA. 

Definition. — The neuroses are nervous affections, provisionally desig- 
nated "functional," since no anatomical basis has been discovered. 
Mobius considers hysteria "a state in which ideas control the body and 
produce morbid changes in its functions." The school of Charcot estab- 
lished its psychogenic nature. It is a cerebral, cortical condition, in 
which the sensory and motor centres are affected, the perception, asso- 
ciation and recollection of ideas are disturbed and trophic and vasomotor 
disorders occur. As its name implies, hysteria was long thought to be due 
to the uterus; Sydenham first called it a nervous affection. 

Etiology. — (a) Age: It is most frequent at puberty and adolescence (fif- 
teen to twenty-five years) . It is occasionally seen in children and rarely 
in middle or advanced life. (6) Sex: Women are ten times as frequently 
affected as men, although in the lower French classes it is more frequent 
in males, (c) Race: The Jewish, Latin and Slavic races are most fre- 
quently affected, (d) Heredity: Charcot and the French school hold 
that this is the sole cause, other factors being only agents provocateurs. 
Parental intoxications, toxemias, constitutional diseases, as gout, diabetes, 
arthritis deformans and a neurotic taint are important in the transmission 
of a congenitally weak nervous system, (e) Acquired hysteria may be 
due (i) to various intoxications, notably lead, alcohol and drugs; (ii) 
to infections, as typhoid, malaria, diphtheria and syphilis; (iii) to con- 
stitutional maladies, as gout, diabetes, chlorosis, secondary anemia 
or cancer; (iv) to exhaustion from mental or physical overwork or ex- 
cesses; (v) to emotional disturbance; (vi) to trauma, especially psychic 
shock; (vii) it may occur as an associate with epilepsy, syringomyelia, 
tabes, brain tumor and multiple sclerosis ; (viii) imitation is an important 
factor in schools, hospitals and at religious revivals; endemics occur now 
as they did in the middle ages. (Refer to Zola's Lourdes.) Reference 
to sexual factors is considered under Therapy. 



906 THE NEUROSES 

Symptoms. — The disease is much more commonly polysymptomatic 
than monosymptomatic. French writers distinguish two main groups 
of symptoms, the stigmata and accidents. 

Stigmata. — The stigmata are usually persistent symptoms. 

1. Sensory Stigmata. — Sensory symptoms (in 85 per cent.) are more 
frequent than the motor and are often combined with them, (a) Hys- 
terical anesthesia is very seldom absent. It must often be looked for, 
without too obviously suggesting it to the patient. It may be absolute, 
affecting appreciation of touch, pain, heat and cold. Analgesia is its 
most common form and, in decreasing order of frequency, there may be 
complete anesthesia, hypesthesia, loss of tactile sense, loss of all sensation 
save to the faradic current or loss of faradic response alone. The same 
deficit frequently occurs in the mucosae and sometimes in the bones, 
ligaments, joints and muscles. In rare cases there is universal cutaneous 
and muscular anesthesia; the following are more frequent: Hysterical 
hemianesthesia, which involves precisely one-half of the skin, accessible 
mucosa? and special senses; segmentary or geometrical anesthesia, which 
affects one limb, variously described as "mitten or stocking" anesthesia 
and frequently associated with other disturbance in the part affected, 
as paralysis, aphonia, amblyopia and deafness; and insular anesthesia, 
which affects small areas, and is therefore frequently overlooked. 

Characteristics. — The anesthesia is psychical, is associated with the 
functions of the part affected and does not follow the area of distribution 
of the peripheral nerves or spinal segments; it is not noted by the patient, 
at least until suggested; it may be localized because of injury or disease 
in the part. Babinski holds that all anesthesias are initiated by sugges- 
tions. The anesthetic areas may last during life, but they move even 
under examination or disappear from emotion, strongly aroused attention, 
drugs or on application of various substances, as metal or wood (trans- 
ferring it to the opposite side). Most of the reflexes usually altered by 
organic disease remain normal, as the pupillary, lachrymal, epigastric, 
cremasteric, patellar and organic reflexes, while the pharyngeal in 90 
per cent, of cases is lost, as well as the plantar. 

Hysterical hyperesthesia and hyperalgesia are very common in localized 
areas, but never in universal or hemiplegic distribution. They occur 
spontaneously or from attention directed to a part or organ, as by trauma- 
tism. A joint may be affected with or without contracture (Brodie's 
joints) and this often leads to great and unfortunate errors. There is 
sometimes hyperesthesia in the sphere of any of the special senses. 
The feeling of a nail in the top of the head (clavus hystericus), sensitive 
spots in the mammae, epigastrium, groins or spine are the most common 
forms and may occur in the midst of anesthetic areas. The so-called 
ovaralgia is cutaneous; it has no relation to the location or to disease 
of the ovary; it occurs also in men. Because hysterical attacks have been 
initiated and sometimes stopped by pressure over this and other sensitive 
areas they have been called hysterogenic zones, but attacks are only so 
produced in patients already hysterical, from some associated memory 
of the patient, or from < suggestion. Taste and smell may be dulled or 
hypersensitive, and hearing may be blunted, or more rarely complete 
central deafness results, usually associated with anesthesia in and about 



HYSTERIA 907 

the auditory meatus. Complete loss of vision is both rare and transitory. 
Hemiopia and scotomata are almost always organic. Partial stigmata 
are more common. Concentric contraction of the visual field is usually 
bilateral, and generally greater on the side of the cutaneous defects. 
Concentric contraction of the field for colors (dyschromatopsia) is more 
characteristic. In the normal eye, blue has the largest field, then yellow, 
orange, red, green and violet; in hysteria the red field is often wider than 
the blue and is the last color lost. Achromatopsia designates the com- 
plete loss of color perception. Errors in accommodation (always ex- 
cluding abnormal corneal curvatures) may cause double images in one 
eye (monocular diplopia), triple images (polyopia) or large or small 
images (macropsia, micropsia). In hysterical amblyopia impairment of 
vision in the affected eye is decreased when the other eye is opened. 

2. Motor stigmata are much less conspicuous but foreshadow the 
motor accidents (v. i.). Voluntary movements are weaker, slower, less 
coordinate and with a tendency toward contractures. 

3. Mental Stigmata.- — Hysteria is always a psychic affection. The most 
conspicuous alienation is impairment of memory {amnesia), which con- 
cerns memory in the ordinarily accepted sense, as memory for persons, 
things, words, hysterical paroxysms experienced, etc., or concerns mem- 
ory and associations for speech, writing, walking or standing. The 
amnesia, like paralysis and anesthesia, is functional and like them returns, 
save in rare cases. Mental power is distinctly decreased, will-power is 
lost (aboulia) or lessened and the patient becomes the ready victim of 
impulses, sensationalism, suggestions, fixed ideas and misconceptions 
both on his own part and on that of others who incorrectly consider him 
deceitful, vain or erotic. 

Accidents. — The accidents of hysteria are the incidental seizures or 
paroxysms. They are usually transient or intermittent, but may become 
fixed and are then ranked as stigmata. 

1. Motor Accidents. — (a) Convulsions occur in 25 per cent, of all and 
50 per cent, of female hysteria. They are much less frequently the 
hysteria major (grande attaque of Charcot) than the partial, modified 
type (hysteria minor). The "grand attack" comprises (i) a prodromal 
stage, with mental depression or exaltation, palpitation, vasomotor 
symptoms, nausea, polyuria, an aura beginning in the epigastrium 
and culminating in choking (globus hystericus), vertigo and unconscious- 
ness ; (ii) a period of epileptiform convulsions (so-called hystero-epilepsy) 
in which, in exceptional cases, there may be biting of the tongue or even 
the cry of epilepsy; the face is at first pale, then red; the teeth are 
ground; the convulsion is most pronounced on the anesthetic side, 
toward which the face turns; the tonic spasm lasts less than two minutes 
and is often characterized by stupor, stertor and slow, wide movements 
of supination, circumduction and overextension, for the trunk and body 
are tetanically rigid; then the clonic spasm develops, with sobbing 
respiration, audible swallowing, abdominal rumbling and small, clonic 
movements, (iii) The period of "clownism" is characterized by con- 
tortions, opisthotonos {arc de cercle), bowing movements, violent strug- 
gling, screams, strikes and bites, (iv) There is next a period of " passional 
attitudes," in which the subject mimics terror, rage, joy and love, fol- 



908 



THE NEUROSES 



Lowed by (v) a stage of delirium with hallucinations, perhaps of animals 
(zoopsia). The attack covers fifteen to thirty minutes and frequent 
repetitions constitute the "status hystericus/' 

The partial attack contains some of the elements of the major type, 
and infinite variations occur; the globus type is extremely common; 
there are also the vertiginous, tetanic, emotional and syncopal types; 
trance-like sleep, with catalepsy in which the limbs retain any attitude 
given them, with sleep, which is apparent only, for the subject later recalls 
everything; there may be attacks of somnambulism, in which patients 
run miles or undertake distant travel without recollection of the trans- 
pired interval. (6) Paralysis is an accentuation of the stigmatic muscular 
weakness. In over 50 per cent, it develops after convulsive paroxysms; 
again it follows emotional causes, traumatism or organic brain disease. 
It assumes the paraplegic five times as often as the hemiplegic form; 
the monoplegic variety is less frequent; the triplegic, diplegic (quadri- 
plegic) or crossed forms are most common. They are rarely complete; 
often gesticulatory movements may be seen; the antagonistic muscles 
are involved, thus, in attempted flexion of the knee the knee ex- 
tensors contract; the paralyzed part may be limp or contractured ; the 
paralyses may be ephemeral or life-long in duration; paralysis may be 
"ideal," i. e., only for standing or walking. Vasomotor changes and 
edema are rare; the tendon, skin and electrical reactions are usually 
normal, although the tendon reflexes may be increased. Hysterical 
hemiplegia occurs three times as frequently on the left as on the right 
side. 



Organic Hemiplegia.- 



-Hysterical Hemiplegia. 



Coma: often complete. 

Reflexes: tendon and bone reflexes abolished 
at first ; later increased. Ankle-clonus. 

Cutaneous reflexes (abdominal and cre- 
masteric) early lessened or abolished; 
Babinski toe sign; lachrymal reflex 
abolished. 

Paralysis: (1) Unilateral; (2) not system- 
atized; face, arm and leg are weak during 
bilateral synergetic movements. (3) In- 
volves subconscious as well as conscious 
voluntary movements, producing the 
platysma sign (lessening of its contrac- 
tion on the hemiplegic side, e. g., on open- 
ing the mouth forcibly), and the com- 
bined flexion of the thigh and trunk 
(when the patient attempts to sit up). 
(4) Paralysis slowly improves some, but is 
not variable. 

The tongue deviates slightly toward the 
paralyzed side. 

Lower muscular tone, as lowering of the 
eyebrow or exaggerated flexion of the 
forearm, in early cases. 

Contracture cannot be voluntarily repro- 
duced; at first flaccid paralysis, then 
contracture. 

Hemianesthesia: rarely total ; , of stereog- 
nostic and muscle sense; rare; coarser; 
more lasting when present; often with 
bilateral hemianopsia. 



Rarely complete (automatic movements.) 
Rarely abolished; no clonus (or only a 

spurious ankle-clonus due to contraction 

of the calf muscles, Gowers). 
Skin reflexes normal; no toe sign. 



Never abolished. 

(1) Not always unilateral; if face involved, 
usually on both sides. (2) Paralysis 
sometimes systematized; and hemiplegic 
side functionates perfectly in bilateral 
synergetic movements. (3) Subconscious 
voluntary movements are not involved; 
absence of the platysma sign and that 
of combined flexion of the thigh and 
trunk. (4) Variable paralysis, improve- 
ment alternating with relapses. Absolute 
aphasia with ability to write (Charcot). 

Very slightly, very greatly or even toward 

the sound side. 
None. Asymmetry of the face is due to 

spasm, and exaggerated flexion of the 

forearm is absent. 
May be reproduced; variable paralysis, 

now flaccid, now spastic from onset, with 

increased reflexes. 
Often total, involving special senses, pain 

and pressure sense; frequent; variable 

in duration; usually with contraction of 

visual field. 



___ 



HYSTERIA 909 

In hysterical paraplegia there are usually no trophic changes, no 
bed-sores, no electrical alteration, no incontinence of urine or feces 
and rarely retention of urine; many errors in diagnosis are made. Hys- 
terical monoplegia usually occurs with anesthesia of even greater extent; 
it is lawless and illogical, viewed from the standpoint of organic disease. 
In astasia-abasia (Charcot and Blocq) the patient is unable to stand or 
walk, although the muscles concerned may be efficient in other move- 
ments. Lesser degrees are called dystasia or dysbasia. The term staso- 
basophobia is self-descriptive. Mobius* akinesia algera is similar, (c) 
Hysterical contractures precede, succeed or alternate with paralysis, or 
occur alone; these "rigid palsies" usually persist during sleep and yield 
to ether anesthesia, save in severe protracted cases with irremediable 
deformity. In the arms, contracture of the flexors predominates; in 
the legs, that of the extensors (club-foot). Spinal deformities may 
develop, most frequently from pseudosciatica. The muscles may so 
contract as to resemble muscle tumors. It is stated that the face escapes 
paralysis, but its lower portion may be weak; more often, however, it is 
contracted early, even when paralyzed ; hemispasmus glossolabialis and 
trismus have been observed. Spastic or pseudoptosis may resemble 
the paralytic form, but spasticity, the lowered or more level eyebrow 
and the concentric or parallel folds in the lid are distinctive of contracture. 
The ocular muscles are seldom involved; voluntary movement may be 
impossible, but associated and reflex movements are normal; con- 
vergent squint may occur, but never the divergent type nor contracture 
of a single rectus or oblique muscle; pain suggests hysteria. Karplus 
maintains that the pupil light reflex is lost during convulsive seizures. 
Organic disease of the hip may be simulated; local hysterical edema 
may occur. Brodie (1827) first drew attention to this group of cases. 
Many avoidable diagnostic errors are constantly made, (d) Rhyth- 
mical spasms, chorea major, the saltatoric chorea (v. i.) and local mani- 
festations, as barking cough or the various tics, may occur. Hysterical 
tremor occurs without voluntary movement. It may resemble the 
senile, Basedow, paralysis agitans or lead, but rarely the multiple 
sclerosis tremor. 

2. Sensory Accidents. — These are frequent, severe and painful. Head- 
ache is often dull or may resemble trigeminal neuralgia, migraine or 
organic disease, as tumor. Meningitis (hysterical pseudomeningitis) 
may be closely counterfeited. Spinal or vertebral pain is frequent and 
sometimes suggests tumor or caries. One and three-tenths per cent, of 
cases of sciatica are said to be hysterical. Joint disease and various 
visceral lesions (v. i.) may be closely mimicked. Dieulafoy collated 59 
cases of hysterical blindness, in 5 of which this accident was the only 
symptom. 

3. Visceral Accidents. — (a) Cardiac accidents include tachycardia, 
palpitation and pseudo-angina pectoris. (6) Respiratory accidents: 
Aphonia, usually attended by normal capacity to cough and often also 
to sing, has been described under Paralysis of the Vocal Cords. It is 
usually due to an "idea," as in a motor aphasia which allows the patient 
to write. Stammering, cough and cries may be provoked by local naso- 



910 THE NEUROSES 

pharyngeal disease. Dyspnea, resulting from paralysis of the diaphragm, 
and laryngeal spasm have been considered. Rapid breathing (tachyp- 
nea) also occurs; dyspnea, aphonia and paralysis of the diaphragm 
constitute Briquet's syndrome. Hemoptysis may occur, sometimes 
without phthisis, possibly as a vasomotor derangement; one fatal case 
is on record, (c) Digestive accidents: Hysterical anorexia results from 
cortical conception, stomach pain, dysphagia from spasm or simple 
sensory perversion; it may endure for weeks and cause extreme inanition 
or even death. Hysterical (pseudo-) hydrophobia is an analogous aver- 
sion to water. Vomiting is sometimes simulated by protracted globus 
or esophageal spasm, in which the food is simply regurgitated. Vomiting 
itself may be occasional or attacks may last weeks or months, often with 
remarkably little malnutrition; it is rarely fecal but substances injected 
by rectum may be vomited in a few hours; or again vomitus may be 
blood-tinged, possibly from vasomotor disturbance or more often from 
actual disease; ulcer may be simulated by pain and tenderness, which 
are surprisingly well confined not to one spot, but to the exact outlines 
of the stomach. The vomitus contains vicariously large amounts of urea 
when the urine is suppressed. Eructations are frequent from swallowed 
air; this also causes tympanites, as air reaches the gut through the 
incompetent pylorus. Phantom tumors or spurious pregnancy (pseudo- 
cyesis) are explained as protrusion of the distended bowel by tonic 
contracture of the diaphragm. Peristaltic unrest, diarrhea on eating, 
enteritis membranacea, spastic constipation, simulation of peritonitis, 
rectal stricture and intestinal obstruction also occur, (d) Genito-urinary 
accidents: Anuria has existed for ten days without uremia. Renal pain 
is not frequent, but hyperesthesia of the bladder is common. The urine 
is often greatly increased, with low specific gravity and solids. During 
attacks of the major type the solids are reduced, the urea one-third 
and phosphates one-half; the phosphates, which normally have a pro- 
portion of 3 of the alkaline to 1 of the earthy phosphates, show nearly 
an equal proportion of each. Depression of sexual desire is more common 
than exaltation; anesthesia is frequent; vaginismus may be observed. 
Hysterical ovarian and other pains are not related to pelvic disease. 

Hysterical fever is a disputed topic. Severe forms may suffer a rise to 
105° or 110°; this may lead to a diagnosis of meningitis, peritonitis, etc.; 
simulation by the patient rubbing the thermometer, or of confusion with 
tuberculosis or typhoid; must be kept in mind> 

4. Vasomotor and trophic accidents are rare. Erythema is the most 
common. Gangrene, falling out of the hair or nails, Raynaud's local 
asphyxia, cutaneous hemorrhages (crucifixion stigmata, stigmata diaboli), 
bloody sweats, lachrymation, hemoptysis, hematemesis, sudden tender 
swellings in the mammae and angioneurotic edema, which is sometimes 
blue in color, have been recorded. 

Course and Prognosis. — The course is always chronic. If we regard 
the disease as congenital the prognosis is poor as to total recovery, espe- 
cially with fixed psychical alteration and major manifestations. In 
mild forms, relapses may occur on disproportionately^slight provocation. 
The outlook is better in infantile and adolescent forms. The stigmata 



HYSTERIA 911 

may be ephemeral or life-long. Marriage may benefit light cases, but, 
with maternity, it is injurious in the severe type. 

Diagnosis. — The stigmata, mental, motor and sensory, are highly 
characteristic. The accidents are unequivocally hysterical or prove 
hysterical after consideration of their associations. The danger lies in 
overlooking concomitant disease (a) nervous, as multiple sclerosis, brain 
tumor, paretic dementia; (b) postinfectious hysteria, as hysteria plus 
neuritis; (c) lung, heart and other visceral diseases, all of which, as 
Sydenham remarked, may resemble hysteria. Stimulation does not 
include mimicry of symptoms by hysterics; simulation of hysterical 
stigmata and accidents is practically impossible. 

Treatment. — 1. Prophylaxis. — When the earliest manifestations occur 
in childhood, home treatment is impracticable because of the family 
tendency. The etiological factors must be studied, especially the hygiene 
and hours of sleep. Useful occupations, as out-of-door gardening, are 
preferable to more artificial plans of distraction. Cultivation of courage 
and self-control, is sought. Servants who teach fear of the dark and 
tell fairy stories should be watched. 

2. General Treatment of the Cause. — As the disease depends 
on disturbed cortical relations between the psychical and material 
processes, the principal treatment must be psychical. The "fixed idea" 
must be grasped and eradicated, which is best accomplished in ordinary 
circumstances by isolation of the patient from home or psychical or 
emotional circumstances surrounding the inception of the disease. Then 
the undue susceptibility incident to the disease may be turned to thera- 
peutic advantage by the self-confidence of the physician and by his covert 
suggestions. Babinski defines hysteria as that series of phenomena 
produced by suggestion and cured by persuasion. The Weir Mitchell 
rest-cure may result in great benefit, and later "vague hints regarding 
the curative power of nature," and fresh air and sunlight may captivate 
the patient. Symptoms must not be suggested to the subject, as anes- 
thesia or pelvic disease, and examinations, especially of the pelvis, 
should be omitted. Hysterics should not be allowed to associate with 
each other for obvious reasons. This general plan is psychotherapy, 
which might include hypnotherapy, as advocated by the Nancy school, 
Bernheim and others. Hypnotism is generally dangerous in its ultimate 
and often in its immediate effects ; the danger of hypnotism is shown by 
the fact that Strumpell considers it an "artificial hysteria," and Fere 
defines it as a "transformation of hysteria." "It is easier to make a 
sound person hysterical by hypnosis than to cure an hysterical one by it" 
(Liebermeister) . Treatment is sometimes frustrated by the patient's 
vanity. Successful treatment requires unusual tact, profound knowledge 
of human nature, strong sympathy (but dominance of the patient) and 
enormous optimism; certain single qualities in an ignorant quack 
may effect cures. 

According to Breuer and Freud, certain sexual activities, mostly of a 
perverse nature, develop before puberty; these phantasies are mostly 
repressed by the hysteric and after puberty these repressed perversions 
come in conflict with the normal sexual proclivities. Freud traces even' 



912 THE NEUROSES 

hysteria back to sexual trauma in childhood. The analytic or cathartic 
method consists of full narration or confession by the patient. The 
repressed complexes, parasitically attached to or dominating the mental 
states, are analyzed and replaced by proper mental reactions — a process 
of reeducation. The subconscious, repressed complexes are brought back 
into higher consciousness, lived over, given verbal expression and there- 
fore eliminated, forgotten. 

3. Symptomatic Treatment. — (a) In relieving pain the physician 
should first acknowledge its existence and intensity to soothe the patient 
and then apply blisters, liniments or the galvanic current with the 
anode on the painful area. Ovaralgia in most cases should be ignored; 
in exceptional cases pelvic surgery has given relief. (b) Convulsions are 
treated by dashing cold water into the face, by suggestive measures or, 
if severe, by etherization. Bromides are of little value, valerian is some- 
times beneficial and turpentine is recommended by Gowers as most 
efficient, 10 drops of the oil being given until slight vesical symptoms 
appear. Pouring water into the mouth or nose, which causes coughing, 
or holding a towel over the nose and mouth for fifteen to twenty seconds, 
may also serve, (c) Paralysis and contracture should receive early treat- 
ment, for neglected cases may necessitate surgical intervention. Massage, 
faradism, blisters and fixation in new postures are indicated and especially 
should their significance be minimized and the patient be assured that 
they are not organic. In 2 cases the author has seen the paralysis 
disappear at once on administration of asafetida in an effervescing 
mixture, (d) Anesthesia should be ignored, (e) Aphonia is treated by 
intralaryngeal faradization. Laryngeal and other respiratory spasms 
usually answer to energetic traction on the tongue. (/) For insomnia, 
the patient should retire at an absolutely regular hour; nervines should 
be given rather than bromides, and hot milk should be very slowly 
sipped, (g) Dysphagia, vomiting and anorexia may be treated by rectal 
feeding or by forced feeding through the stomach-tube. Constipation 
is often obstinate and its mixed spastic character is shown by the sheep- 
like feces. Olive oil by mouth and rectum, cold abdominal compresses 
and endorectal galvanization are usually effective. 

NEURASTHENIA. 

Definition. — Neurasthenia is a diffuse neurosis, which affects the 
entire nervous system, but chiefly the brain; it is characterized (a) 
by morbid irritability of the nervous system with a tendency to its 
rapid exhaustion ("irritable weakness"), and (b) particularly by psychical, 
motor, sensory, vasomotor, secretory and vegetative disturbances in func- 
tion. The nervous tissue responds unduly to stimuli, its reaction time 
is short and ready exhaustion results. It seems probable that the slight 
cellular and protoplasmic changes in nerve cells, noted by Hodge to follow 
fatigue, may have some bearing on its pathology. The affection described 
and named by Beard, in 1869, whose description, first received with 
skepticism and ridicule abroad, later gained universal recognition. It 
is possible that the disease is more frequent than formerly because of the 



NEURASTHENIA 913 

more strenuous life and methods of education. The difference between 
"nervousness" and neurasthenia is only quantitative. 

Etiology. — Neurasthenia constitutes 35 per cent, of nervous diseases 
and 50 per cent, of neuroses, (a) A neuropathic tendency is observed in 
50 per cent, of cases, especially among Hebrews whose proneness to ner- 
vous diseases is referred by Erb to inbreeding and desire of gain. Other 
neuroses, as hysteria, epilepsy or migraine, the psychoses and parental 
infirmities or intoxications may be obtained in the family history, (b) 
Age and Sex: 75 per cent, of cases occur in persons between the twentieth 
and fiftieth year. Women are more disposed but men more exposed, 
to the disease by their excesses in work, sexual activity and alcoholism, 
(c) Psychical causes include sorrow and care; hard mental or physical 
w T ork rarely produces neurasthenia. Worry is a prolific factor; it is the 
irritable weakness of work. Hard work is injurious when combined 
with excesses in tobacco, alcohol, coffee, drugs or venery. Certain 
occupations entailing responsibility or emotional factors predispose to 
nervous weakness, as in railway or telegraph employees, board-of-trade 
men, teachers, actors, artists and musicians. Trauma operates chiefly 
through psychical causes, as in the traumatic neuroses (q. v.). (d) In- 
toxications, as from stimulants, drug habits, lead or arsenic poisoning, 
infections, especially typhoid, grippe, malaria and syphilis, and gout, 
anemia or diabetes may be indirect factors, (e) Sexual life: Excessive 
coitus and coitus interruptus, sometimes promote neurasthenia, but their 
importance is enormously overestimated. Masturbation produces less 
direct physical than psychical injury, for it leads to brooding over its 
possible results (v. s. Freud's theory). Continence is never injurious, 
as sexual indulgence is rather a habit than a necessity. In neurasthenic 
women gynecological complaints are more often subjective, secondary 
and neurasthenic than objective, primary and organic. The same state- 
ment holds in male neurasthenics with chronic urethritis or prostatitis. 
Pregnancy and lactation are sometimes apparent causes. (/) Organic 
diseases may possibly be factors, but it is questionable to what extent 
enteroptosis, chronic gastric or other somatic lesions promote neuras- 
thenia. 

Symptoms. — A clinical description holding for all cases is impossible. 
A patient presents himself for the treatment of some single visceral com- 
plaint or describes symptoms in his head, heart, lung, stomach, sexual 
or other organs. The various types will be considered in the general 
picture, for pure forms are rare; they are the cerebral (cerebr asthenia) , 
spinal (myelasthenia) , cerebrospinal (the general type), the sympathetic 
or vasomotor and the visceral (cardiac, sexual, gastric) types, (a) The 
acute form from simple nervous exhaustion in normal individuals, or 
in those with neurotic stigmata; (b) the subacute or chronic acquired 
form and (c) the chronic constitutional neurasthenia, which is usually 
hereditary. 

1. Cerebral Symptoms. — These are most important. Headache is 

almost invariable, is more often dull than acute, produces a sense of 

pressure ("lead-cap" headache) or intracranial paresthesia and is most 

often occipital. Vertigo is frequent. Insomnia is extremely common, 

58 



914 THE NEUROSES 

but rarely absolute, which always suggests organic brain disease; sleep 
is slow in onset, the patient being kept awake by his fear of sleeplessness, 
by a rapidly moving circle of uncontrollable memory pictures or by 
indigestion or palpitation; sleep, when once attained, is restless or the 
patient awakes in the night or early morning. It is broken by dreams, 
startings or sometimes emissions. In mild cases distinct alterations in 
temperament and character develop, as loss of courage and confidence, 
depression, irritability, undue response to emotional stimulation, as on 
seeing sad plays or hearing hard-luck stories, slight ethical blunting, 
tendency toward extremes and development of quiet self -concentration 
or obtrusive egotism. The brain tires readily on mental or bodily exertion, 
especially as the irritable patient is often prodigal of time and energy. 
It is remarkable how in some cases the morning depression may disappear 
before an afternoon or evening excitement, but this is notably followed 
by reaction. Psychical processes are disturbed; perception is blunted 
and memory is weakened or often temporarily lost (dys-, para-, amnesia), 
as shown by the copious notes of his symptoms which the patient pro- 
duces in the physician's office ("I'homme aux petits papiers," as Charcot 
called him); association and combination are difficult, as in thought, 
composition, judgment or conclusions, whence the speech is often slow 
and disjointed, names are forgotten and the patient re-reads addresses, 
runs repeatedly to see if the door was closed, etc. Compulsory conceptions 
may lead to homicide or suicide in highly psychopathic types. Fear, 
being an attribute of the weak, is common enough, and may in marked 
types assume the form of various phobias, as the fear of open places 
(agarophobia), of enclosures (claustrophobia), rivers (potomophobia), 
high places (acrophobia), stars (asterophobia), railways (siderdromo- 
phobia), dirt (mysophobia), of high things falling (batophobia), of stand- 
ing (stasophobia), or walking (basophobia), of darkness (nyctophobia), 
of a single thing (monophobia), of all things (pantophobia), of places 
(topophobia), of men (anthrophobia) or of disease (nosophobia). Fibril- 
lation of the lids and wide, variable, sensitive and unequal (3 per cent.) 
pupils are frequent; permanent irregularity is almost always organic. 
Asthenopia is very common, especially in hypermetropia from weakness 
of the ciliary and int. recti muscles. The field of vision may be concen- 
trically limited, but this is rarely marked or permanent, and Forrter's 
shifting type may be found, in which objects brought from without into 
the field are better seen than those moved from within the field outward. 
Hyperesthesia of the retina and ear, ringing in the ears, Meniere's 
complex and disturbance of taste or smell are not common. 

2. Spinal Symptoms. — These include the so-called "spinal irritation." 
Many symptoms ranked as spinal are essentially cerebral. In women 
they are more common and are localized chiefly to the upper dorsal 
and coccygeal regions; in men they are lumbodorsal and most frequent 
in the sexual type. Sensory symptoms are constant. Hyperesthesia 
is common in the bodies of the muscles; paresthesia is frequent, as 
tinglings, girdle sensation or itching. Paralgesia in the form of headache 
(rhachialgia) is as frequent as headache and the pain may radiate into 
the various nerve plexuses; it is very often sacral and cutaneous; the 



NEURASTHENIA 915 

spine may be exquisitely sensitive to pressure. Neuralgia is rare. Anes- 
thesia is no part of neurasthenia. Of the motor symptoms, myasthenia 
is the rule, spinal and cortical in origin and conspicuous in the morning. 
The muscles often show fibrillary contractions and a tremor (85 per cent.) 
which is as fine and frequent as that of alcoholism or Graves's disease. 
Muscular fidgets, starts, cramps and irritability of the nerve trunks, as 
in tetany, are also observed. Actual ataxia is most rare, although sug- 
gested by the writing. The akinesia algera (Mobius) or the abasia- 
astasia of Blocq, as in hysteria or the psychoses, is the result of a phobia 
or a fixed conception. One of Erb's patients remained in bed for fourteen 
years. The skin, tendon and periosteal reflexes are increased. 

3. Vasomotor Symptoms. — These produce many central, visceral 
and peripheral manifestations. During brainwork the cerebral vessels 
normally dilate while those of the arm contract; this does not occur in 
neurasthenia. The manometer in normal cases reveals no essential 
variation during work, while in neurasthenia marked manometric varia- 
tions occur. Neurasthenics often suffer from cold and wear more clothes 
than is necessary; the skin is cold, clammy, even cyanotic or locally 
asphyxiated. On the other hand, the skin may be flushed and hot. 
Salivation or a dry mouth, polyuria, pseudo-angina pectoris, the wide 
temporal vessels, epigastric pulsation, edema, urticaria and dermograph- 
ism are but vasomotor manifestations, 

4. Visceral Manifestations. — (a) Some of the cardiovascular signs 
and symptoms have been treated. The arteries relax and throb, the pulse 
may be slightly of the "water-hammer" type and capillary pulsation is 
often apparent in the lips or nails. Palpitation, precordial anxiety and 
dyspnea are frequent. The pulse is frequently faster and may increase 
10 or 20 beats on pressure over some sensitive area (v. i. Traumatic 
Neuroses). Many neurasthenics seek consultation for cardiac disease. 

(b) Gastric symptoms (in 60 per cent.) are functional in character, as achlor- 
hydria, hyperchlorhydria, hyperesthesia. Anorexia is usually mental, 
as are polyphagia, polydipsia and adipsia (see Neuroses of Stomach). 

(c) Intestinal symptoms. Diarrhea is less common than constipation, 
which, like previous sexual abuses, often occupies the patients' thoughts. 
They "would be perfectly well if they could have one natural move- 
ment," and when they do they complain of "exhaustion during the 
entire day afterward." A sense of pressure, peristaltic unrest, hyper- 
esthesia, burning and flatulency torment the patient. Enteritis mem- 
branacea and enteroptosis are not infrequent, (d) The amount of urine 
is equally often increased or decreased. The specific gravity is lowered, 
but the urates, uric acid and urea are increased. Phosphaturia and 
oxaluria occur, often attended by flatulent dyspepsia, melancholia and 
nervous depression. Vesical tenesmus is an occasional complaint, (e) 
Genital symptoms. Fear of the results of previous excesses or of self- 
abuse may dominate the patient's mind, but the trouble is more a 
matter of conception than of reality, since the sexual appetite is actually 
decreased as a rule. In most cases there is premature ejaculation and in 
some patients there is psychical impotence. Emissions are frequent, but 
their importance is greatly overestimated. 



916 THE NEUROSES 

Course and Prognosis. — Acute cases are rare and fatal cases extremely 
exceptional. The usual chronic course is one of slow onset; it is attended 
by evidences of nervous fatigue which are at first relieved by rest, but 
which later persist in spite of rest and incline the patient to stimulants 
or drug habits. Later the signs of cerebral irritability, disturbed sleep, 
vasomotor disorders, reduced mental and psychical capacity, pains, 
spinal tenderness, paresthesia or paralgesia, sympathetic dyspnea or 
palpitation develop, sometimes with temporary remissions. The outlook 
is poor in severe hereditary forms or when there are complicating psy- 
choses or drug habits. In other types recovery is usual, although long 
deferred. 

Diagnosis. — The diagnosis is generally made with ease, but several 
rules must be borne in mind: (1) No single symptom is pathognomonic; 
(2) neurasthenia may precede, follow or complicate organic nervous or 
visceral disease, as arteriosclerosis. The subjective signs, irritable weakness, 
emotivity, muscular weakness, headache, backache, insomnia, amnesia, 
impaired psychical coordination and the phobias, together with objective 
findings, as asthenopia, insufficiency of the internal recti, tachycardia, 
epigastric pulsation, vasomotor alteration, as disturbed secretion of 
urine or sweat, increased reflexes, fibrillation and tender muscles cannot 
be mistaken. Psychasthenia is made by Janet to include all cases, with 
doubts, phobias, fixed ideas, obsessions, dazed conditions or a sense of 
unreality. The neurasthenic prodromes of progressive paralysis (q. v.) 
are usually distinguished on careful search for organic disease. Hysteria 
is typical in its stigmata and accidents; anesthesia, persistent contrac- 
tion of the fields of vision, dyschromatopsia, achromatopsia, monocular 
diplopia, convulsions, paralyses, contractures and anuria are foreign to 
neurasthenia. Hypochondriasis differs from neurasthenia in that it is 
a pure psychosis, its concepts are primary, ill-based, illogical or absurd 
and cannot be eradicated even for a time. 

Treatment. — 1. Prophylaxis. — Prevention is difficult, but even with 
hereditary stigmata much may be done. Treatment starts with the 
education of both child and adult. Children are mimics and the clearest 
of all observers. The inculcation of self-control, fearlessness, self-sacrifice, 
moderation in all things, truthfulness, prompt decision and constancy of 
purpose must be based on actual parental example, and in this way 
the child should also educate the parent. The child must learn to give 
up, to sleep alone, to stop at the right time, to finish what he has begun, 
to obey and to learn that he is not the centre of the family. He should 
be taught without being forced. Out-door living is more important than 
the school-room. The English method of treating children with reserve 
has some advantages over American demonstrativeness. Simple, varied 
food, without tea, coffee or alcohol, and long sleeps develop a strong 
nervous system. The sexual instinct requires attention. 

2. Therapy. — When once manifested, the disease should be treated 
as above outlined and causal factors should be investigated. Work alone 
is seldom injurious and while the modern complexity in the struggle 
for existence is increasing the number of neurasthenics, work should not 
bear the stigma nor should disappointment, for both make character. 



NEURASTHENIA 917 

Work must be systematic, not slavish. Hurry, failure to learn indi- 
vidual limitations, uncontrolled planning beyond the immediate day's 
work and worry cause the damage, especially when work produces 
indifference to nature, family life, exercise, rest and the things higher 
and above one's own small life and ambition. The time for exercise should 
be taken from the work hours, it should not follow them, nor should it 
be enforced in every case, for some are hurt by it; work under stimulation 
is injurious. The chief element in treatment is psychical and the physician 
accomplishes more than do drugs. He carefully examines and reexamines 
the patient and his assurrance that no organic disease exists has its 
weight for the time. Conversely, careless diagnoses, as of fatty heart, 
work damage to the patient's mental balance. The hygiene should be 
regulated. Strict dietaries and stimulants should be avoided, moderate 
out-of-door life or exercise enjoined and in pronounced cases absolute 
rest from work, with sojourn near the sea or at a moderate altitude free 
from sudden changes or high winds is recommended. Sexual matters 
should be left alone unless gross violations are found. The patients 
need sympathy — in moderation for their sake; but the patient must be 
taught that he alone can cure his malady by self-control and by avoiding 
extremes in everything. 

Pronounced cases in thin women, especially those with gastric symp- 
toms, are often helped by the Weir Mitchell rest-cure, which consists of 
absolute rest in bed, isolation, forced feeding, massage and faradization. 
The patient is not allowed to lift a hand and sees only the nurse, who is 
selected for her strength, optimism and lack of nerves. The patient is 
fed milk every three hours and the muscles are rubbed and faradized. 
Thus weight and strength are gained without muscular degeneration. 
Few men will tolerate this method and obese do not fare as well as lean 
women. No greater mistake is made than to give all patients a rest-cure; 
they often want work and occupation, harmonized with rest. 

3. Diet. — No one dietary is essential; some physicians favor a meat 
diet, others give well-cooked vegetable albumins, cooked fruit, fats, milk 
and eggs, especially in cardiac types. In mental anorexia, feeding by 
mouth or rectum must be forced. Water in abundance is indicated. 
Gastric hyperesthesia is relieved by small doses of phenol. Eructations 
must be controlled, since the air admitted exceeds the gas expelled; 
asafetida is excellent because it makes as strong an impression when 
swallowed as when eructed. Electricitv is largely suggestive. With 
massage and vegetable diet, endorectal faradization relieves constipation. 
In cardiac types alcohol and tobacco are interdicted and small doses 
of belladonna and bromide usually control palpitation; other vasomotor 
symptoms are relieved by these remedies, ergotin or nitroglycerin, 
according as they are angioparetic or angiospastic; or arsenic in anemia. 

Insomnia is often difficult to relieve; the following measures are valu- 
able: avoidance of evening work, stimulants or excitement; a cool bath, 
the wet pack or an ice-bag over the heart; small doses of bromide with 
valerian for the "expectant attention" which wards off sleep; 20 grains 
of sulphonal in hot milk, which should be slowly sipped; codeine with 
hyoscine; and chloral (the continued use of which induces vasomotor 



918 THE NEUROSES 

disturbance). The habit of sleep must be cultivated and the patient 
must not get up to read. Local, urethral and uterine affections are best 
ignored. 

THE " TRAUMATIC NEUROSES." 

This is a practical grouping of traumatic neurasthenia, hysteria, 
chorea and hypochondriasis. Hysterical forms were first described by 
Walton and Putnam; Erichsen (1866) wrote on trauma to the spine, on 
which the illogical name of railway spine was later conferred, and Oppen- 
heim (1877) termed the group the "traumatic neuroses." All organic 
affections must be excluded, whether trauma seems directly or indirectly 
causal, as vertebral caries, tumor, chronic ankylosis, rarefying osteitis 
which Kocher refers to fracture; hematorrhachis, meningeal hematoma 
or pachymeningitis; and cord affections, as poliomyelitis, myelitis or 
lateral sclerosis. Experimental trauma may produce molecular nervous 
changes, and trauma may hasten arteriosclerosis. Alcoholism and 
syphilis are predisposing factors. Traumatic neuroses are purely func- 
tional affections caused by trauma, which operates psychically rather 
than somatically. 

Symptoms. — The symptoms are those of hysteria, neurasthenia and 
hypochondriasis, singly or in combination. The patient may feel well 
for a day or two and then pain develops at the seat of injury or in the 
spine; anxiety, fear of his financial future or for his family, a "fixed 
idea" of his incapacity and the development of "litigation symptoms" 
are typical of hypochondriacal neurasthenia. Psychical symptoms are 
usually prominent; they are accentuated by repeated, sometimes sug- 
gestive, physical examinations, visits of lawyers or adjusters, court-room 
suspense, reversals of judgment or appeals. Vertigo, backache, headache, 
sleepiness by day and nocturnal insomnia may cause great distress. 
Pain, which seems to be nervous, may prove organic on examination by 
the a>rays ; it may be simulated, but is often real, as shown by persistence 
after award of damages. Tender areas are difficult to pass upon, because 
of exaggeration or simulation; Mann, Kopf and Rumpf found that press- 
ure on areas which are actually tender increases the pulse-rate by 10 
to 30 beats; this sign is subject to several conditions: (a) it is not always 
present; (b) its absence is no proof of simulation; (c) in simulation, 
the writhing which occurs when certain areas are touched may increase 
the heart's action. Paresthesia and hyperesthesia of the skin or special 
senses are frequent. Anesthesia indicates traumatic hysteria. Hysteric 
or neurasthenic contraction of the visual fields may remain the same from 
day to day and not vary with approach or withdrawal of the test object ; 
this is not a sign of simulation; Forster's type cannot be assumed. The 
pupils may vary, especially by dull illumination; reflex immobility 
indicates organic disease. Motor symptoms may embrace all those of 
hysteria or neurasthenia, abasia, astasia, paralyses, contractures sug- 
gesting vertebral injury or joint disease (Brodie's joints), pseudospastic 
or -tabetic gaits, tremor (forme trepidante) or sometimes muscular atrophy 
about the joints. Hysterical convulsions are rare; the author twice saw 
choreiform affections in telephone girls who sustained slight shocks 



EPILEPSY 919 

and once a genuine chorea. Patients must often be watched ; one of the 
author's cases, with spastic gait, shuffled out of the office but walked 
perfectly well around the corner. The reflexes are often increased, 
perhaps asymmetrically; ankle-clonus, which is probably spurious, is 
sometimes reported. When there is albuminuria and glycosuria the 
question arises whether they were previously present. 

Diagnosis. — Several points are often difficult to establish, because 
objective findings are frequently few: (a) It is usually possible to state 
whether one of the neuroses is present or whether organic disease obtains. 
(b) Exaggeration and simulation are difficult to estimate, as shown by the 
change of professional opinion from the idea that most cases are simulated 
to the present statement of some writers that it is present in 4 per cent, 
of cases only, (c) If disease is present is it directly due to injury? (d) 
If so, the most difficult of all questions is presented, namely, the degree 
and duration of the disease and the damages to be awarded. 

Prognosis. — (a) As to life, the outlook is usually good, though some 
cases become insane or suicidal. (b) As to complete recovery, it is less 
favorable. In most cases it is surprising how soon symptoms disappear 
after satisfactory legal settlement is made; this is said without cynicism. 
Many persons do not then recover completely and symptoms may endure 
in those who reject litigation. Hysterical are more favorable than neu- 
rasthenic or hypochondriacal symptoms. 

Treatment. — Treatment is psychical. The physician dreads the effect 
of litigation on the patient, assures him that there is no organic lesion 
and advises early settlement and return to work. 



EPILEPSY. 

Definition. — Epilepsy, by derivation, "being seized upon," has been 
called the "falling sickness" and morbus sacer. It does not include 
Jacksonian or symptomatic epilepsies. Classified with hysteria and 
neurasthenia as one of the "three great diffuse neuroses," it probably 
includes more than one disease. It is a disturbance of balance between 
the central exciting and inhibiting nervous processes attended by (a) a 
typical chronic, convulsive disorder, affecting the entire central nervous 
system, each attack being followed by loss of consciousness, (b) partial 
or atypical manifestations of these characteristics, or (c) concomitant 
or consecutive psychical or other symptoms. It occurs in from one to 
six persons per thousand. 

Etiology. — Of the ultimate causes, the neuro- or psychopathic tendency 
of Griesinger is found in 37 per cent, of cases; only the tendency is trans- 
mitted by inheritance, rarely the disease itself. Neurotic or psychopathic 
antecedents, parental alcoholism (51 per cent.), morphinism, plumbism, 
syphilis, tuberculosis, gout, diabetes, or ovarian and testicular diseases 
lessen the nervous resistance of the offspring. The disease rarely develops 
after the thirtieth year; 75 per cent, of cases develop before twenty; 
46 per cent, between ten and twenty, mostly at puberty; 28 per cent, 
before ten. The sexes are equally affected. 



920 THE NEUROSES 

Inciting causes include infections, as malaria or typhoid; syphilis may 
be hereditary, induce the Jacksonian type from cortical gumma, or it 
may be parasyphilitic ; intoxications, especially alcoholism; exhausting 
affections, as diseases of the blood or metabolism; and trauma or fright. 
Inciting causes are found in 37 per cent, of cases. 

Reflex epilepsy is said to occur from painful scars, nerve tumors, or 
foreign bodies in the ear, nose, nasopharynx or larynx; diseases of the 
digestive tract, uterus and heart; onset of the menses or their monthly 
appearance; pregnancy, phimosis or onanism; from gall-stones, colic or 
abdominal paracentesis. 

Pathology. — There is no characteristic macro- or microscopic change. 
The usual finding after death is that of any convulsion, viz., venous en- 
gorgement and punctate ecchymoses. Induration of the cornu ammonis, 
induration in the medulla, neurogliar increase in the cortex, thickening, 
asymmetry or deformity of the skull and persistence of the thymus 
have not been proved causal. 

Symptoms. — The symptoms are best studied from the completely devel- 
oped attack, in which there are three component parts: (a) The prodromal 
stage is not always present. Its "warnings" are either distant or imme- 
diate. The distant warnings (in 10 per cent, of cases) may precede the 
seizure by hours or days and take the form of restlessness, dispositional 
changes, depression, thoracic or cephalic oppression, insomnia, vertigo, 
nausea, grinding of the teeth, hyperesthesia of the special senses, angio- 
neurotic palpitation or cerebral congestion. The immediate warning, the 
aura proper, is the beginning of the convulsion rather than a warning. 
It is a central cortical irritation; its frequency is 40 per cent.; it is rarer 
in sudden, stormy, generalized seizures. The psychical aura is rare and 
is manifested by emotional or intellectual alteration and anxiety. The 
sensory aura consists of paresthesia and a sense of deadness in a limb or 
joint, attacks of migraine and epigastric sensations (from the pneumo- 
gastric nerve, pressure or irritation of which sometimes inhibits the 
convulsion). The special senses may be irritated or blunted; there may 
be flashes of light or colors, hallucinations, blackness before the eyes and 
less often anomalies of hearing, taste or smell. The motor aurse are 
circumscribed clonic or much less often tonic twitchings, as in Jacksonian 
epilepsy, from which they are distinguished by a rapid loss of conscious- 
ness; automatic movements, like stamping or buttoning the coat, are 
rarer and motor weakness and singultus, coughing or sneezing are least 
frequent. Vasomotor aurse may be localized or generalized, as rushing of 
blood to the head, palpitation, anesthesia, increased temperature, in- 
creased arterial tension, pallor or chilling. The patient then falls, pale 
and unconscious, or is thrown with force, often on his face, when (6) the 
convulsive stage begins. First a tonic convulsion affects all voluntary 
muscles, due to infracortical irritation. The initial cry, guttural or 
groaning from' tonic abdominal, thoracic and laryngeal spasm, is heard 
in 50 per cent, of cases The head is held back ; the eyes are open and 
staring, the jaw set, the face flushed, the neck tense, the body often 
opisthotonus, breathing and pulse are suspended, the muscles are hard 
but slightly vibrating to the palpating hand, the arms are turned tetanic- 



EPILEPSY 921 

ally inward, the hands are clenched with the thumb adducted and under 
the fingers, the legs are extended, the thighs adducted and the toes 
flexed or extended and spread apart. In some cases the head, eyes and 
even trunk deviate and in a few instances the tetanic spasm spreads 
gradually, instead of the usual instantaneous tonic spasm. The tonic 
phase lasts ten to thirty seconds, relaxing in inverse order from the limbs 
to the neck and face. The second phase of clonic convulsion occurs 
at once, appearing first in the limbs, which are not yet free of the tonic 
spasm. This stage is bilateral, highly irregular and violent, with very 
short remissions, leading perhaps to injury, fracture, luxation, breaking 
of teeth, laceration of skin, tongue and cheek, or rupture of muscles. 
It consists largely of alternating flexion and extension; the head strikes 
the ground, the body turns violently, the eyes jerk and protrude, the face 
is distorted, the tongue is bitten as it is thrust out, bloody saliva is 
expressed by the masseters, inarticulate sounds arise from the move- 
ments of the diaphragm and respiratory muscles and gurgling results 
from intestinal movements; vomiting movements, filling of the stomach 
with air, cyanosis, swelling of the jugular veins, ecchymoses in the 
conjunctiva, skin, retina or larynx, involuntary and sometimes forcible 
evacuation of the bladder, less often of the rectum, and occasionally 
ejaculation, occur. The clonic phase lasts one-half to three minutes, 
ending in a fine generalized tremor, (c) The comatose stage often begins 
with a deep sigh; respiration and circulation become normal, the limbs 
relax and the condition resembles a sound sleep, from which the patient 
awakes in from fifteen minutes to several hours, sometimes suddenly, 
more often gradually and in a more or less dazed condition. He recalls 
nothing of the attack and the loss of memory may extend back of the 
seizure (retrograde amnesia). He experiences pain in the muscles, joints 
or head, nausea, mental irritability or depression and finally a group of 
exhaustion symptoms, viz., (i) sensory exhaustion, expressed by hypesthesia, 
anesthesia, hypalgesia or analgesia; (ii) exhaustion of the special senses, 
as concentric limitation of the visual and color fields, dulling of hearing, 
taste or smell, and (iii) motor exhaustion due to cortical fatigue. 

During the attack vasomotor constriction often occurs, as shown by 
the initial pallor of the face, cardiac overaction or perhaps irregularity. 
The ecchymoses and retinal congestion are due to the convulsion. The 
pupil is reactionless, narrow at the onset, and dilated widely in the 
second stage; afterward it may oscillate; the pupils are sometimes 
unequal. The tendon and skin reflexes are weak or lost in complete 
attacks and for hours afterward, whence we may judge of the severity 
of the seizures. The temperature may be elevated 2° or 3°. Voisin found 
albumin in 50 per cent., though others consider it infrequent. The 
author has often noted transient albuminuria and cylindruria (granular 
casts) after marked paroxysms; glycosuria is uncommon. The phos- 
phates and nitrogen are increased; polyuria is common in the third 
stage. The sweat is increased. 

Types of Epilepsy. — 1. The completely developed attack (epilepsia 
gravior, grand mal) consists of (a) the classic type (29 per cent.), as above 
described, with loss of consciousness, and tonic followed by clonic con- 



922 THE NEUROSES 

vulsions; or (b) the slightly atypical type (19 per cent.), in which, e. g., 
the spasm may not always be generalized. 

2. The rudimentary attack (21 per cent.) consists of loss of conscious- 
ness, plus tonic or clonic spasms. This includes the apoplectiform cases, 
especially the senile (arteriosclerotic) form; forms resembling myo- 
clonus; cases which do not fall but stumble along at the onset (epilepsia 
procursiva) or turn (epilepsia rotatoria). 

3. The third form is the abortive attack (epilepsia mitior, petit mat, 
31 per cent.). Its importance is underestimated by the profession and 
the public; two main types, with endless variations, are distinguished: 
(a) one with loss of consciousness with few or no motor signs, and (b) 
motor and vasomotor signs with no loss of consciousness, or very slight 
clouding of the intellect. The loss of consciousness is often very slight 
or may last for a few seconds, so that a scarcely perceptible break occurs 
in the patient's occupation, reading, speaking, playing the piano or a 
game of cards; it is described by the French as "absence." He may 
move his lips inarticulately or there is nystagmus, a chewing or swallow- 
ing movement, tremor or twitching of the face, monospasm or vertigo. 
A cry may be the sole symptom. Some patients seem to fall suddenly 
asleep. Nothing, or everything, may be remembered. Aurse may con- 
stitute the whole attack, which aborts without unconsciousness or spasms. 

4. The psychical equivalent of Sammt, also known as transformed or 
larvated epilepsy or the epileptoid condition is often mistaken. Mental 
symptoms may precede, succeed, alternate with or replace the ordinary 
convulsive type, which must be first recognized to establish this variety. 
The mental changes are slight (petit mal intellectuel) or marked (grand 
mal intellectuel) and include excitement, emotional outbursts, narcolepsy, 
incoherent conceptions, amnestic attacks and mania. The patient may 
act like a hypnotized subject; he may take sudden long journeys or 
commit assault, arson or murder, whence the great medicolegal signifi- 
cance of this variety. 

The Interparoxysmal State. — Signs of psychical degeneration, poorly 
differentiated or large, small or prominent ears, hematoma of the ear, 
deformed teeth, lips or palate, coloboma, strabismus, nystagmus, small 
eyes, irregular pigmentation of the iris, deformed genitals or fingers, 
disorders of speech or irregular facial innervation may indicate hereditary 
taint. Neurasthenic symptoms are not unusual. The expression is often 
dull. When idiocy occurs with epilepsy, both are coordinate results of a 
common cause, or early and repeated attacks have initiated mental 
degeneration. However, many brilliant men have been epileptics, as 
Julius Caesar, Napoleon, Carl V, Peter the Great, St. Paul, Mohamed, 
Petrarch and Rousseau. The importance of organic disease of the heart, 
lungs, stomach and kidney is difficult to estimate. Epileptics often sweat 
profusely, are usually constipated and frequently become obese from 
inordinate eating and the bromide treatment. 

Diagnosis. — The diagnosis concerns the convulsive seizures and the 
abortive types. Similar convulsions must first be excluded which occur 
in (a) organic brain disease, as syphilis, tumors, vascular lesions, paretic 
dementia, multiple sclerosis and infantile cerebral paralysis. These 



EPILEPSY 923 

affections may produce generalized or Jackson ian fits. Jacksonian 
epilepsy is more clonic (cortical irritation) than tonic (infracortical 
irritation), is often associated with paresis or sensory alteration, occurs 
less often with coma and in 50 per cent, of cases is due to small cortical 
tumors. Epilepsy rarely develops after thirty years of age (E. tarda) 
and 90 per cent, of cases which occur after thirty — excluding alcoholism 
and uremia — are syphilitic. After forty-five, vascular lesions are a 
very common cause, (b) Convulsions may occur in alcoholism, uremia 
(eclampsia), plumbism or drug poisonings, (c) Reflex epilepsy {v. s.). 

Simulation of epilepsy is impossible. In the complete type, the tongue 
biting, cry, stertor or involuntaries may be absent. Scars are often of 
diagnostic value. Nocturnal epilepsy occurs in 33 per cent., often coming 
on when the patient drops off to sleep or on awakening in the morning; 
the depression, bitten tongue, ecchymoses and involuntary evacuations 
are unmistakable. 

Differentiation from hysteria is usually easy: 

Epilepsy. vs. Hysteria. 

Distant warnings: few, mental. Frequent, emotional. 

Aura: more frequent, momentary, oftenest Less frequent, longer, bilateral, foot aura, 

unilateral or epigastric. globus. 

Cause: none. Emotional. 

Onset: always sudden, often with pallor, More gradual, rarely with pallor or cry, 

cry which is never verbal, immediate which may be repeated or verbal, and 

falling and complete unconsciousness, recur. Rarely brusque falling, slower and 

with rigidity, etc. less complete unconsciousness, and may 

react to suggestion. 

Tongue biting, frothing: very common. Exceptional, or seemingly purposive. 

Convulsions: generalized, tonic followed by Rigidity, to carry out semi-intentional 

clonic spasms, very rarely tonic alone; movement; struggling; clonic, irregular 

flexor spasm predominates. spasms; extensor spasm predominant, 

"arc de cercle," clownism. 

Reflexes: pupils contracted at onset, dilated Pupils usually wide and react (may be 
later, immobile (in clonic period). Ten- immobile, Westphal, Karplus). Some- 
don and skin reflexes absent during and times convergent strabismus. Reflexes 
after attack. rarely absent; or increased. 

Involuntary evacuations: frequent. Absent or most exceptional. 

The urine: solids always increased, both Solids decreased; altered ratio of earthy 

nitrogen and phosphates. and alkaline phosphates. 

Temperature: sometimes elevated, 2 °— 3°. Practically never. 

Coma: complete. No real coma. 

Duration of seizure: very short. Longer, recurrent, relapsing. 

Postparoxysmal: sensory and motor ex- Depression, fatigue, pain in the head or 

haustion, ecchymoses, absent reflexes, stomach, nausea, some memory of 

mental incapacity, with no memory of attack, 
transpired events. 

Most difficult to differentiate are petit mat and transformed epilepsy, 
in which the history of major attacks is important. Petit vial may be 
confused with cardiac syncope, labyrinthine vertigo, etc. 

Course and Prognosis. — When one attack has occurred a second may 
be expected in 33 per cent, of cases in less than one month, in 33 per 
cent, in from one to twelve months, in 33 per cent, in over one year; 
and when epilepsy is once established, daily attacks occur in 11 per cent., 
in 50 per cent, they occur at intervals of less than two weeks, and in 
75 per cent, they occur at intervals of less than one month (Gowers). 



924 THE NEUROSES 

The mode of life, stimulation, excitement, pregnancy and sexual excesses 
may increase their frequency and cessation during fevers is not uncommon. 
In some, fortunately rare, cases the attacks occur in quick succession 
(status epilepticus, etat de mat), as many as 10 or over 100 occurring 
in 'one day. In one case 2500 seizures occurred during a month; the 
stage of coma may last from two or three days to a week, with a tem- 
perature of 105-7° and death then results. The outlook (a) as to recovery 
is poor. Five to 10 per cent, of cases may recover spontaneously. The 
prospects are best in cases which begin before twenty in males, in cases 
with long intervals between attacks and in hereditary forms. After two 
years' duration the outlook is unfavorable, (b) As to life, the average 
duration of life is shorter than normal. A few cases drown, suffocate 
from turning on the face or are fatally burned during the seizure. Some 
patients die during the insult from vascular lesions of the brain or less 
often from heart rupture, respiratory cramp, edema of the lungs or 
vomiting into the larynx. One-sixth of epileptic deaths are sudden. 
Epileptics frequently become tuberculous. In 10 per cent, dementia 
occurs. Bodily health and intellectual vigor may be remarkably preserved. 
Treatment. — 1. Causal. — Syphilitic epilepsy, unless due to gummata 
or secondary anemia, does not respond to antisyphilitic remedies. Avoid- 
ance of alcohol may be almost curative in this form. Reflex factors 
should be removed. In Sweden epileptics cannot marry; 50 per cent, of 
hereditary epileptics transmit some transformation of the taint to their 
offspring. 

2. Hygienic. — Children should receive the general care outlined under 
the other neuroses. School work should be limited and country is prefer- 
able to city life. For poor subjects, institutional treatment is indicated. 
Many neurologists restrict the consumption of meat. Richet withdraws 
salt and gives a milk and cereal diet, which promote the affinity of the 
bromides for the brain cells. 

3. Bromides. — Introduced by Laycock (1853) and developed by Voisin, 
the bromides act directly on the nervous tissue; they depress the cortical 
cells, inhibit reflex action and lessen centripetal conduction. Untotvard 
symptoms may result even within therapeutic limits. Intellection may be 
dulled and muscular depression occur, but these may often be counter- 
acted by coffee; the frequent stomach symptoms can be avoided by free 
dilution with water; diarrhea, which results especially from potassium 
bromide, is relieved by opium if marked, or if less, by salicylate of bis- 
muth, gr. x, after meals; in its elimination by the skin, acne is common, 
which is lessened by large quantities of water, small doses of arsenic and 
washing the skin with green soap. Belladonna in small doses modifies 
the respiratory catarrh or salivation. The anaphrodisiac effects cannot 
be prevented. In some individuals there are marked idiosyncrasies, as 
mental excitement, hallucinations, emaciation ("bromide cachexia") 
with lessened physiological resistance to acute diseases. Toxic symptoms 
may be acute, but more commonly are chronic, resembling those of 
paretic dementia; bromism is most likely to develop in those with weak 
digestion or circulation and when the drug is given carelessly for a long 
time, because its elimination is slow. In the former, hydrotherapy, 



EPILEPSY 925 

massage and tonics should be used as preliminary or concomitant measures. 
Cardiac symptoms are due almost wholly to the potassium salt, but 
especial care in the use of all bromides is indicated in senile epilepsy 
(myocarditis, arteriosclerosis, endocarditis) or great nutritive exhaustion, 
in which combination with digitalis or strychnine is indicated. In bromism 
the reflexes are decreased; the pharyngeal reflex is weak in 17 per cent, 
and absent in 25 per cent, of normal individuals, whence Ziehen watches 
the corneal reflex, which is never normally absent. In advanced bromism 
there are low temperature, bronzed skin, vasomotor relaxation, somnol- 
ence, paralytic speech, muscular relaxation, ataxia, tremor, fetor ex ore, 
anorexia, slow respiration (the usual cause of death), weak heart, abolition 
of sensation and of all reflexes and decrease or suppression of urine. 
Therapeutically the drug unites with the nerve cell and depresses its 
activity and metabolism and toxicologically it causes its degeneration 
or atrophy. The drug must be used for months or years and the symp- 
toms above enumerated must be watched for; epileptics have a tolerance 
for bromides which Voisin regards almost as a food in this affection. 

Results. — Seguin's results were: cessation of attacks in 23 per cent., 
notable decrease in 40 per cent., no great effect in 26 per cent., no effect 
in 10 per cent. Gowers noted immediate relief in 43 per cent., improve- 
ment in a short time in 47 per cent, and no effect in 10 per cent. He 
gives a dram a day of the potassium salt, for two years, for larger doses 
are no more efficacious; in nocturnal epilepsy a large dose should be 
given at bedtime. Charcot gave a daily dose of one dram, which was 
gradually increased to two, and then slowly decreased to one. Erlen- 
meyer's formula gives excellent results (sodium and potassium bromide, 
each two parts and ammon. bromide one part). The best results are 
obtained in cases treated early in their course and early in life and in 
those in which there are long intervals between attacks. Children 
tolerate large doses. Opium, belladonna, digitalis, thyroid extract and 
chloral are of but secondary importance. Nitroglycerin may be useful 
in petit mat. 

4. The Attack. — This is confined to cases in which aurse are present. 
The patient is placed on the bed or ground to avoid injury and a towel 
inserted between the teeth to prevent biting of the tongue. Compression 
or manipulation of the limb in which the aura is felt may in a few instances 
avert the spasm. Charcot placed an ice-bag over the head and one 
over the heart. Inhalations of amyl nitrite, ether or chloroform are 
sometimes beneficial. 

5. Surgical Indications. — Biswanger's conclusions are (a) that only 
a small percentage of traumatic cases recover; operation is indicated 
(b) when convulsions emanate from a small cortical focus or (c) are of a 
type intermediate between the Jacksonian and generalized forms; (d) 
when, with generalized convulsions, there is a suggestive scar, bone 
defect or localized tenderness; (e) the site of trephining should be governed 
by focal symptoms, motor or sensory aurse, or " exhaustion" signs; 
(/) cysts, tumors, bone, membrane or scars may be removed, but not the 
cortex; (g) operation must be followed by the bromide treatment; (h) 
operation is contra-indicated in ordinary epilepsy. 



926 THE NEUROSES 



INFANTILE CONVULSIONS. 



In young children many axis-cylinders are not yet clothed with myelin 
sheaths and the lower dominate the upper segments, thus predisposing 
to disproportionate nervous reaction. 

Etiology.— (a) Rickets as a cause was especially emphasized by Wm. 
Jenner. Many cases of carpopedal spasm, tetany and laryngismus 
stridulus have a rhachitic basis; spasmophilia occurs between the eighth 
and twenty-fourth months of life, is prone to recur and disappears after 
the second year. (6) Reflex spasms may be caused by peripheral irritation, 
as from dentition and worms, though this type has been greatly over- 
estimated; gastro-intestinal irritation or auto-intoxication, phimosis and 
otitis media are possible causes, (c) Gastro-intestinal intoxication results 
in debility, malnutrition or a "hydrencephaloid" condition described 
above under various captions and usually of most serious import, (d) 
Nervous affections, trauma during delivery, meningitis, tumor, sinus 
thrombosis, severe coughing, acute encephalitis (cerebral hemiplegia) 
and acute poliomyelitis are etiological factors, (e) In acute infections, as 
scarlatina, measles or pneumonia, convulsions and vomiting often 
replace the chill which is more common in adults, (f) Genuine epilepsy 
in 12 per cent., according to Gowers, occurs in the first three years of 
life. 

Symptoms. — The symptoms resemble those of epilepsy in most of 
its phases; the eclampsia of children usually begins in the hands and the 
seizure is partial, tonic, intermittent and carpopedal rather than general- 
ized. Screaming and grinding of the teeth may occur. Laryngeal spasm 
is described under Affections of the Vagus. 

Treatment. — The occurrence of the convulsion is the first indication 
for treatment and should be met symptomatically by inhalations of 
chloroform or nitrite of amyl, followed by gr. v-x of chloral and 
5ss of bromide by rectum. The bromide is given for several days, for 
its effects are cumulative rather than immediate. Opiates should gener- 
ally be avoided in children under five years, especially in nurslings, 
weak or marantic infants; the hot bath is of little service. 

The cause is then determined and treated, as rickets, tetany, peripheral 
irritation; lancing of the gums is practised less and less; in gastro- 
intestinal intoxication the stomach should be emptied by ipecac or 
the stomach-tube; lavage of the bowel is indicated in acute cases and 
stimulants may be indicated. 

CHOREA AND CHOREIFORM AFFECTIONS. 

Chorea or St. Vitus 's dance, known to Paracelsus, and endemic in the 
middle ages is now known as chorea major; it was hysteria. Chorea 
in its usually accepted sense was described by Sydenham and is known as 
Sydenham's chorea or chorea minor. 

Definition. — Sydenham's chorea is (a) a neurosis of late childhood; 
(b) it is characterized by subacute onset, limited duration and, usually, 
recovery; (c) it is probably cortical in localization, as indicated (d) 



CHOREA AND CHOREIFORM AFFECTIONS 927 

by involuntary irregular spasmodic movements, and (e) increased in- 
coordination on voluntary efforts; (/) it is always associated with some 
psychical weakness or irritability and (g) is frequently associated with 
rheumatism and endocarditis. 

Etiology. — (a) Age: 80 per cent, of cases occur between the fifth and 
fifteenth years; 90 per cent, between the fifth and twentieth years; it 
is most frequent at the sixth and seventh years of life or at puberty. 
(b) Sex: Seventy per cent, of cases are in girls, (c) Rheumatism has been 
considered a cause since Bright' s time, especially by English and French 
writers. Rheumatism is a factor in at least 20 to 25 per cent. (Hughes and 
See) ; endocarditis, rheumatism and chorea are too frequently associated 
to escape serious attention; they are probably correlated, i. e., due to a 
common virus. Rheumatism occurs usually before the chorea; in but 
4 per cent, of cases do the two occur simultaneously, (d) Other acute 
infections are causes in 43 per cent, of cases (Neumann), e. g., gonorrhea, 
puerperal fever, sepsis, pertussis, measles, typhoid, etc. (e) Pregnancy 
is a predisposing cause, particularly before the twenty-fifth year. Chorea 
occurs in the first three months, especially in first pregnancies, and is 
most severe in character. It rarely occurs postpartum. Giles de la 
Tourette justly holds that many cases classified as chorea are really 
hysteria. (/) Neuropathic heredity is observed in 16 per cent, of choreic 
subjects, particularly among Hebrews, (g) Other causes are sometimes 
operative, as fright, trauma and reflex irritation from nasal or digestive 
disease. It occurs more largely in the lower classes, is sometimes due to 
iodoform or mercurial poisoning and is influenced by the poor hygiene, 
excitement, exhibition and competition of the school-room, the "school- 
made chorea" of Sturges. 

Pathology and Pathogenesis.- — The disease is a provisional neurosis, 
since no constant pathological findings exist. The following changes 
have been recorded: hyperemia, exudation about the arteries, areas 
of softening, punctate hemorrhages, round hyaline bodies in the peri- 
vascular lymph sheaths and swelling of the large pyramidal cells of the 
cortex; none of these are characteristic or constant. In fatal cases 
endocarditis is the most frequent finding (90 per cent.) and Osier notes 
that its frequency is greater even than in rheumatism. Kirke's theory 
of cerebral embolism has been abandoned. The bacteriological reports 
are conflicting. The irritation, due to exhaustion or toxemia, is probably 
cortical or in the basal ganglia. 

Symptoms.- — 1. Onset. — Prodromes are infrequent, as irritability, 
restlessness, depression, disturbed sleep, headache, anorexia, rheumatic 
pains, or sensory irritation. The affection usually begins with motor 
disturbance in the form of involuntary movements and incoordinate volun- 
tary movements; the latter are often misunderstood and punished, for 
the child cannot sit still or breaks or drops things. 

2. Chorea Movements. — These are involuntary, although they may 
seem voluntary, as the thrusting out of the tongue or the reaching 
of the arm at an object. They are "irregular in time, character and 
degree," are not usually attended by fatigue or pain, are incomplete and 
without motive, are increased by attention being drawn to them and by 



928 THE NEUROSES 

excitement and cease during sleep. They usually begin in the arms and 
later extend to the face and legs. Chorea very often begins on one side, 
especially the right, whence it extends to the other side, but sometimes 
remains largely, though never entirely unilateral (hemichorea) . The face 
is contorted with varying expressions, now grimaces or again motiveless 
smiles, the fades choreatica of Sachs. The eyes roll, and diplopia is not 
uncommon. The pupils are often wide and react slowly. The author 
recently saw a case in which many of the teeth were broken. Speech 
is involved in 25 per cent, of cases, due rather to difficult articulation by 
the tongue and lips than to phonation. Speech is quicker than normal 
and may be aggravated by irregular movements of the glottis and respira- 
tory muscles, resulting in panting, irregular inspiration or expiration or 
sobbing sounds in which the diaphragm participates. Aphasia is less 
frequent. The arms are most involved; they are flexed, extended, pronated 
and supinated in tireless succession — Bouillaud's folie musculaire. The 
trunk is sometimes involved in light cases and distinctly so in severe 
types. The violent movements may throw the patient out of bed. The 
legs are less involved; there is a zig-zag gait and walking may be im- 
possible. Besides hemichorea, other irregularities are encountered, as 
monochorea, chorea paraplegica or chorea alternans. The muscular 
poiver and endurance are said to be normal (Wallenberg), but Gowers 
and Osier speak of marked muscular weakness. Two forms are dis- 
tinguished: (a) paresis with chorea, in which the muscular power is 
reduced, as in the usual case, and (b) limp or paralytic chorea (choree 
molle). The paresis may be of the mono-, para- or hemiplegic type. 

3. Psychic changes are constant and the irritability and ready fatigue 
resemble an acute neurasthenia. The subject is wilful, forgetful, 
emotional, irritable, unable to concentrate the attention or to remember 
perfectly. Marked alteration may occur, as complications, viz., delirium, 
mania, melancholia or hallucinations; chorea insaniens has a most 
unfavorable prognosis. Combination with hysteria is frequent, with 
epilepsy infrequent. Hughlings Jackson found paroxysmal headache in 
90 per cent, of cases. 

4. Sensation. — Sensation is normal or slightly blunted. Tenderness 
over the spine and peripheral nerves is not common, though S. Weir 
Mitchell and Triboulet described a painful chorea. Occasionally there 
is a tingling sensation and numbness. 

5. The reflexes are normal in light cases but may be decreased 
or absent. The bladder and rectum are normal save in the severest 
forms. 

6. Electrical Reactions. — The electrical reaction and mechanical 
irritability of the muscles are with few exceptions unaltered. 

7. The Heart. — Irregularity is common and is often due to irreg- 
ularity in breathing (pseudo-arrhythmia). A slight increase in rate 
is due to the general neurosis. Ollivier, Roger and Simon claim that 
chorea may affect the "muscles of organic life", but a cardiac chorea is 
improbable. Functional murmurs are frequent, especially in thin, nervous 
children, from anemia, toxemia and tachycardia. Great conservatism 
must be exercised in their prognosis and diagnosis (see page 358). 



CHOREA AND CHOREIFORM AFFECTIONS 929 

Endocarditis has been mentioned in the definition of the disease and 
its causation and pathology (90 per cent, of fatal cases). It was found in 
66 per cent, of Osier's cases without rheumatism. It is rarely malignant, 
but may produce embolism. Mitral lesions, especially insufficiency, 
are the most common form. The importance of endocarditis without 
clinical symptoms is vast. Pericarditis is not frequent. Heart disease 
follows 50 per cent, of cases having two attacks of chorea, and 100 per 
cent, of those having over three. 

8. The Skin. — Herpes and pigmentation result from arsenic. Urti- 
caria, erythema nodosum, purpura and rheumatic nodes (v. page 284) 
are sometimes observed. 

9. General Symptoms. — Emaciation occurs chiefly in severer types. 
The urea and phosphates are often increased. Albuminuria is rare, 
except as a result of renal embolism. The temperature is not often 
elevated, save from cardiac and other complications; even in chorea 
insaniens it rarely passes 102°. 

Course and Prognosis. — The average course of mild cases is from six 
to ten weeks, and six weeks to six months is the average duration of all 
varieties. In very rare instances the disease may last years. Three 
main types are distinguished: (a) The mild type, in which the patient is 
nervous, irritable, has but slight choreic movements and is often dyspeptic 
and sometimes anemic ; (b) the severe form in which the spasmodic move- 
ments are severe and general; (c) the maniacal type (chorea insaniens), 
which is most often observed in adult or pregnant women, and sometimes 
at puberty. The movements are incessant, extreme and often associated 
with fever, constant insomnia and great psychical disturbance. "As 
a rule, the shorter the duration the more intense are the symptoms. 
Sydenham noted the tendency to recurrence (in 25 to 33 per cent.). 
One year is the average interval and when there is no recurrence within 
one and one-half years, relapse is improbable (Gowers). Recovery is the 
rule; the mortality averages between 2 and 3 per cent. Twenty to 25 
per cent, of pregnant cases die. Fatality is greatest at the age of puberty 
and in adults. As Charcot remarked, death occurs less often from com- 
plications, as endocarditis, than from toxemia, fever, emaciation, delirium 
and coma. Fever or obstinate insomnia is ominous. Though the im- 
mediate outlook is not influenced by endocarditis, it is a most important 
feature in the ultimate prognosis of a complete recovery. Intercurrent 
fevers may dissipate the spasms. In rare instances distinct psychical 
changes (Jolly) or permanent chorea remain (v. s.). 

Diagnosis. — Recognition of the disease is usually most easy when one 
bears in mind 'the conception (definition) of the disease. 

Differentiation. — Simple tremor or the intention tremor of multiple 
sclerosis is easily separable. The hemichorea of hemiplegia (see page 722) 
or the bilateral chorea of infantile cerebral paralysis (q. v.) is distinguished 
by the history and course. Friedreich's ataxia is differentiated by its 
slow, irregular, incoordinate movements, nystagmus, its frequent family 
incidence, the scoliosis, talipes, and slow, scanning speech. Hysterical 
chorea (so-called) is rhythmic, more regular and frequently produces 
sudden ("electrical") movements, as bowing or salaaming, nodding the 
59 



930 THE NEUROSES 

head, etc. Chorea major in the original sense is of historical interest; it 
was a pandemic or epidemic hysteria provoked by religious excitement. 
Its victims made pilgrimages to the shrine of St. Vitus. Similar out- 
breaks occurred in Kentucky among the early settlers. This form closely 
resembles the saltatoric spasm described by Bamberger, in 1859, in which 
the legs contract on attempting to stand, causing jumping or springing 
movements. It may be transitory or may last for years. Beard and 
Thornton described a similar neurosis endemic in Canada among the 
"jumping Frenchmen." The "holy rollers," and jumpers of Russia and 
Java come under this head or under impulsive tic (v. L). 

Huntingdon's chorea has no connection with Sydenham's type. Chronic 
chorea comprises two forms: (a) The senile form, in which the mind is 
less involved, the course more benign than in (6) the hereditary form of 
Huntingdon who, in 1872, brought out the cardinal features of the disease 
as observed on Long Island, viz., (i) the late and gradual onset after the 
thirtieth year, especially in males ; (ii) its hereditary character, sometimes 
involving 25 or 50 per cent, of the family, sometimes skipping generations 
or lasting for generations or even for two centuries in a family (Osborn) ; 
(iii) its progressive character, and (iv) the ultimate slow dementia, often 
with epileptiform attacks or suicidal tendencies. The precise pathology 
of Huntingdon's type is not known. Pachymeningitis, hematoma of the 
dura, or less often chronic encephalomeningitis, vascular disease and 
atrophy of the convolutions are present in the isolated autopsies. The 
etiology is unknown. Clinically it is characterized by irregular move- 
ments, which usually begin in the hands, are somewhat controlled by 
voluntary effort and are more irregular, incoordinate and slow than in 
acute chorea. Slow, spasmodic facial contortions are observed, and the 
speech becomes first slow and hesitating, and later quite indistinct. 
The gait is unsteady and swaying. Writing is interfered with, the reflexes 
are moderately increased, sensation is normal, save that the muscular 
sense is somewhat blunted, and dementia develops. The disease is in- 
curable. 

Tic. — The term is now. used to designate an "habitual, conscious, 
convulsive movement resulting in the involuntary contraction of "one 
or more muscles, abruptly reproducing some reflex or automatic action 
of every-day life" (G. Guinon). There are three forms: (a) In simple 
tic, (i) localized spasm, habit spasm or habit chorea, which is said by 
S. Weir Mitchell to occur in girls between seven and fourteen years 
of age, may result from lesions of the nose or throat or possibly from 
eye-strain, and includes movements such as winking, drawing of the 
mouth, sniffing, shaking the head and shrugging the shoulders. It 
usually ceases, but may last into adult life; the child's attention should 
not be drawn to the movements, although the writer believes that judi- 
cious reminders and discipline inhibit these habits. Arsenic may be 
beneficial, (ii) The electric chorea (Henoch and Bergeron) consists of 
short, lightning-like contractions in special muscles, as those of the neck 
or shoulders, as though the muscles were electrically stimulated, (iii) 
Dybini's disease (1846) consists of contractions of the arms and legs, 
followed by hyperesthesia, pain in the head and back, muscular atrophy, 



CHOREA AND CHOREIFORM AFFECTIONS 931 

paresis and sometimes fever and convulsions. It is endemic in Lombardy, 
its cause is unknown, and it is usually fatal from apoplexy or coma. 
(iv) Paramyoclonus multiplex, or myoclonia, described by Friedreich, 
in 1881, is an affection of sudden onset, with symmetrical, involuntary, 
arrhythmic, quick, clonic contractions of the upper parts of the arms, 
legs and trunk, sometimes of the face and tongue, and occurs without 
loss of consciousness. The contractions number from 10 to 150 a minute 
and may terminate in a tetanic contraction. It affects male adults 
chiefly (75 per cent.) and follows mental or emotional agitation, so that 
some would classify it under hysteria. The myotatic irritability and 
reflexes are increased, the mind is usually normal, though sometimes 
fixed ideas are observed, hiccough is occasional from involvement of the 
glottis or diaphragm, voluntary movement is decreased or sometimes 
arrested, there are no sensory symptoms and the outlook is usually good. 
Treatment consists of administration of voltaic electricity, nervines and 
bromides. The family form (Unverricht) with epilepsy and spasms of the 
tongue and pharynx, is probably a subtype of hereditary chorea. 

Tic and Chorea. 

Form of movement: pseudo-intentional, with Incoordination and great variability. 

repetition. 
Rhythm: rhythmic, brusque, short, syn- Arrhythmic, slow, not synchronistic. 

chronistic. 
Will: suspends movements. No effect. 

Accessory signs: muscular power preserved; Myasthenia; modified reflexes and sensation. 

normal tendon reflexes. 
Etiology: hereditary degeneration. Neuropathic tendency. 

(b) Tic with explosive utterances, impulsive tic or Giles de la Tourette's 
disease, is closely affiliated with hysteria and monomania. It occurs in 
neurotic individuals between the sixth year and puberty. The cardinal 
features of the psychosis are : (i) Involuntary movements in the face and 
arms or in all the muscles in severe types, when the movements become 
violent or explosive, (ii) Explosive utterances, resembling a bark; the 
patient repeats words he hears (echolalia), mimics movements (echo- 
praxia) or uses obscene or profane words (coprolalia) . (iii) The subject 
has fixed ideas, as arithmomania, in which every action is preceded by 
counting or doing a certain thing a given number of times; a fear of 
contamination (delere du toucher) ; onomatomania, or repetition of a given 
word or name; folie pourquoi, demanding the reason for everything. 
The prognosis is usually unfavorable. 

(c) In complex coordinate tic, as thumb-sucking, rocking in the bed 
and bumping the head, the outlook is favorable, except in feeble-minded 
children. 

Treatment of Acute Chorea.— 1. Prophylaxis. — Sensible methods of 
education should be adopted, the hours in the overheated, foul school- 
room should be short, and the useless forcing of children by marks, prizes 
and exhibition abandoned. Children can be taught more in an hour 
or two of judicious individual instruction than in the five or six confining 
hours which their wandering attention must endure. Prevention may 
concern other etiological factors (q. v.). 



932 THE NEUROSES 

2. Rest. — The results obtained by rest in bed and isolation are as, 
rapid as those of any medicinal therapy. It not only saves tissue waste, 
but is the best treatment of endocarditis. 

3. Skin. — The dry and harsh skin must be given special attention — 
stimulation of the skin by proper covering, refrigerant diaphoretics and 
full warm baths. The skin must be kept clean and in severe cases the 
water-bed must be used. 

Trauma. — Trauma is prevented in severe types by padding the bed 
by mattresses and pillows, since the violent movements may throw the 
patient to the floor. Sepsis is a frequent and most dangerous occurrence. 
The temperature must be taken by rectum. 

5. Exhibition of Drugs. — (a) Fowler's solution is the most frequently 
used and the oldest remedy. It should be given in increasing doses 
(see page 677); children tolerate large doses of arsenic exceptionally 
well. It may be administered hypodermically or by clyster when the 
digestive tract is irritable. Arsenic is not without its dangers. C. Gamble, 
Jr., records an instance of fatal arsenical poisoning in a case to whom 
about If ounces of Fowler's solution was given in three weeks. Rest 
in bed gives equally good results. (6) Salicylates are of benefit only 
when rheumatism actually coexists and acetanilide is indicated only 
in the initial stages, i. e., antirheumatic remedies are less important in 
the treatment than is rheumatism in the etiology, (c) Depressomotors: 
The bromides rarely cure the movements, although they often quiet 
mild psychic manifestations. Chloral, given in large and continued 
doses to produce continuous sleep, merely demonstrates the tolerance 
of the body for dangerous remedies and chloral cannot be given safely 
in amounts exceeding a dram for adults in three divided doses at intervals 
of an hour. Morphine is generally dangerous and inferior to chloral. 
Small doses often accentuate the mental agitation, but if combined 
with chloral, hyoscine and bromide, it may give some temporary relief. 
(d) Strychnine is valuable, especially when recovery is slow, (e) In 
chorea gravidarum, abortion or premature delivery is indicated. 

OCCUPATION OR FATIGUE NEUROSES; WRITER'S CRAMP. 

The continuous, hard, improper use of coordinate, functionally asso- 
ciated muscles may result in their cramping. Writer's cramp (grapho- 
spasmus, mogigraphia) was first described by Charles Bell (1830) and 
especially studied by Duchenne and Benedict. Neuropathic tendencies 
are noted in most cases; 83 per cent, occur in males, 93 per cent, occur in 
those between twenty and sixty years of age and most cases develop 
between twenty-five and thirty-five. Worry is a frequent factor ; toxemia, 
cold, trauma, neuritis and neuralgia are possibly factors. The disease 
practically never occurs in those who write properly, i. e., move the arm 
from the elbow or the shoulder, but develops in those who use the little 
finger or wrist as the basis of movement. Some accuse the coordinating 
cortical or subcortical centres; the occasional atrophy and paresis 
suggest localization in the cord or nerves. Meige terms it a functional 
anarchy. 



MYOTONIA 933 

Symptoms. — Gradually fatigue, pain aud cramping in the muscles of 
the forefinger and thumb, may extend to the forearm or shoulder. There 
may be the "lock spasm" of Mitchell, in which the pen is spastically 
held or thrown from the fingers. On rest, the tonic spasm disappears, 
but reappears with attempts to write. In Benedict's classification we 
find the spasmodic, paralytic, tremulous and neuralgic forms, which are 
of less interest as types than as showing the various symptoms, which 
are often combined in a single case. Vasomotor symptoms may occur, 
as. flushing or glossy skin. 

Differentiation. — Differentiation, according to the type, from hemiplegic 
weakness, paralysis agitans, musculospiral paralysis and neuralgia, is 
easy. Similar cramps are observed in telegraphists, milkmaids, weavers, 
cigarette rollers, tailors, shoemakers, miners, athletes, watchmakers and 
violin and piano players. Neuroses of the throat in public speakers, 
jaw spasms in gum chewers and lumbar spasm in physicians who drive 
much are described. 

The outlook is poor, because the unfortunate sufferer is often com- 
pelled to write until the affection is firmly fixed and when able, usually 
returns to the same work. In some cases the muscles may waste. 

Treatment. — Rest is essential to recovery, because treatment for the 
usual nervous symptoms alone never succeeds. Plaster casts are some- 
times successfully employed. Even when the subject learns to write 
with the other hand it often develops there. Prevention is possible by 
writing free-hand from the shoulder; holding the pen between the first and 
second fingers, use of pens with large handles, of quills and of forearm 
splints with the pen attached to the extremity, are also helpful. Active 
systematic gymnastics, passive manipulations and weak phenol solutions 
injected into tender neuritic spots are helpful. 

MYOTONIA (THOMSEN'S DISEASE). 

Myotonia is usually called myotonia congenita from its leading causal 
element, heredity. It was described by Ley den but more fully by Thom- 
sen (1876), who was a victim among 20 cases in his own family in five 
generations. This rare affection, of which there are 102 reported cases 
(Koch, 1904), occurs chiefly in males and in Germany and Scandinavia. 
Its pathology is obscure, for the only two necropsies showed no nervous 
alteration. Muscle fibers, excised during life, show hypertrophy, de- 
creased striation, nuclear multiplication and slight interstitial increase 
suggesting a myopathic process. 

Symptoms. — A peculiar transient tonic muscular rigidity develops 
when the muscles are first used, which limits or arrests movement, 
but wears off as their use is persisted in. It is intense when a new kind 
of movement is undertaken. The longer the muscles are rested the 
more severe is the initial spasm on exertion. Rigidity does not follow 
passive muscle movement, although firm pressure or a sharp blow initiates 
it. It appears perhaps "in the cradle," but generally between the ages of 
four and ten; it increases as the muscles develop and then becomes 
stationary for life. In one case improvement was observed. The legs 



934 THE NEUROSES 

are more affected than the arms, but in exceptional cases the face, tongue, 
bladder or the respiratory muscles may be affected. They are usually 
stronger and sometimes larger than normal. Sedgwick noted von Graefe's 
sign in five generations. 

Though the tendon reflexes and the mechanical and electrical excit- 
ability of the nerves are practically normal, application of the galvanic 
current to the muscles produces sluggish, prolonged closing contractures, 
with either pole and become tetanic with strong currents, the myotonic 
reaction of Erb. Undulatory contractures follow strong faradic stimula- 
tion. Subjects of myotonia are frequently irritable or hypochondriacal. 

Treatment. — Thomsen believed that exercise retarded the disease. 
Strychnine is apparently of value. Cold, dampness, excitement and 
fatigue are to be avoided. 

The following are allied affections: the congenital paramyotonia of 
Eulenberg, consisting of tonic spasms, which occur especially in the 
arms, and often affect the eyes and mouth; the ataxic paramyotonia of 
Gowers, in which tonic spasms may last the entire day, with muscular 
weakness, ataxia, especially in the hands and disturbed sensation or 
anesthesia in the fingers. In myotonia atrophica, there are (1) weakness 
and wasting of the orbicular muscles of the mouth and eyes ; the temporals 
and masseters; the vasti muscles of the thighs with the recti femoris 
frequently escaping completely; the muscles of the anterior tibial groups, 
resulting in bilateral foot-drop. (2) The myotonic phenomenon evidenced 
more particularly by a marked difficulty in extending the fingers from 
a flexed position. (3) The deep reflexes are depressed according to the 
degree of muscle wasting. 

PARALYSIS AGITANS. 

This affection is also known as shaking palsy or Parkinson's disease; 
it was first described by Parkinson in 1817. 

Etiology. — (a) Most cases occur between the ages of forty and sixty- 
five, (b) Sixty-six per cent, of cases are men. (c) A neuropathic tendency 
is present in 15 per cent. 

Pathology. — It is classed among the neuroses, because of the absence 
of any constant pathological finding. Arteriosclerosis is often found, 
since paralysis agitans occurs in the early degenerative period ; Gordinier 
shows that (a) general arteriosclerosis is less marked than that of the 
nervous tissue; (6) the arteries in the cord are markedly changed and 
around them are (c) neurogliar sclerosis and (d) pigmentation and atrophy 
of the nerve fibers. Camp found swelling, increased nucleation, hyaloid 
changes and atrophy of the muscle fibers. 

Symptoms. — The cardinal symptoms are tremor and stiffness, slowness 
of movement, shortening and weakening of the muscles, (a) Tremor 
in 66 per cent, of cases is the first symptom; it is sometimes absent 
(paralysis agitans sine agitatione). It is most marked in the hands. 
It affects first one hand and usually next reaches the leg of the same 
side, then the opposite hand, the opposite leg, and lastly the trunk, so 
that it is successively a monoplegic, hemiplegic or finally a diplegic 



PARALYSIS AGITANS 



935 



tremor. It is slow (4 to 7 oscillations per second), rhythmic, fine at the 
onset but somewhat coarser later, persists during rest, ceases during sleep 
and ceases momentarily on voluntary action. In rare cases it appears 
only on movement, as intention tremor. In the hands it may affect 
chiefly the flexors and extensors at the metacarpal joints or the interossei, 
which give the spinning or pill-rolling movement. The wrists may be 
abducted and adducted, rarely supinated and pronated, and the arms 
and shoulders are implicated but little. The writing is tremulous. The 
feet are mostly involved at the ankles 
and the toes but little. The thigh 
adductors often tremble. Trembling 
is infrequent in the face, neck and 
back, while the abdomen entirely es- 
capes. The head and body may of 
themselves tremble, but much of it is 
imparted to them from the limbs. 
In the rarest cases the tongue, palate, 
larynx and epiglottis tremble. 

(6) Muscular rigidity and shorten- 
ing, weakness and slowness of move- 
ment usually follow the tremor; slight 
symptoms are detected early and 
anticipate tremor or exist without it. 
These changes result in the follow- 
ing: (i) The mask-like Parkinson 
fades, which is devoid of lines or ex- 
pression; the eyelids wink seldom. 
The forehead shows transverse 
folds because of the bowed head and 
body. The eyes move tardily in 
reading, and the entire body must be 
turned to enable the patient to look 
laterally. There is also slow, mo- 
notonous, monosyllabic speech, with 
hesitation at first, but hurried at 
the finish, (ii) The attitude is char- 
acteristic, because of the flexor posi- 
tions assumed ; the head and the chin 
are held forward, the neck is ex- 
tended and rigid, the body is inclined 

forward, the elbows are fixed and brought somewhat forward and away 
from the body; the forearms are brought toward the body, the trembling 
thumb and index-finger are apposed, or the fingers deviate toward the 
ulnar side as in arthritis deformans, and in standing the knees are some- 
what bent and at times closely apposed. The body expression, we may say 
is like that of the face, (hi) The gait is equally characteristic. Like the 
speech, it is initially hesitant, later hurried. The patient, when once 
started, may not be able to stop himself. Trousseau spoke of the patients 
as "chasing their centre of gravity." This destination or propulsion is 




Fig. 78. — Side view of a case of par- 
alysis agitans, showing forward inclination 
of the trunk. Tendency to propulsion. 
(Dercum.) 



936 THE NEUROSES 

purely mechanical from the forward bodily inclination, although inter- 
preted by Charcot as a forced movement. To counteract the throwing 
forward of the centre of gravity the arms may be carried behind the back. 
In some cases, if the patient is pushed backward or sidewise, he may not 
be able to stop for some steps; this is retro- and later opulsion. (iv) The 
palsy is often slight and rarely extreme, although simulated by the help- 
lessness caused by rigidity. The patient is not inclined to exertion, 
"moves like a piece of machinery," as Parkinson describes it, and may 
not be able to turn over in bed. Patients have drowned from falling 
on the face in a small puddle of water. Muscular reaction requires 
40 per cent, more time than normal. 

The mind is clear, but stiff like the face and limbs, and a certain rest- 
lessness, irritability or apathy may be detected; insomnia is common. 
Sensation is essentially normal, although pains, pruritus, paresthesia and 
hypesthesia are seen in 35 per cent, of cases. Vasomotor disturbance 
most often assumes the form of a feeling of heat; indeed the peripheral 
temperature may be increased several degrees. Severe sweats are common. 
The pupillary, cutaneous, tendon and organic reflexes are normal. 

Course and Prognosis. — The onset is usually gradual and the course 
covers several decades. The outlook is most favorable in atypical 
cases. Remissions may occur, but the disease progresses steadily. Death 
occurs from intercurrent pneumonia, arteriosclerosis, cerebral softening, 
myocardial insufficiency, nephritis and kindred lesions. 

Diagnosis. — Confusion is possible in the early hemiplegic forms, but 
the absence of a paralytic stroke and the later course are distinctive. 
Charcot and Orden stein (1868) clearly differentiated the affection from 
multiple sclerosis (q. v.). The fine, senile tremor, the hereditary tremor 
of Dana, tremors due to overexertion or excitement, to toxic causes 
(alcohol, nicotine, lead, mercury, coffee, opium or chloral), weakness of 
convalescence from acute infections, paretic dementia or epilepsy, 
Graves's disease, hysteria and neurasthenia are excluded by the absence 
of the Parkinson rigidity, facies and festination. 

Treatment. — Treatment of the probably fundamental arteriosclerosis 
may possibly retard the disease, but prophylaxis is possible in the early 
stages only. All mental and physical fatigue should be avoided. The 
administration of full doses of iodide, chloral, opiates, bromides, hyoscine, 
or duboisin may mitigate the tremor, but lower vitality and disturb 
function. Parathyroid gland is recommended. 

PERIODIC FAMILY PARALYSIS. 

This affection was first described by Cava re (1853) and more fully 
by Westphal (1885); Holzapple collected 70 cases (1905); Goldflam 
collected 11 cases in one family and E. W. Taylor 12 in another. Most 
cases occur in adolescence, chiefly under twenty-five; it recurs every 
few weeks or months, possibly every day, or only at intervals of years. 
Its symptoms are almost wholly motor, producing a flaccid paralysis in 
the legs and arms, less often in the trunk, and exceptionally in the face, 
neck, tongue and throat. It occurs without apparent cause, usually 



MIGRAINE 937 

during sleep, from which the patient awakes with a sense of weakness or 
dulness which develops into paralysis within twentj^-four hours. Mental, 
sensory, cranial nerve and special sense symptoms are rare. The pulse 
is often slow and cardiac dilatation has been observed. Sudden death 
sometimes occurs in an attack. The deep reflexes are decreased or 
abolished, often also those of the skin, and the faradic excitability of 
the nerves and muscles is lessened or absent. The patient is well in a 
few hours or days, until another attack occurs. The disease usually 
subsides spontaneously after the fiftieth year of life. Goldflam's theory 
of auto-intoxication is supported (a) by J. K. Mitchell, Flexner and 
Ebersoll, who found increased secretion of kreatin before and during the 
attack; (6) by Crafts and Irwin, who isolated toxins from the feces; 
(c) possibly by the fact that potas. citrate sometimes lessens or aborts 
the seizure. Bernhardt and others consider the disease affiliated with 
myotonia and progressive muscular atrophy. Holzapple administers 
potas. bromide in .doses of thirty grains. 

MIGRAINE. 

Hemicrania, megrim, is an hereditary neurosis, with paroxysmal aura?, 
headache and vomiting. 

Etiology. — (a) Heredity is a conspicuous cause (90 per cent. Mobius), 
directly as migraine or indirectly from neurotic, gouty or epileptic ante- 
cedents, (b) Thirty-three per cent, of cases begin between the fifth and 
tenth, 40 per cent, between the tenth and twentieth years, and the 
remainder usually before the thirtieth year, (c) Exciting causes are 
constipation, dyspepsia, overexertion, alcohol or sexual abuse, emotional 
factors, pelvic disorders and lactation. 

Symptoms. — As preliminary symptoms the patient may feel depressed, 
or, in some cases, especially well and energetic. They occur in cases in 
which the sensory symptoms are least marked. Sometimes the pupils 
are dilated. Most attacks develop during the night. 

Aur^e. — In over 50 per cent, of cases, auras are (a) sensory, as visual 
aura?, a cloudiness before the eyes, sparks, lightning, zig-zag forms, 
etc.; they are most often bilateral and affect the homologous half-fields; 
taste and smell may be similarly affected ; paresthesia may occur, usually 
as hemiparesthesia ; (b) motor auras are much less common, as aphasia, 
dysphasia or motor weakness on the contralateral side; in the very rare 
ophthalmoplegic migraine, there are fugitive ptosis, outward strabismus, 
double vision and a dilated immobile pupil; mental auras are uncommon, 
as anxiety, confusion and double consciousness. The auras last for ten 
to fifteen minutes. 

The Attack. — (a) Headache, the cardinal symptom, at first is intense 
and circumscribed, over the eye, temple, occiput or forehead; then it 
spreads over one side (hemicrania), sometimes affects the opposite side 
or rarely reaches the neck or arm. The pain is deep, being most often 
boring, and even as intense as in brain tumor or meningitis. It is in- 
creased by movement, stooping or lying down. The special senses are 
hyperesthetic. The mind is usually clear and often acutely active, 



938 THE NEUROSES 

sometimes there is double consciousness, and in rare cases stupor, (b) 
Nausea follows, often with vomiting of undigested food and finally of 
bile — "bilious headache." Feeding and medication are impossible in 
severe cases. Vomiting may be attended by hyperacidity or moderate 
collapse, as in sea-sickness, (c) Vasomotor symptoms may be present, 
of the spastic type with pallor, coldness, wide pupils and retraction of the 
eye-balls. Thoma found the temporal artery sclerotic on the side of lesion, 
and de Giovanni noted a marked arcus senilis on the same side. The 
pulse may be slow and tense and the breathing superficial. In the 
paretic type, there are redness of the skin, small pupils, sweating and 
increased flow of saliva or tears. Very rarely is there erythromelalgia, 
edema or ecchymosis. It is best to regard these sympathetic symptoms 
rather as a result than as a cause of the attack. 

The attack ends with the vomiting, after which the patient frequently 
sleeps, or with almost critical sweating, lachrymation, polyuria or epistaxis. 
The attack lasts from ten to twelve hours; the term status hemicranicus 
is used for cases of long duration or those in which the attacks overlap. 
Most attacks are atypical, as headache alone, vomiting alone, or headache 
with vomiting; in a few cases the attack aborts with the aura. The 
aurse, pain, gastric and cardiac inhibition, vasomotor symptoms and 
vomiting prove that migraine is a functional cerebral affection. 

Course and Prognosis. — When the disease is established in youth its 
attacks become more frequent in adolescence and usually last until the 
forty-fifth or fiftieth year. The periodicity, noted by Tissot, Trousseau 
and Liveing, has not been explained. Overwork, worry, menstruation 
or change of routine may precipitate an attack at a regular or irregular 
interval. Attacks may cease during an intercurrent pregnancy, tabes or 
gout. The school of Charcot emphasized the fortunately rare danger 
of transformation into epilepsy, labyrinthine vertigo or some psychosis. 
Complete cases are more obstinate and dangerous than light forms. 

Diagnosis. — With a history of heredity and development in childhood, 
the full attack is most characteristic. "Sick headache" is practically 
always migraine. Atypical forms may be confused with various head- 
aches, classified as follows: 

1. From nervous affections, as (a) cerebral neurasthenia, in which there 
is a sense of constant pressure rather than actual headache, without 
nausea, but with paresthesia, and in location frontal or general, some- 
times occipital or temporal; (6) hysteria, which is less common (clavus 
headache, "neuralgic headache"), and sometimes is precisely like mi- 
graine; (c) epilepsy, which some consider as identical with migraine; 
the epilepsy aura is shorter and loss of consciousness is the most con- 
stant symptom; (d) meningitis, which in all types is early and severe; 
(e) hydrocephalus, which is often severe, especially in acquired forms ; (/) 
brain tumor, which is constant, generalized, often very severe and some- 
times typically hemicranic ; (g) paretic dementia, in which migraine is fre- 
quent; care is necessary when migraine occurs after syphilitic infection. 

2. From affections of the special senses, as eye-strain, hypermetropia ; 
glaucoma, which most often produces frontal headache; nasal disease, 
which may cause sinus involvement with frontal headache. 



NEURALGIA 939 

3. From toxemia, (a) Those due to acute infectious are usually frontal 
and dull, but sometimes occur in other locations and are severe, deep- 
seated and increased by stooping ; the rheumatic or indurative headache 
is oftenest occipital, attended by tenderness, often by induration and 
pain on motion; it is severe; (b) intoxication by alcohol, nicotine, 
lead, nitroglycerin and opium, and (c) constitutional states, as gout or 
arthritis, (d) In nephritis they are usually frontal, remittent or contin- 
uous, but sometimes sharply hemicranic. (e) In gastric affections they are 
exceedingly common, mostly occipital, but sometimes vertical or frontal. 

4. From circulatory causes, as from wearing a tight collar, repeated 
coughing, cardiac disease or arteriosclerosis (with vertigo), and usually 
increased by lying down. 

5. From anemia, especially from chlorosis, as a "tugging" sensation 
back of the eyes or frontal or generalized headache, and often relieved 
by lying down. 

Treatment. — Prophylaxis is said to be of little value, but many subjects 
recognize the warnings and avert the attacks by resting, on noting unusual 
mental or physical capacity for work or an unusual appetite, which ushers 
in some attacks. Migraine subjects should observe moderation in eating, 
especially of meat, in work, exercise or recreation, narcotics, stimulants, 
as coffee or tobacco, and in sexual matters. Immoderation is a neurosis 
in itself. Hurry, worry and tension must be avoided and their first 
manifestations must be learned and treated. The extract of cannabis 
indica, gr. \-\, given for weeks or months, after Seguin's plan, is almost 
the only remedy which helps the condition, and then only in some cases. 
Mobius finds that salicylate of soda, gr. xv, in black coffee, given the even- 
ing before the attack, often wards it off. Nitroglycerin in full doses 
sometimes aborts it, as may washing out the stomach and following the 
lavage with a saline. 

In the treatment of the established attack, bromides constitute the best 
remedy; they are given not only during the attack in the mild type, 
but continuously, as in epilepsy, when the type is severe and frequently 
repeated (Liveing and Charcot). Phenacetin often helps mild forms 
and those with initial rise of blood-pressure. Morphine is to be avoided. 
The stomach sometimes rejects all medication, which must then be 
given by rectum. Application of cold to the head, hot foot-baths and 
sinapisms to the nape of the neck and epigastrium are subordinate helps. 



NEURALGIA. 

Pain is only a symptom, usually of an affection of a peripheral sensory 
nerve, although in rare cases affections of the cortex, pons, medulla or 
parts near the thalamus may cause peripheral pain. The pain of neuralgia 
and neuritis may be confused. 

Etiology.- — (a) Neuralgia occurs mostly in adult life (twenty to sixty) 
and rarely before puberty or after sixty, in which case it is usually severe 
and intractable. (6) Most cases occur in women, (c) Heredity is an 
apparent factor in 25 per cent, of cases, especially in neuropathic, weakly 



940 THE NEUROSES 

or gouty families, (d) Debility from exhausting conditions, as lactation, 
anemia, overwork, sensory fatigue, as from eye-strain, sexual or other 
excesses, emotional conditions and trauma may cause it. (e) It may 
result from acute infections, notably influenza, typhoid at its onset, 
malaria, the causal importance of which has been much overestimated, 
rheumatism (from exposure to cold) particularly of the fascial type, and 
sometimes syphilis. (/) Alcoholism, diabetes, plumbism, gout and neph- 
ritis may produce it; most of these are also causes of neuritis, differentia- 
tion from which may be difficult, (g) Nerve affections, as sciatica and 
neuritis, herpes zoster, reflex irritation, as radiated from a carious tooth, 
compression of a nerve trunk by varices, aneurysms or neuromata or the 
root pains of tabes, may cause neuralgia, (h) Arteriosclerosis may affect 
the nutrient nerve vessels. 

General Symptoms. — The pain presents the following characteristics: 
(a) It is always paroxysmal, with intervals of total or relative relief; 
intense pain is never constant, (b) It recurs irregularly at intervals 
varying from hours to months or with surprising periodicity on a given 
day or hour, perhaps at the menstrual period; periodicity is as frequent 
in non-malarial as in malarial cases, (c) It is usually unilateral, generally 
constant in its seat, and most often found over the distribution of a single 
nerve or several nerves; bilateral pain is usually symmetrical. The pain 
may shift from place to place, especially when due to systemic causes. 
It is probable that the spinal cord may be the medium of radiation of 
pain from one region to another and that pain may follow the distribution 
of the spinal segments rather than that of the peripheral nerves, as in 
herpes zoster, (d) Its onset and cessation are sudden and spontaneous; 
an imminent attack may be precipitated or existing pain may be aggra- 
vated by muscular movements, a breath of air or a simple touch; the 
character of the pain is sharp, stabbing, rarely pulsating; if it travels 
along the nerve trunk its shooting direction is usually centrifugal, rarely 
centripetal; if it is localized it is commonly burning or boring, (e) 
The pain is usually deep, but the skin is very hyperesthetic. (/) The 
"tender points" of Valleix (1811), later called maximal points by Head, 
are found in the nerve (50 per cent.) both in the attack and the free 
interval, especially where the nerve emerges from the bone or fasciae, lies 
on hard surfaces, divides or anastomoses. The occasional tenderness over 
the spine at the origin of a nerve (Trousseau's point apophysaire) occurs 
in many other conditions. In neuritis the nerve trunk along its entire 
accessible course is tender, (g) Vasomotor constriction, followed by dilata- 
tion, is fairly common. Edema, erythema, blanching or falling out of the 
hair, secretory disturbances, herpes, pigmentation, numbness or tingling, 
trophic alteration of the skin, localized hypertrophies and reflex twitch- 
ings of the muscles are much less frequent than in neuritis. Persistent 
pain or its etiological factors may reduce the general nutrition. 

Local Clinical Varieties. — 1. Trifacial neuralgia (prosopalgia, tic 
douloureux) is the most important, severe and frequent type, because 
the fifth nerve is most exposed to trauma, compression and infection, by 
way of the eye, nose and ear. The entire nerve is not usually affected, 
though pain may radiate from one division into another; indeed only the 



NEURALGIA , 941 



secondary branches of a single division may be involved. The general 
features of neuralgia are present, as already described, (a) Involvement 
of the first branch is the most common form; pain occurs over the eye, 
forehead and frontal sinus (in which the familiar pain is experienced 
after eating ice-cream) ; it sometimes radiates into the second and third 
branches; there are "tender points" over the lower edge of the nasal 
bone, the supra-orbital notch, less often over the supra-orbital nerve, 
even to the vertex, sometimes over the occiput or over the cervical spines ; 
cold, carious teeth, disease of the sinus, glaucoma, hypermetropia, etc., 
are causal factors. (6) When the second branch is involved there is pain 
over the side of the nose and cheek from the infra-orbital region to the 
upper lip; there are "tender points'' over the lower border of the nasal 
bone, the malar bone, the infra-orbital foramen, the gums over the 
canine teeth, and sometimes in the hard palate; among other causes is 
the dental alveolitis in the aged, due to sclerosis. Diseased teeth may 
cause neuralgia without local dental symptoms and in every severe case 
the dentist should be consulted, (c) Involvement of the third branch 
is the least frequent form; inframaxillary pain, along the lower teeth, 
tongue, chin, external ear and maxillary region; and tenderness over 
the auriculotemporal nerve and inferior dental foramen may occur. 
In old persons the loss of the teeth brings the jaws closer and therefore 
stretches the inf. dental nerve; it is relieved by proper plates. In severe 
forms vasomotor symptoms and increased secretion from the eyes, nose 
and salivary glands are usually present. Hyperalgesia is such that the 
face cannot endure simple contact, and drinking, mastication and wiping 
the nose cause great suffering. Herpes and trophic changes are probably 
neuritic rather than neuralgic symptoms. In rare instances facial spasm, 
transient reflex ptosis, internal strabismus or myosis coexists. Differ- 
entiation: In headache and migraine there are no tender points; intra- 
cranial disease, as tumor or syphilis, is usually excluded by systematic 
examination. The prognosis is doubtful in severe forms, which are often 
life-long in duration and agonizing in degree. 

2. Cervico-occipital Neuralgia. — There is pain in the first four 
cervical nerves, especially the inferior occipital and auricularis magnus; 
this pain sometimes radiates into the fifth nerve; there is tenderness 
half-way between the mastoid and spine, over the parietal eminence and 
over the cervical plexus between the sternomastoid muscle and trapezius ; 
this form is often bilateral and is less intermittent than other neuralgias, 
which facts are explained by its frequent connection with cervical caries 
and syphilis, and with tumors, meningitis, root disease and affections 
of the ear. 

3. Phrenic Neuralgia. — Phrenic neuralgia is rare; it sometimes 
occurs in pericarditis and diaphragmatic pleurisy; it is usually left-sided, 
with pain and tenderness over the insertion of the diaphragm and nerve 
trunk in the neck; movements involving the diaphragm are painful. 
Differentiation is usually uncertain. 

4. Cervicobrachial Neuralgia. — Any nerve may be involved, 
especially the ulnar and circumflex. Pain may radiate over the entire 
plexus and chest; the tender points are most often in the axilla, shoulder 



942 THE NEUROSES 

and ulnar distribution; it is often confused with neuritis from trauma, 
compression, rheumatoid arthritis or other organic disease. 

5. Intercostal neuralgia ranks third in frequency after trifacial 
and sciatic neuralgias (neuritis). Pain is felt along the intercostal nerve 
and tenderness over the points of emergence of its three branches, over the 
angle of the ribs, in midaxilla and near the mammary line. It is more 
easily distinguished in the upper than lower interspaces. Differentiation 
may be difficult in muscular rheumatism in which movement is more 
painful. Peritoneal disease, ulcer, spinal caries, aneurysm and tabes 
must be distinguished. It is most common in gastrohepatic affections 
and neurotic women. 

Herpes zoster is an acute inflammation of the posterior root ganglia 
(Barensprung and Charcot) which are the seat of a cellulohemorrhagic 
exudation; its fibers to the posterior column degenerate. It is mentioned 
in this connection because of the acute pain preceding and associated 
with the rash, which appears after three or four days; the pain is often 
protracted and intractable ; the pain on the trunk follows the distribution 
of the spinal segments rather than that of the intercostal nerves. J. 
Ramsay Hunt collected 15 cases of herpes of Gasserian origin, associated 
with ocular palsies, and 60 palsies associated with herpetic inflammation 
of the geniculate ganglion, and also describes herpes zoster of the face 
and neck with auditory symptoms and facial palsy. 

6. Lumbar Neuralgia. — This infrequent type occurs in the ilio- 
hypogastric, ilio-inguinal and genitocrural, sometimes in the ext. cutane- 
ous, obturator and crural nerves. The pain is felt over the iliac crest, 
inguinal canal, labium or testis (irritable testicle). 

7. Sacral Neuralgia. — Coccygodynia is neuralgic and occurs mostly 
in women. The pain is increased by sitting, coitus and defecation; it is 
obstinate and resists even operative measures. 

8. Pododynia. — Neuralgia of the heel is termed pododynia; plantar 
neuralgia, which is mostly neuritic, occurs in acute infections and caisson 
disease. Morton's metatarsalgia, regarded as bony compression of the 
fourth metatarsophalangeal nerve, usually occurs in one foot and mostly 
in women; operation is usually indicated. 

9. Visceral Neuralgias. — (See Diseases of the Heart, Stomach and 
Kidneys, Hysteria and Neurasthenia). Under this caption may be given 
Head's areas of pain referred to visceral disease : the organ is first given, 
and following it is the area to which its pain is reflected: Heart: 1st, 
2d, 3d dorsal segments. Lungs: 1st, 2d, 3d, 4th, 5th dorsal segments. 
Stomach: 6th, 7th, 8th, 9th dorsal; cardiac end from 6th and. 7th. 
Pyloric end from 9th. Intestines: (a) Down to upper part of rectum, 9th, 
10th, 11th and 12th dorsal, (b) Rectum, 2d, 3d, and 4th sacral. Liver 
and gall-bladder: 7th, 8th, 9th, 10th dorsal; perhaps 6th dorsal. Kidney 
and ureter: 10th, 11th and 12th dorsal. The nearer the lesion lies to the 
kidney the more is the pain and tenderness associated with the 10th 
dorsal. The lower the lesion in the ureter the more does the 1st lumbar 
tend to appear. Bladder: (a) Mucous membrane and neck of bladder, 
1st, 2d, 3d, 4th sacral. (6) Overdistention and ineffectual contraction, 
11th and 12th dorsal and 1st lumbar. Prostate: 10th, 11th, 12th dorsal, 



NEURALGIA 943 

1st, 2d, 3d sacral and 5th lumbar. Epididymis: 11th and 12th dorsal 
and 1st lumbar. Testis and ovary: 10th dorsal. Appendages: 11th and 
12th dorsal and 1st lumbar. Uterus: (a) In contraction. 10th, 11th, 
12th dorsal and 1st lumbar, (b) Os uteri. 1st, 2d, 3d and 4th sacral. 

Treatment. — Logically, the treatment of the cause (q. v.) should precede 
that of the symptoms, but practically, pain is the prime indication for 
therapeutic measures. 

1. Local Measures. — Pressure on tender points may diminish or 
abolish pain. As in sciatica, blisters and sinapisms (both of which may 
leave permanent pigmentation on the face), the cautery, local heat, 
acupuncture or injections of water or cocaine may give relief. Freezing 
the skin by ethyl chloride often gives better results. Menthol, camphor- 
chloral (equal parts) and liniments are of some value (tr. aconiti, tr. 
chloroformi, tr. belladonnas aa 3ij> linimentum saponis^iv). Injections 
of 1 per cent, solution of osmic acid into the nerve trunk are very success- 
ful; they were recommended by Billroth and Neuber (1884). Schlosser 
(1900) recommended alcohol injections; Patrick treated 75 cases without 
a failure and Kiliani 190, with 5 failures. Massage is often beneficial, 
for the muscles and nerves have common veins. 

2. Nutrition. — A full diet, with milk and cod-liver oil, the Mitchell 
rest-cure, hydrotherapy and massage, are often beneficial, especially with 
change of climate or surroundings. Alcohol, which is always dangerous, 
is most often indicated in older subjects. The beneficial effects of castor 
oil are often great, probably because it promotes elimination. Gouty 
subjects may thrive on a vegetable diet. 

3. General Drug Treatment. — Dana gives strychnine hypoder- 
mically in doses of -§-$ gr. even up to \ gr. Arsenic, iron and phos- 
phorus are excellent in anemic, malarial and degenerative types; quinine 
is beneficial in non-malarial as well as malarial types and in trifacial 
neuralgia especially, although its value is overestimated. Valerian, 
cannabis indica and bromides should be given for irritability; salicylates 
for rheumatism and colchicum for gout ; iodides are sometimes of benefit 
to non-syphilitic subjects; full doses of nitroglycerin are frequently helpful. 

4. Analgesics. — Acetanilide (gr. v) and the other coal tars should 
be used in fresh cases. Extr. cannabis indicse (gr. J) and fluidextr. 
gelsemii (ITlij-iv) should be administered every three to six hours in 
the less severe cases. In acute febrile or rheumatic cases, fluidextr. 
aconiti (TTlj-ij) should be given every two hours until tingling in the 
mouth or extremities and slowing in the pulse intervene. Liebreich 
advocates croton-chloral, gr. v, or with care even gr. xx, for several 
doses. Finally, in severe cases, morphine, as far as possible, should be 
avoided; sometimes its administration is inevitable; though some writers 
find that it tends to prevent recurrence, the pain often develops again, 
intensified; atropine sometimes more permanently controls the pain than 
does morphine. 

5. Electrotherapy sometimes relieves pain, as galvanization with a 
weak current, just strong enough to produce a sensation of burning and 
applied with the sponges warm and with the anode to the painful area, 
especially in newly developed cases, 



944 THE NEUROSES 

6. Surgical therapy includes nerve section, resection, stretching 
or divulsion; these procedures often fail. In incoercible trigeminal 
neuralgia the Gasserian ganglion may be extirpated (Rose, 1890), but 
this operation entails a high mortality, and loss of the eye may result. 

VASOMOTOR AND TROPHIC NEUROSES. 

Vasomotor centres exist in the cerebral cortex and medulla. The 
fibers probably run in the lateral columns of the cord and leave by the 
anterior roots. Vasomotor paralysis occurs independently or with func- 
tional or organic disease. Paralysis of the cervical sympathetic may 
result from trauma, aneurysm, tuberculous apical or glandular disease 
or disease of the cord. It is attended by redness, rise of temperature, 
pulsation and tortuosity of the vessels, sweating, unrest, ringing in the 
ears and palpitation. In paralysis of the cervical sympathetic there 
are pupillary narrowing from the unopposed action of the third nerve, 
slight ptosis, narrowing of the interpalpebral fissure from paresis of 
Miiller's muscle, salivation, lachrymation and in cases of long standing, 
retraction of the eye and flattening of the cheek. The pupil reacts 
somewhat to light but not to stimulation by pain or pinching of the skin 
of the neck (Mobius); the pupil can be widened by atropine, but to a 
less degree than the normal eye. 

Vasomotor spasm presents converse symptoms — pallor, coldness, 
small vessels and frequently a sense of tingling or arterial pain. Two 
examples are nervous angina pectoris and Raynaud's disease; spasm 
(contraction, irritation) of the cervical sympathetic produces wide 
pupils, an increased interpalpebral fissure and exophthalmos. 

Little is known of the trophic nerves, if indeed separate nerves sub- 
serve nutrition. If they exist they are probably closely related to the 
vasomotor tracts. Trophic changes may be symptomatic of disease of 
the nerves or cord, as in neuritis or nerve trauma, facial hemiatrophy, 
tabes, syringomyelia and myelitis. 

Erythromelalgia. — Erythromelalgia, described by Graves (1843) and 
S. Weir Mitchell (1872), indicates redness and pain in the extremities. 
It occurs mostly between the years of twenty-five and forty and is slightly 
more frequent in males. Pathologically, Mitchell and Spiller find neuritis 
and sclerosed arteries. The toes (less often the fingers) and balls of the 
toes are the seat of severe, paroxysmal pain, swelling and redness, par- 
ticularly when the limbs depend; the arteries throb and the veins are 
engorged; the color is sometimes blue. Pain is occasionally experienced 
in the head or neck and vertigo and muscular weakness may be noted. 
The symptoms occur mostly in warm weather and generally disappear 
in winter. The clinical course is long, the prognosis doubtful and the 
treatment consists of electrotherapy, cool baths, acetanilide and iodides. 

Acroparesthesia. — Closely related to erythromelalgia, it was described 
first by Nothnagel, and F. Schultze (1890) named this very frequent 
affection; its derivation signifies paresthesia of the extremities. More than 
90 per cent, of cases occur in women between thirty and sixty years of 
age. The etiology is doubtful (stasis or arteriosclerosis). The chief 



VASOMOTOR AND TROPHIC NEUROSES 945 

feature is an unpleasant crawling, tingling sensation, sometimes amount- 
ing to actual pain in the fingers or hands, less often in the toes or feet. 
The discomfort is greatest at night and in the early morning; it is per- 
ipheral and symmetrical but does not correspond with any nerve area. 
Generally there are no objective findings other than occasional vasomotor 
disturbance or slight sensory blunting. The outlook is favorable, the 
course is chronic and the faradic brush frequently affords relief. 

Spontaneous Symmetrical Gangrene. — Raynaud's disease was first 
described by Raynaud (1862). Sixty-six per cent, of cases occur in 
women, who are usually delicate, anemic and neurotic, and most cases 
develop in persons between twenty and forty-five years of age. In 10 
per cent, it is hereditary. Other causal factors are uncertain, as expo- 
sure to cold and dampness, exhaustion and acute infections. Occasional 
coexistence is noted with hysteria, neurasthenia, epilepsy, tabes, syringo- 
myelia, angioneurotic edema, neuritis, acute mania, etc. Its pathology 
is not established, but arterial spasm, endarteritis and neuritis are said 
to exist. There are three stages: (a) Local ischemia (or syncope) begins 
with pallor and coldness of one or two fingers, perhaps of the entire 
hand or of the toes and is attended by numbness or severe pains. The 
"dead fingers" or toes appear on exposure to slight cold or on emotion 
and reaction occurs after a variable period. The process may not pass 
this stage. (b) Local asphyxia (or cyanosis) develops in the parts in- 
volved, at times with some swelling or anesthesia. It is most severe 
in winter and chilblains are regarded as the mildest type of this stage, 
(c) Local gangrene, which is spontaneous, symmetrical and fortunately 
rare, is the last stage. It is dry, sometimes vesicular and its extent is 
always less than the area of ischemia and asphyxia. The tips of the 
fingers or toes dry up, fall off and scars mark successive attacks. Less 
often the tip of the nose, ear, buttock, heel, shoulder or abdomen is 
involved and very rarely the tongue, penis, elbow or knee. In some 
instances there is severe general disturbance, as fever, chill, enlarged 
spleen, colic, hemoglobinuria, uremia, stupor, coma, convulsions, transient 
hemiplegia, neuritis and spastic retinal vessels. The severe or fatal 
cases occur especially in children. The course is chronic and consists of 
repeated attacks, which often abate in summer. 

Differentiation. — Differentiation is usually easy from hysterical gangrene 
(self -injury), diabetic, arteriosclerotic or embolic gangrene, syringomyelia, 
leprosy, ergotism and acute arteritis, as in typhoid. 

Treatment. — Narcotics are given for pain; warmth and elevation 
promote venous return and nitroglycerin dilates the arteries. Gushing 
advised Esmarch's constrictor for a few minutes. In actual gangrene 
surgical interference should be postponed until complete demarcation 
develops, because the area is much more circumscribed than at first 
indicated. 

Acute Angioneurotic Edema. — It was first fully described by Quincke 
(1882), although Milton (1876) described "giant urticaria." It occurs 
most frequently between the years of twenty and thirty-five and is 
slightly more frequent in women than in men. It is allied to urticaria, 
erythema nodosum and possibly to some forms of purpura, and consists of 
60 



946 THE NEUROSES 

a circumscribed edema, which is sudden in onset and in disappearance, is 
tense and pale, does not pit on pressure, sometimes causes burning and 
appears mostly on the eyelids, lips, cheek, tongue, hands or genitalia, some- 
times on the buttocks, in the pharynx, larynx, lung or digestive tract. It 
sometimes attacks several areas simultaneously. Gastro-intestinal symp- 
toms occur in 33 to 50 per cent, of cases, as epigastric pain, vomiting, colic 
or diarrhea (see p. 693). Hemoglobinuria, albuminuria and polyuria are 
less frequent. The outlook is good, except that laryngeal or pharyngeal 
localization may cause sudden death. Recurrence is not uncommon, 
perhaps with considerable periodicity. 

Treatment. — Treatment is symptomatic; nitroglycerin is recom- 
mended. Bloodgood employed deep incisions with great benefit. Wright 
exhibited calcium lactate (gr. xx) with success. 

Herz described a pseudoperiostitis angioneurotica, occurring especially 
on the thoracic bones; it is periodic, transitory, painful, tender and 
associated with neurotic cardiac disturbance. 

Chronic Hereditary Trophedema.— Twenty-two cases of chronic 
hereditary trophedema in six generations were described by Milroy 
(1893) of Omaha, 8 cases in four generations by Meige (1898) and 13 
cases in five generations by Hope and French (1898). A firm, pale, 
painless edema, chiefly below the hip or knee, develops toward puberty, 
without cardiac, renal or apparent local cause. It may appear in the 
arm and leg of the same side, including probably some of the so-called 
local hemihypertrophies. The first cases recorded were thought to be 
phlebitis. Health and life are not threatened, although treatment 
produces no results. 

Hydrops Articulorum Intermittens. — Hydrarthrosis intermittens occurs 
in 71 per cent, in persons between ten and forty years of age; about 
70 cases are on record. Its etiology is not known. Some cases present 
malarial, gonorrheal or traumatic antecedents. The knee is usually 
involved when several joints are affected and in 33 per cent, is alone 
involved. The effusion wholly disappears after two or three days, but 
it reappears obstinately every one to four weeks. There is no fever and 
usually no pain. Treatment is general. 

Scleroderma. — Described by Lusitanus and Alibert, Thirial (1845) 
gave the first full account. It is a chronic thickening and hardening of 
the skin, followed by atrophy. It is a rare affection, but is more common 
than is generally recognized. The localized form usually develops before 
and the generalized form after the twenty-fifth year. Seventy-five per 
cent, of cases occur in women. The causation is obscure; erysipelas, 
trauma, cold and neuropathic disposition are sometimes considered 
etiological and association with other neuroses, general and vasomotor, 
is frequent. Anatomically the skin and all the contained structures are 
fibrosed. In the localized form it occurs in spots or streaks, which often 
correspond to the course of given nerve trunks or spinal segments. In 
the general form the body may be literally "hide-bound." Its distribu- 
tion in order of frequency is the upper extremities, trunk, head and face, 
lower extremities, and generalized. The skin is usually first painful and 
sensitive, then reddened and thickened, and finally pale, glossy, dry, 



VASOMOTOR AND TROPHIC NEUROSES 947 

atrophic and parchment-like. It is rigid and without folds, inhibiting 
the mimetic play of the features. The nose is peaked, the lids cannot 
close over the eye-ball and may become everted. The mouth is so small 
as to sometimes necessitate extraction of some of the teeth and rigidity 
in the neck may render swallowing difficult. In the fingers it occurs in 
5 per cent, of cases (sclerodactylia, Ball). The close skin produces decided 
deformity and loss of function. Sensation is usually preserved, the secre- 
tion of sweat is usually reduced and pigmentation and trophic changes 
in the hair and nails are occasionally seen. In some cases it occurs 
with herpes (the herpetiform morphea of Hutchinson). Circumscribed 
atrophy of the bones is said to occur. Only 30 per cent, of cases improve 
and 15 per cent, recover. 

Treatment. — Treatment is unsatisfactory. Improvement has followed 
administration of salol and inunctions with oil ; thyroid extract, especially 
if used early in the disease, may promote recovery. 

Ainhum. — Ainhum was first observed by Clark (1860), then by Da 
Silva Lima (1866). It is a chronic affection, usually limited to the great 
toe, which at its plantodigital fold suffers a slow, painless, non-inflam- 
matory circular constriction and spontaneous amputation. Ainhum 
is chiefly found in the colored races of Brazil, Africa, India and sometimes 
in this country. Its nature is disputed; an ingrowth of the epidermis 
and scleroderma have been thought to be causes. It is not amputating 
leprosy, as has been claimed. 



SECTION X. 

DISEASES OF THE L0C0M0T0K SYSTEM. 



DISEASES OF THE MUSCLES. 

MYOSITIS. 

Inflammation in the muscles may be single or multiple; it may be 
an independent or a secondary affection. It may reach the muscles by 
contiguity from adjacent disease, may result from trauma, trichinosis, 
cysticercus, echinococcus, myxo- sarco- and microsporidia, sepsis, puer- 
peral fever, rheumatism, scarlatina, gonorrhea, syphilis or erythema 
multiforme. The muscles are the seat of serous, sometimes hemorrhagic 
or diffuse purulent exudation in septic forms and of fatty degeneration. 
In a form, endemic in Japan, the Staphylococcus pyogenes aureus occurs 
in pure culture. The muscles are usually friable and sometimes frag- 
mented. Polymyositis, first described by Wagner (1887), Hepp and 
Unverricht, occurs most often in youth and adolescence and is attended 
by pain, especially near the tendons, swelling and often edema in the 
muscles, and decreased tendon reflexes. The skin may participate, 
with herpes, erythema, bullse or purpura (dermatomyositis) ; the infection 
may involve the tissue in which the afferent nerves originate (muscle 
spindles), (neuromyositis, Senator). In some cases there is arthritis or 
phlebitis. Oppenheim describes a case of dermatomucomyositis with 
stomatitis, iritis and conjunctivitis. The inflammation occasionally 
reaches the tongue, pharynx, larynx or respiratory muscles and may cause 
difficult mastication or swallowing, ptosis or dyspnea. The systemic 
reaction is severe, marked by fever, chills, sweats, splenic tumor, some- 
times by angina, bronchitis, albuminuria or leukocytosis. Death is the 
usual issue. 

In muscular fibrositis, the morbid process is an inflammatory exuda- 
tion into the fibrous tissues; the swelling and thickening may be slight 
and impalpable; severe and definitely tumor-forming; acute and trans- 
ient; chronic, and eventuating in hard, fibrous lumps. The most con- 
stant symptoms are pain and tenderness; if vigorously rubbed, the swelling 
and the pain are greatly increased. If a patient presents himself with 
any of the ordinary manifestations of chronic rheumatism, as a lumbago, 
sciatica, pleurodynia, or a cephalalgia, and with any obscure myalgic 
or neuralgic pain in any part of the body, Telling urges that a careful 
investigation should be made of the fibromuscular tissues of the affected 
areas. 



950 DISEASES OF THE MUSCLES 

Differentiation. — Differentiation concerns multiple neuritis (tenderness 
over the nerve trunks, motor and sensory findings) ; trichinosis (trichinae 
in the tender, swollen muscles, eosinophilia and digestive symptoms); 
and periarteritis nodosa (q. v.). 

Treatment. — Treatment is symptomatic and is identical with that of 
sepsis. Sweats and salicylates are beneficial. 

Myositis Ossificans. — Myositis ossificans usually develops acutely 
in the muscles of the neck or back before the fifteenth year and leaves 
residual foci of infiltration, partly in the periosteum and partly in the 
fasciae and tendons, which gradually calcify. The thigh and arm are 
most severely and permanently affected. The process occurs in the 
strongest muscles and at an age when they develop most actively ; it may 
affect many muscles and runs a chronic course, perhaps of several decades. 
Schutz collected 275 cases of the localized form and A. R. Elliott, 107 
cases of the progressive inflammatory type, often associated with infan- 
tilism, microdactylia, etc. Massage is sometimes beneficial. 

MUSCULAR RHEUMATISM (MYALGIA). 

This includes many vague but important affections. It occurs par- 
ticularly in men, promoted by cold, dampness and certain occupations. 
Muscular overexertion, as straining and lifting, is frequently a part of the 
history. Rheumatic and gouty subjects are specially and recurrently 
exposed. Disorders of metabolism or mental as well as physical over- 
work mark some cases. Other forms are, as Leube insists, probably 
infectious, for fever occurs in 33 per cent, and occasionally endocarditis; 
muscular rheumatism in this sense does not generally involve many 
muscles, but usually one muscle or a single group. The pain is not 
paroxysmal, as in neuralgia, and is experienced in the muscle or reaches 
it from its tendons or fasciae. In some cases it is a mild neuromyositis. 
Its varieties are : Myalgia capitis, affecting the fascia of the head ; omalgia, 
involving the muscles of the shoulder, or rheumatic torticollis, which is 
usually unilateral; pleurodynia, which affects the pectoralis, intercostals 
and serratus, limits respiratory movements and is likely to be confused 
with intercostal neuralgia, pleurisy, periostitis of the ribs or vertebral 
disease; lumbago, which involves the lumbar muscles, and is the most 
frequent, painful and obstinate form, causing great pain on movement 
or on efforts of the uninvolved muscles to maintain quiet; it is probably 
due in some cases to muscular rupture, as after lifting. In the abdominal 
muscles and glutei it may simulate pelvic disease. In treatment, rest is 
indicated, for use of the affected muscles aggravates pain and protracts 
the condition. Involuntary movement is prevented by careful strapping 
with adhesive plaster. A hypodermic of morphine into the muscle is 
often indicated. Deep injection of water into the muscles of the affected 
part may relieve pain. Ringer's method of acupuncture with long needles 
which are pushed three inches into the back and left there for from five 
to ten minutes is beneficial, but is usually vigorously opposed by the 
patient. Very energetic massage, with the local application of heat, 
probably gives the best results. The actual cautery and constant cur- 



ARTHRITIS DEFORMANS AND CHRONIC RHEUMATISM 951 

rent give good results. Belladonna plasters afford relief. Gelsemium 
acetanilide and salicylates may relieve certain cases. 

Chronic cases, with vague, fugitive pains which come on with change 
of weather, are treated in the same way. Confusion is frequent with 
chronic alcoholism, tabes, gout and diabetes. 

AMYOTONIA CONGENITA. 

Of Oppenheim's disease, Griffith (1910) collected 49 cases. Some 
cases are apparently myopathies and others of spinal origin. This con- 
genital condition is characterized by extreme flaccidity and weakness, 
smallness and softness of the muscles, oftenest of the legs and most rarely 
of the face. The deep reflexes are lost, the faradic excitability of the 
muscles is lessened and contractures are likely to develop. There is a 
tendency toward slow improvement. 

Myotonia, paramyoclonus multiplex and myasthenia gravis are de- 
scribed elsewhere. 



DISEASES OF THE JOINTS. 

ARTHRITIS DEFORMANS AND CHRONIC RHEUMATISM. 

Excluding gouty, traumatic, trophic, tuberculous, syphilitic, gonor- 
rheal and hemophilic affections, there remains a group of articular 
affections of which the chief are arthritis deformans and the so-called 
chronic rheumatism. Several totally different affections are most un- 
satisfactorily gathered under these names. 

. Arthritis deformans is a progressive or at least chronic affection, 
marked by changes in the synovial sac, cartilages and bone, causing func- 
tional disturbance and usually symmetrical and polyarticular deformity. 

Etiology. — (a) The predisposing factors are (i) heredity, which is causa- 
tive in 13 per cent. (Garrod) ; (ii) age; 55 per cent, of cases occur between 
twenty and fifty years of age; 5 per cent, under twenty years and 40 
per cent, over fifty years of age (Garrod) ; (iii) sex; Stewart and McCrae 
consider that the sexes are equally involved; (iv) fatigue, cold, dampness, 
poor hygiene or trauma may be predisposing factors, (b) The immediate 
cause is unknown; the infective theory is based upon finding bacteria 
in the joint, enlarged spleen and lymph glands and its occasional 
development after infections; some cases can be traced to disease of 
the tonsils, sinuses, gall-bladder, appendix, tubes, prostate, pyorrhea 
alveolaris, etc. 

Pathology and Symptoms. — Whether the synovia or cartilages are first 
involved is undetermined; the x-tsljs do not solve the question; prac- 
titioners, who see cases early, hold that the serous sac is first affected and 
surgeons find the cartilages most often diseased. The synovial villi 
hypertrophy and the cartilage slightly fibrillates, cleaves and finally 
atrophies. The bone becomes thin in some places and tuberous in others 



952 DISEASES OF THE JOINTS 

from periosteal proliferation (Haygarth's nodosities); the joint surfaces 
become eroded and in part grow together. 

1. Diffuse Progressive Type. — (a) The acute form is less common. 
There is some fever, rise in the pulse-rate and general depression and the 
joints become red and swollen, resembling acute articular rheumatism, 
but differing from it in that arthritis deformans is less fugitive, involves 
the small joints less frequently, is attended by less sweating, and seldom 
by heart complications, does not react to salicylates and runs a longer 
course. In some cases it even resembles typhoid, because the fever and 
splenic enlargement antedate the arthritis, (b) The more frequent 
chronic form develops insidiously, with uncomfortable sensations in the 
joints or racking nocturnal pains about the joints and vasomotor skin 
symptoms. It begins most often in the small joints of the hands, with or 
without swelling, and remits and recurs. The hands often sweat. The 
fingers become fusiform from joint changes, capsular thickening and 




Fig. 79. — Rheumatoid arthritis. (Musser.) 

collateral edema which separate the fingers from each other. The edema 
often disappears, showing more clearly the osseous and capsular thicken- 
ing. The cartilages become uneven and crackle on movement, loosened 
villi may become free bodies and the adjacent bursa? and tendons may 
swell. The fingers deviate and become angular from flattening of the 
saddle-shaped epiphyses and extensor or flexor muscular contractures. 
Extension to other joints occurs; the elbow becomes flexed, the shoulder 
often crackles and becomes fixed ; the large toe is bent out and lies under 
the other toes, which are often extended at their first and flexed at their 
two distal articulations; the ankle is often abducted; the knee is swollen, 
shapeless and flexed from effusion or contracture; in a few cases the hip, 
jaw and spine are involved. The vertebrae may be affected (v. i.). 

Motion is limited by the swelling, muscular contractures or articular 
fixation by interlocking extracapsular nodosities and capsular induration. 
The contiguous muscles atrophy from disuse, local inflammatory in- 
vasion or reflex influence on the cord. The skin may become puff} 7 , 



ARTHRITIS DEFORMANS AND CHRONIC RHEUMATISM 953 

glossy or atrophic. The reflexes are increased. Neuritis is not uncommon. 
The heart was not affected in any of Garrod's 500 cases. Anemia, epi- 
scleritis and other complications are uncommon. The majority of 
patients do not improve or recover and recurrence of the disease is very 
common. In some cases the process is arrested. Aside from atheroma 
and nephritis few intercurrent diseases develop. 

2. Monarticular Type. — Pathologically, this type resembles the 
form described, but differs from it in that it presents more profound 
changes and is limited to one or few articulations. There is the same 
capsular thickening and cartilaginous fibrillation; the cartilage often 
softens, ossifies or hypertrophies; the bone rarefies or becomes cystic 
and soft in some places, with flattening of the bone heads and widening 
of the sockets, particularly in the shoulder and hip; in other places bony 
overgrowths form, known as Haygarth's nodes or a new socket may 
develop; the bone may eburnate and the joint may be either smooth or 
ridged. As a rule the atrophic prevail over the hypertrophic changes. 
They resemble the extreme senile change (morbus coxce senilis); trauma 
or a nervous basis is considered causal; it occurs in old persons and 
largely in males. Clinically, compared with the general progressive type, 
it is single or at least rarely symmetrical, occurs in the proximal large 
joints (hip and shoulder), and is less often attended by subluxation. 
The elbow, spine and smaller joints are less involved. 

3. Vertebral Type. — Stnimpell (1885) named this type chronic 
ankylosing spondylitis; vertebral arthritis deformans occurs with anky- 
losis of the spine, shoulders and hips. Marie (1898) made it a separate 
type (spondylose rhizomyeliqve) , characterized by complete vertebral 
ankylosis, scoliosis, ankylosis of shoulders and hips, exemption of all 
other joints, incidence almost exclusively in males, and its appearance 
in the young immediately after bony development has ceased. Von 
Bechterew (1892) described a similar type due to heredity, trauma or 
meningeal inflammation and characterized by paresis of the muscles of 
the neck, trunk and extremities, some atrophy of the back and shoulder, 
involvement of the spinal nerves (hyperesthesia, pain and paresthesia) 
and an ascending degeneration in the cord. These are probably subtypes 
of arthritis deformans. 

4. Juvenile Type of Still. — (a) The ordinary progressive form 
may be observed in children, as in adults, and often with almost uni- 
versal ankylosis; in some cases the great toes are lengthened, (b) 
" Still's type" occurs largely in poor children; 70 per cent, of cases are 
girls; 30 per cent, occur between the second and seventh years, 32 per 
cent, between the seventh and thirteenth years, and 20 per cent, between 
the thirteenth and seventeenth years. The onset is often subacute. The 
multiple arthritis affects chiefly the extracapsular tissues and there is 
seldom crepitus. The spleen is always enlarged and the lymph glands 
near the affected joints are hard and large. Anemia and retarded develop- 
ment are common. 

5. Heberden's Nodes. — Bony nodes develop on the sides of the 
end phalanges near the joints. They begin between thirty and forty 
years, but are seen chiefly at about sixty years of age. At first soft 



954 



DISEASES OF THE JOINTS 



and sometimes painful and red, they become hard, indolent and as large 
as a pea. Their growth is more intermittent than continuous. Dis- 
turbance in function is not uncommon, but only in extreme cases is 
deformity observed, as flexion of the end phalanges into the palm or 
deviation toward the radial side. Involvement of the large joints is 
rather uncommon, whence the prognosis is favorable. 

Diagnosis. — (a) In gout, the history, localization, fine (not coarse) 
crackling in the knee-joint and radial articulation of the elbow, greater 
spontaneous pain, infrequent generalization, and symmetry, the uratic 
deposits and tophi in the ear are characteristic, (b) Acute rheumatism 
(v. s. Acute Form), (c) Multiple tuberculous arthritis may cause diag- 
nostic difficulty, particularly in children, for pulmonary tuberculosis may 
complicate arthritis deformans; but the tuberculous hip and knee in- 
volvement, the fusiform fingers, the hectic fever, involvement of the 
glands and serous membranes are generally distinctive. Poncet's anky- 
losing tuberculous pseudorheumatism may cause confusion (v. p. 182). 




Fig. 80. — Heberden's nodes. (Musser.) 

(d) Syphilis (q. v.) of the joints occurs particularly in persons between 
four and fifteen years of age and in about 40 per cent, of hereditary 
forms; the epiphyses are irregularly deformed, (e) Hemophilic arthritis 
is distinguished by the family history and its three stages, hemarthros, 
panarthritis and adhesions, erosions, deformity and ankylosis. (/) 
Chronic articular infections, especially subchronic gonorrheal arthritis 
(q. v.), begin acutely, usually affect the knees first, then possibly after 
months the ankles, hands (in women particularly), sternoclavicular and 
other joints; similar chronic arthritides may follow scarlatina, pneumonia, 
tonsillitis (v. s.), etc. (g) Nervous arthropathies exhibit much the same 
pathology; (i) the arthropathies of tabes (q. v.) occur rapidly and early, 
without pain, tenderness or other inflammatory evidence; are attended 
by much effusion, are atrophic or flail-like rather than hypertrophic, 
in 80 per cent, involve the lower extremities and are accompanied by 
other signs of tabes, (ii) In syringomyelia (q. v.) the effusions are great, 
painless, in 80 per cent., involve the upper extremities and are accom- 
panied by panaritia and dissociated anesthesia. (//) " Chronic rheumatism" 



ARTHRITIS DEFORMANS AND CHRONIC RHEUMATISM 955 

rarely follows acute rheumatism; the changes involve less the bone, 
cartilage and serous sacs than the capsule which becomes fibrous. The 
cartilage may become somewhat fibrillated and fibrous, but is seldom 
hypertrophied or destroyed. The vascular bands become callous (Jac- 
coud's fibrous rheumatism) and ankylosis may result. Some maintain 
that ankylosis by connective tissue and the joint obliteration differentiate 
fibrous rheumatism from arthritis deformans, but clinical differentiation 
is often impossible. 

X-ray examinations detect the synovial or periarticular changes (the 
so-called rheumatoid arthritis), the atrophy of bone or cartilage and the 
hypertrophic alterations (osteo-arthritis) . 

Treatment. — Arrest of the process results rather from spontaneous ex- 
haustion of the disease than from therapeutic efforts, (a) Possible causal 
conditions should be corrected, as pyorrhea, tonsillar or antral disease, 
otitis or genito-urinary infections. Autogenous vaccines, in the writer's 
hands, have proved futile, (b) " Rheumatic" influences, as exposure 
to cold and dampness, overheating while at work and resting in damp 
garments are to be carefully avoided. Woolen underwear should be worn. 
General hydrotherapeutic measures are illy borne. A warm climate 
benefits especially those cases resembling (or including) chronic fibrous 
rheumatism, as Mexico, West Virginia and Arkansas, (c) Diet is not 
of such importance as in gout; liberal feeding always is strongly indicated. 
(d) In acute exacerbations rest, salicylates and coal-tar derivatives are 
indicated, (e) Passive movements and massage relieve stiffness and 
muscular contractures. Massage reduces the edema and adhesions. 
In some cases forcible pressure, as with the thumb, will cause absorption 
of the fresh osteoplastic nodes; it may be easily overdone, and once every 
day or two on the same area is sufficient. Cautious active exercise is 
essential. (/) Extension by pulley weights sometimes produces wonderful 
results, according to Hoffa, in lessening pain and exostosis, though the 
author has never observed any benefit, (g) Local measures. The x-rays, 
local applications of warm water and strong electric lights may afford 
temporary alleviation from pain but do not seem to affect the basic change; 
fibrous rheumatism is more benefited than arthritis deformans. Hot 
air causes hyperemia of the parts and is sometimes of real benefit; cages 
of wire, asbestos and felt are devised to enclose the joint, leaving around 
it an air space; the temperature is gradually raised by a lamp placed 
under a connecting elbow to 200° or 250° F. and then gradually lowered. 
Bier's method of venous hyperemia, used in tuberculous joints, is also 
advocated; the Esmarch constrictor above the joint should produce 
swelling but not pain. "Firing" the skin with the Paquelin is beneficial 
in lighter grades. Operation: resection may be considered in non- 
progressive, monarticular forms, but the general poor health and age 
of the patient rather contra-indicate it. (h) Internal medication, as cod- 
liver oil, arsenic, thyroid extract and syrup of iodide of iron may help 
a few cases. Luff uses guaiacol carbonate; the initial dose of five grains, 
t. i. d., is increased two grains every week till a single dose of twenty 
grains is given. 



956 DISEASES OF THE BONES 



DISEASES OF THE BONES. 

For hypertrophic pulmonary arthropathy, leontiasis ossea and osteitis 
deformans, see page 722. 



OSTEOMALACIA. 

Etiology. — Osteomalacia is a chronic nutritive disorder, characterized 
by decalcification and progressive softening of the bones, with bend- 
ing, fracture or deformity. It occurs especially in adults and women 
(90 per cent.), particularly nursing or pregnant multiparas. 

Pathology and Symptoms. — The pelvis, vertebrae and ribs are oftenest 
affected, with pain which is considered "rheumatic," disturbances in 
walking, etc., and deformities. The osteomalacic pelvis, often first de- 
tected by a pelvic examination during pregnancy, exhibits an approach 
of the sacral promontory and the acetabula; scoliosis, lordosis or kyphosis 
develops; the bones of the leg curve and spontaneous fractures occur. 
The flaccid and atrophic muscles exhibit tremor or fibrillation. Radio- 
graphic and autopsy examination reveals decalcification in the spongy 
and compact bones, with replacement by vascular, gelatinous, perhaps 
cystic or hemorrhagic tissue. The urine contains an excess of calcium 
and phosphorus. 

Prognosis and Treatment. — The chronic, usually progressive, course 
covers five to ten years; it is sometimes acute or at times arrested. 
Asthenia or intercurrent disease is the usual cause of death. Calcium 
and phosphorus are beneficial. That the disease may be related to the 
ductless glands, is shown by occasional cures by ovariotomy in advanced 
cases and by full doses of adrenalin (Bossi). 



ACHONDROPLASIA. 

Pathology. — From unknown causes, perhaps from pituitary or thyroid 
disease, there is a dystrophy of the epiphyseal cartilages (chondrodystro- 
phia fetalis) ; connective-tissue invasion from the periosteum prematurely 
unites the diaphyses and epiphyses, thereby preventing development of 
the long bones. The intermediary cartilage is narrowed, irregular and 
zig-zag and stray nests of cartilage cells may develop into chondromata, 
exostoses or rapidly growing malignant osteocartilaginous tumors. The 
x-rays show the small or deformed epiphyses. 

Symptoms. — In achondroplastic dwarfism, intelligence is normal, 
the head and trunk are nearly normal but the decreased stature (3-4 
feet) is due to the short extremities. The humerus and femur may 
measure less than the tibia and ulna. The fingers are nearly equal in 
length and diverge. The hand is short and the fibula is longer than 
the tibia. The pelvis ,is contracted and lumbar lordosis follows tilting 
forward of the sacrum. The root of the nose is depressed. 



OXYCEPHALY 957 



FRAGILITAS OSSIUM. 



Ostheim (1914) collected 193 cases, "including two types of cases, (1) 
the fetal type found either at birth or soon afterward, associated with 
imperfect bone formation and multiple fractures (imperfect osteogenesis 
or periosteal dysplasia), these cases commonly not surviving beyond the 
second year of life; and (2) the congenital type, found in infants and 
children, at birth or later, with fractures recurring often until puberty 
or even until adult life, associated with similar bone changes (idiopathic 
osteopsathyrosis), which children if well cared for, survive, but often in 
a badly crippled condition." 

The bone trabecular are produced by calcification of the cartilage 
cells, whereas normally new bone is produced by osteoblasts on a car- 
tilaginous matrix, the periosteum forming imperfectly laminated, dense 
bone with large spaces; the bones contain little calcium. Fractures occur 
in the diaphyses only. The fetus exhibits imperfect cranial ossification, 
apparently shortened, bowed extremities and many fractures. 

OXYCEPHALY. 

Steeplehead, thurmschadel, tete a la Thersite, caput turritum, is 
usually congenital and is due to early synostosis, especially of the cor- 
onal and sagittal sutures, whence the head grows sloping upward to 
compensate for the lack of growth laterally and anteroposteriorly. 
The x-rays show a dimpling of the inner table, considered characteristic 
by Fletcher, who collected under 90 cases (1910). Intelligence is normal, 
the eyes are prominent or actually exophthalmic and headache and optic 
neuritis or atrophy are usual. Decompressive operation is indicated. 



SECTION XI. 

INTOXICATIONS. SUNSTROKE 



ALCOHOLISM. 



I. Acute Alcoholism. — (a) The highest brain centres are first affected, 
judgment (emotion predominating), motility next (disordered speech, 
gait and vision), then the lower centres (respiratory, circulatory and 
spinal), (b) The pulse becomes more rapid, though alcohol does not 
stimulate the heart. Full doses make the pulse slow and small. The 
face is flushed and the vascular tone is lax; for this reason alcoholics 
suffer little shock from traumatism, (c) Respiration is slow, deep, 
seldom stertorous, (d) The pupils are more often dilated than narrow 
and reactionless. (e) The temperature may fall markedly, even as low as 
75°, from vasoparesis, usually with cyanosis and failing of the bulbar 
centres. Involuntary evacuations occur in the severest cases. 

Dipsomania is intermittent, acute alcoholism, an hereditary psychosis 
in which, after intervals of abstinence and no craving for liquor, the 
subject becomes intoxicated. 

Diagnosis. — The alcoholic breath is usually suggestive but epileptics 
and uremics while drunk may suffer skull fracture or apoplexy. Many 
mistaken diagnoses result from carelessness, but many are unavoidable; 
the apparently drunk patient should be treated for alcoholism, while 
other possibilities are carefully considered. As a rule the patient can be 
aroused, but in "dead drunks" this is not the case and incomplete coma 
may occur from other causes. The pupils are usually dilated in alcoholic, 
contracted in opium and uremic, and unequal in apoplectic, coma. Ster- 
torous breathing is strongly indicative of apoplexy or uremia. Convul- 
sions following delirium and muscular twitchings are less common than 
in other similar conditions, but at the time of writing the author observed 
uni- and then bilateral convulsions. The urine rarely contains alcohol, 
as at the most 5 per cent, of ingested alcohol is excreted by the lungs and 
kidneys. Sudden death may occur without adequate necropsy findings. 
One-third of all fatal poisonings are acute alcoholism. 

Treatment. — Gastric lavage is sufficient in most cases. The convulsions, 
when severe, yield to a few whiffs of chloroform. Acute mania yields 
to a hypodermic of apomorphinse hydrochloridum (gr. J). Collapse, 
cold extremities and cardiac and respiratory failure are relieved by hot 
coffee, strychnine, atropine, aromatic spirits of ammonia and local 
heat (v. i. Acute Opium Poisoning). 



960 INTOXICA TIONS— SUNSTROKE 

II. Chronic Alcoholism. — This is less an hereditary tendency than a 
lack of character, though Plutarch said that drunkards beget drunkards. 
Some people can take beer, wine, spirits or patent medicines throughout 
life without apparent injury; in others, even the mildest alcoholic drinks 
may induce visceral alterations, so that as in liver cirrhosis, it would 
seem that there is some other etiological factor. Alcohol in health is a 
bad food, an injurious narcotic or stimulant, a protoplasmic poison to 
the parenchymatous organs and arteries, and a check on metabolism. 

Symptoms. — (a) Nervous manifestations. Functional changes include 
the alcoholic tremor, a most common symptom; mental dulness and 
weakness ; nervousness, jumping from slight stimuli, irritability, impaired 
judgment and feeble will-power; neuralgias and muscular rheumatism. 
The alcoholic is suspicious, cruel, conceited and degenerate. Quinquad's 
sign is elicited by having the patient place his fingers vertically to the 
examiner's hand or body, when a series of jerking shock-like movements 
is noted; (i) if it is absent, alcoholism is absent; (ii) if it is moderate 
there is uncertainty and (iii) if it is marked, in 3 cases out of 5, the patient 
is an alcoholic. Of organic nervous manifestations, multiple neuritis 
is the most common; it may result from small amounts of alcohol, 
when there is a coincident metallic poisoning; epilepsy may result from 
alcoholism; hemorrhagic pachymeningitis, chronic leptomeningitis, acute 
polioencephalitis, degeneration in the anterior horns or Clark's columns, 
degeneration of the cerebral nervous tissue, slight optic neuritis and even 
immobile pupils may be more or less direct sequences, (b) Circulation. 
Arteriosclerosis often develops with its train of sequences, cardiac hyper- 
trophy and dilatation, angina pectoris, cerebral softening or hemorrhage. 
(c) Chronic bronchitis, emphysema, chronic pharyngitis and laryngeal 
thickening are frequent collateral findings, (d) Digestive organs. Alcoholic 
gastritis (q. v.) is common; the quite characteristic vomitus matutinus is 
quieted only by another dose of its cause. Beer drinkers usually have 
large stomachs. Alcoholic cirrhosis has been discussed ; fatty degeneration, 
arterial congestion and hypertrophy may antedate or accompany cirrhosis. 
Beer drinkers have lax bowels, while consumers of spirits are constipated. 
Hemorrhoids are common, (e) The kidneys undoubtedly suffer. Dickin- 
son, Formad and Pitt think that renal disease is less common than is 
usually believed; the kidneys are hypertrophied without other change 
in 43 per cent.; several factors may be necessary to produce indurated 
kidneys. Sterility is common. (/) Metabolic maladies, as gout, obesity 
and some forms of diabetes may result from chronic alcoholism, (g) 
The skin. Acne rosacea is a very common but not, as Trousseau says, 
an "indelible stigma." The vessels of the nose, cheeks and other parts 
are suggestively dilated; the conjunctivae are injected and the eyes water. 

Prognosis. — The prognosis is unfavorable, both from the standpoint 
of curability and complications. English life insurance companies 
estimate that the risk is 33 per cent, less in abstainers than in alcoholics. 
The general resistance is lowered, thus favoring infections, as tuberculosis, 
and raising greatly the death-rate, most notably in pneumonia. Twenty 
per cent, of suicides are alcoholics. The offspring of inebriates are 
disposed to numerous nervous affections. 



ALCOHOLISM 961 

Treatment. — Treatment consists of correction of the habit and care 
of the complications, the latter of which have, in great part, already 
been considered. The cure of the habit is largely personal. Its prophyl- 
axis is better than its cure. No person, however intellectual or strong- 
willed, can safely drink with any regularity. Institutional treatment is 
generally necessary. The vomiting should be treated as in acute and 
chronic gastritis; lavage is probably the most reasonable measure; a 
mixture of bismuth (page 55) and small doses (Tfl,i-ij) of Fowler's 
solution and tr. nucis vom. (Tfl,x) are valuable just before the adminis- 
tration of hot milk with tr. capsici, lUx. Hyoscinse hydrobromidum 
(gr. y-jo") should be given two or three times at three-hour intervals, 
chloral hydrate (gr. x) and sod. bromide (3ss) for three or four doses, 
before bedtime, or sulphonal (gr. xx) in hot milk before bedtime, in order 
to induce sleep. (See Lambert's treatment, page 964). Sipping ice- 
water, sucking lemons or drinking water with tr. quassise may satisfy 
the desire to "drink something." Cocaine and morphine are avoided, 
lest a substitution or succession of habits develop. Relapse is very 
common. 

III. Delirium Tremens. — Mania a potu is an acute accident of chronic 
alcoholism and almost never follows an acute debauch in an otherwise 
temperate individual. It was noted among sailors by Sutton, of Green- 
wich, in 1813, but was probably best described by Ware, of Boston, in 
1831. Sixty-six per cent, of cases occur in men, while multiple neuritis 
is more common in women. The patient, usually between thirty and 
forty years of age, has been, on the average, an alcoholic for eight years 
before delirium tremens develops; strong spirits, rather than beer or 
wine, are the cause, as they are of alcoholic convulsions. It may be 
precipitated by trauma to the chest, fractures, mental shock, sudden 
failure of the stomach to assimilate food, acute withdrawal of alcohol or, 
in 70 per cent, of cases, the shock of onset of an acute infection. 

Symptoms. — It develops with restlessness and insomnia, which re- 
newed drinking fails to allay; for a day or two the mind wanders, but 
can be brought back to realities. The patient may be facetious, but is 
soon disturbed by horrible hallucinations. There is "great versatility 
of ideas." The patient talks volubly, turns suspiciously to the head of 
his bed, drives his horses vigorously and brushes away the vermin from 
the coverlet; hallucinations of hearing are also common. He at first 
knows that the bugs and snakes are unreal, but they soon become actual 
torments, so that unless watched he will leap from the window after 
waiting for his opportunity. The pulse is rapid and soft, the skin is 
flushed or slightly cyanotic and covered with sweat, the tongue is 
tremulous and white, the urine scanty and often albuminous and sleep 
is constantly absent. There may be moderate fever, 101° to 103°. 

Diagnosis and Prognosis. — The diagnosis is rarely uncertain. The 
chief danger of error is in overlooking coincident trauma, and infection. 
In heavy and constant drinkers, a delirium may be delirium tremens 
or an associated delirium, as from pneumonia. 

The outlook is always uncertain. Early convulsions are of no great 
moment. The prognosis is determined by the pulse, general nutrition 
61 



962 IN TOXIC A TIONS—S UN STROKE 

and complicating alcoholic or other lesions. Rigidity of the muscles 
of the neck is ominous and indicates edema of the brain. The average 
mortality is 15 to 20 per cent., but varies as the affection is (a) uncompli- 
cated (1 per cent, die, Lambert); (6) associated with other affections 
(grave outlook) or (c) occurs in the aged or debilitated (probably fatal 
outlook). Recurrence is frequent, 27 attacks being recorded. In fatal 
cases death usually results from exhaustion and heart failure; the tongue 
becomes dry, the delirium constant and the skin cold and clammy. 
The autopsy shows edema of the brain ("wet brain/' Dana), degenerative 
changes in the brain and cord (Bonhoffer), arterial alteration (Collins) 
and hypostasis of the bases of the lungs. 

Treatment. — (a) The patient should be kept in bed and watched con- 
stantly lest he escape. Strapping the ankles and wrists and confinement 
by a straight jacket is a harsh procedure and invites trauma to the hands 
and feet, but is inevitable when the family is indulgent or the nurses 
are negligent, (b) Withdrawal of alcohol is usually advocated but is a 
severe measure; the temporary continuance of moderate doses seems to 
steady the pulse and favor digestion, (c) Sleep is induced with great 
difficulty and, as Ware first pointed out, comes when the disease runs its 
course. Excessive medication should be avoided. Sod. bromide (5ss), 
tr. capsici (ITlv) and whisky (5ij), in hot, peptonized milk should be 
given every three hours, by mouth if possible, or by the nasal catheter, 
for nutrient enemata are difficult to give and are seldom retained. Chloral 
is always dangerous in inveterate alcoholism. Moller administers 
veronal, gr. xv, repeated once. Hyoscine with strychnine may be bene- 
ficial. Morphine should be given only by the hypodermic method, 
for its absorption can then be measured. 1 Protracted warm baths may 
quiet the patient but they are hard to administer. In 6 cases in which 
the violent delirium became ominous the writer etherized the patient, 
and in three instances with excellent results, (d) The circulation should 
be treated as in pneumonia. Large doses of digitalis are tolerated only 

1 In the treatment of 500 cases of delirium tremens, S. W. Ranson's conclusions are as 
follows: (1) In incipient cases the patients respond readily to treatment with chloral, ergot, 
bromides and whisky. (2) Delirious patients are very resistant to treatment. Sedatives 
increase the mortality (scopolamin, 13 per cent.) ; 15 to 30 grains of chloral in twenty-four 
hours may be given with good results, but larger doses increase the death-rate. (3) The 
only drug which reduced the mortality was ergot; the death-rate was reduced 21.6 per 
cent. (4) When whisky was given the mortality was increased 1.8 per cent. Ranson's 
cases were divided into two classes, incipient and delirious. The incipient cases showed only 
insomnia, restlessness and tremor. The fully developed cases were noisy, delirious, and 
had well-defined hallucinations. Of the sedative drugs the bromides were most extensively 
used and severe cases showed a mortality of 45.5 per cent. ; of incipient cases treated with 
bromides, only 32.6 per cent, became delirious; while of similar cases not treated with 
bromides, 52.8 per cent, became delirious. Chloral is of no value after active delirium has 
set in; chloral is of great value in the treatment of incipient cases; chloral is superior to 
bromides because of the greater speed of its action. Morphine has no effect in delirious cases 
and is far inferior to small, repeated doses of the sedatives used in the incipient cases. Scopo- 
lamin, To- -,vo of a grain, in incipient cases has no controlling action, and proved extremely 
dangerous when given to actively .delirious cases. In those cases in which ergot, fluid- 
extract, in dram doses, repeated every four hours was used the mortality was only 30 per 
cent., while among those patients treated without ergot it was 51.6 per cent. Ergot is of 
value in the incipient cases, the percentage of patients developing delirium being reduced 
23.3 per cent, by its use, possibly by decreasing the cerebral hyperemia. Whisky is of use 
in the treatment of incipient cases, lowering the percentage of patients becoming delirious 
by 20.2 per cent. In the delirious patients it is useless. 



OPIUM POISONING 963 

because they are not absorbed; the original treatment by digitalis is 
based on the fact that a nurse by mistake gave a toxic dose of digitalis; 
the patient improved and the "digitalis treatment" was thus insti- 
tuted, (e) Cold affusions upon the neck and chest are recommended 
by Broadbent. (See Lambert's treatment, page 964.) 

OPIUM POISONING. 

I. Acute Poisoning. — This is important chiefly from a diagnostic 
standpoint. In the second stage it is strongly characterized by profound 
sleep, dry, flushed skin, narrow pupils, slow, strong " digitalis pulse" 
and slow, deep, stertorous breathing. The third or terminal stage is differ- 
ent; the skin becomes cyanotic and clammy, the narrowed pupils may 
dilate, the pulse becomes weaker (though the heart centres live after the 
other bulbar centres fail), respiration is very slow and halts. Mistakes 
in diagnosis are made by attributing undue importance to the "pin-point" 
condition of the pupils. Morphine may be detected in the stomach washings. 

Treatment. — This consists of (a) evacuation by repeated gastric lavage. 
(b) Chemical antidotes, such as large amounts of tannic acid, should be 
given with the lavage and removed, as the tannates formed may dissolve ; 
1 to 1000 permanganate of potash (Moor) may be given by mouth or 
hypodermically. (c) Respiration must be sustained by walking the 
patient, but fatigue must be guarded against; phrenic faradization is 
indicated, but care is necessary lest too strong a current produce paralysis 
instead of stimulation; strychnine plus atropine may be given hypo- 
dermically, but the total dose of atropine should not exceed gr. -j^; 
pulling slowly and rhythmically on the tongue may help respiration; 
artificial respiration and oxygen inhalation may be used, (d) The heart 
is stimulated by coffee, strychnine, heat and digitalis. 

II. Chronic Morphinism. — The use of morphine for pleasure only, so 
common in Asia, is rare with us; those taking morphine for pain and 
resisting its attractions are called morphinists; those using it for pleasure 
only are morphinomaniacs. The habit is contracted by its use for in- 
somnia or for mental or physical pain. Forty-seven per cent, of morphine 
victims are said to be physicians; women, particularly prostitutes and 
nurses, druggists and — in Germany — officers rank next. It may be taken 
for years without mental or physical deterioration, but increase in the 
daily dose becomes necessary and the half-oxidized alkaloid produces 
symptoms which are only allayed by larger doses. Morphine acts as a 
nerve poison. The victim becomes restless and irritable without his 
dose. The mental and moral attributes are anesthetized and there is a 
"moral insanity."" The patients lie by choice, neurotic symptoms are 
common, muscular and mental asthenia develop, the pupils are contracted, 
the sweat and saliva are decreased, the teeth decay, the appetite fails, 
the skin becomes sallow, itchy and dry, the hair coarse and gray, con- 
stipation is usual and slight ataxia may develop. 

Prophylaxis. — Physicians should not give opiates freely. When admin- 
istered for severe pain the habit is less often contracted than when given 
to neurotics, At least 20 per cent, of cases relapse after a "cure," 



964 INTOXICATIONS— SUNSTROKE 

Treatment. — Treatment is almost impossible without (a) institutional 
confinement, which must of course be voluntary. The patient will obtain 
morphine if possible, (b) The morphine may be withdrawn abruptly, 
rather suddenly or very gradually; the second method is the best, stopping 
the morphine entirely in four to seven days. Its withdrawal is attended 
by awakening of dormant anesthetized functions; there is at first 
paroxysmal yawning and sneezing; roughening of the voice, paresthesia, 
neuralgias especially in the legs, clammy skin or rapid pulse, wide pupils, 
tremor, sexual excitement, extreme irritability, vomiting, colic and diar- 
rhea also occur. The symptoms were attributed by Marme to di-oxy- 
morphine, the antidote to which is morphine; Hitzig believes that they 
are largely due to hyperchlorhydria, for the gastric nerves under the 
influence of morphine secrete little hydrochloric acid; relief is obtained 
by washing out the stomach with a solution of Carlsbad salts, (c) The 
patient should be kept in bed for a week to obviate vasoparetic cardiac 
collapse, (d) Symptomatic treatment is indicated (i) by the collapse 
(aromatic spts. of ammonia, lUxx, strychnine, gr. ^-, heat) ; (ii) by nervous- 
ness (warm baths, sodium bromide in doses of one dram every four hours) ; 
(iii) by the insomnia (hyoscine, gr. y^-Q every two hours for two to four 
doses, sulphonal or trional, gr. xx) ; (iv) by the gastralgia (gastric lavage 
with alkaline salts) ; (v) by diarrhea and colic (as in enteritis, but vege- 
table astringents, large doses of bismuth, and no opiates should be used) ; 
(vi) by neuralgia (acetanilide, gr. v, fluidextr. gelsemii, Tfljij). Whatever 
treatment is instituted, alcoholism, chloralism, bromism or cocainism 
should not be substituted. Alexander Lambert's treatment aims to 
eradicate the craving for narcotics. 1 

1 Lambert's prescription consists of: ■** 

1$ — Tincturse belladonnas (15 per cent.) .... 20 c.c. flov 

Fluidextracti hyoscyami 10 c.c. or 

Fluidextracti xanthoxyli 10 c.c. aa fl 5hss 

M. et Sig. — Administer as directed. 

He emphasizes the necessity of carrying out his treatment absolutely to the letter, and 
employing profuse catharsis. In alcoholics 6 to 8 drops are given every hour, day and night, 
until either the patient shows symptoms of belladonna excess, or from the cathartics the 
characteristic stool. The dose is increased by 2 drops given every six hours until 14 to 16 
drops are taken. Usually an alcoholic can be given four compound cathartic pills at the 
same time that the specific is begun. After the drops have been given for fourteen hours, 
a further dose of compound cathartic pills is given, either two or four, depending upon the 
amount of action obtained from the previous pills. If the first pills have caused abundant 
action, only two are now necessary. At the twentieth hour of the drops, from two to four 
more compound cathartic pills are given, and after these have acted, the stools should begin 
to be green. An ounce of castor oil should now be given, and a few hours later the char- 
acteristic thick, green, mucous, putty-like stool will appear. Usually the drops must be 
continued, and at the thirty-second hour from two to four compound cathartic pills are 
again given, and a few hours later the castor oil. The drops can now be discontinued. In 
the first twenty-four hours with an older patient, or one in the midst of a spree, whisky 
should be given four or five times, in one- or two-teaspoonful doses, in milk. The whisky 
should not be continued after the first twenty-four hours, and in younger patients it is 
usually not necessary to give it at all. An alcoholic is less tolerant of belladonna than a 
morphine patient, but if they are sensitive to this drug they will show it in the first six or 
eight hours of the treatment. After the patient has been through with this treatment 
the desire for alcohol has ceased, and it is a question for the next few days of proper nutri- 
tion, and sometimes the administration of a drug for sleep. He finds the best hypnotics 
for these alcoholics are chloral and bromides. Whatever tonic is given of course must be 
non-alcoholic. In treating morphinism, patients do not suffer more than a bearable amount 



LEAD POISONING 965 



LEAD POISONING. 

Etiology. — The importance of plumbism or saturnism is increasing. 

(a) Industrial plumbism is very common. Workers in white- or red- 
lead factories usually acquire the disease. Miners of the metal generally 
escape, but smelters of lead ore and even animals and birds near the 
furnaces are frequently affected. Painters, plumbers, glaziers, less often 
tinners, printers, cameo polishers, cartridge makers, etc., may be poisoned. 

(b) Accidental contamination of food or drink. Poisoning may result 
from the action of acids in canned foods on the tin or solder, as in cans 
of sardines; wine or cider may become poisonous in the same way, as 
happened in Devonshire and Poitou (colica pictonum). Chromate foil, 
covering hams or candy, rubber nipples, bullets in pickled game, bread 
ground in lead vessels, chromate used to color buns (D. D. Stewart's 
report of the fatal Philadelphia epidemic), Seltzer or other charged 
waters, wine and eau de vie sweetened or cleared with litharge, are a few 
of the many subtle causes of saturnism. Drinking water conveyed 
through lead pipes is generally protected by the deposit of lime, and other 
salts, but poisoning is possible when the water is exceptionally pure or 
soft, thereby depositing little lime in the pipes, or when it is saturated 
with organic matter or collected from lead roofs, (c) Less frequent 
sources of plumbism are in the environment, and in hair-dyes, powders 
or cosmetics, linen, freshly painted walls, candles, sealing wax, brightly 
tinted toys, false teeth and thread, (d) Therapeutic and criminal plumb- 

of discomfort in breaking away from the drug. First, the patient is made comfortable with 
his accustomed dose of morphine, and then given four or five compound cathartic pills. 
Then the drops should be given as prescribed for alcoholics. If there is a hypersensitiveness 
to belladonna the drops must be stopped and later begun again with a smaller dose. After 
the drops have been started and the time has come for the patient's usual dose of morphine, 
he receives from one-half to two-thirds of the kind of opium that he has been taking, and 
administered in the manner that he has been administering it. After fourteen hours of the 
drop treatment, the patient should be given four compound cathartic pills and five grains 
of blue mass, or some other form of vigorous cathartic such as the vegetable cathartic pills 
of the Pharmacopoeia with ginger and capsicum and ^ of a drop of croton oil to each pill. 
Four or five of these last pills should be administered, if preferred to the compound cathartic 
pills and blue mass. After the twentieth hour of the drop treatment the patient should 
receive four or five more of the vegetable cathartic-ginger-capsicum-and-croton-oil pills 
and blue mass, and, if these do not quickly act, they should be followed by four or five 
compound cathartic pills and then an ounce of Epsom salt or Hunyadi water every half- 
hour for four or five doses. If in an hour or two these do not act, four or five more of the 
vegetable cathartic pills, followed by the salts, should be persisted in until the bowels act. 
Lambert states that this cathartic treatment will appear to be extraordinary, and it is sur- 
prising that the withdrawal of the morphine does not of itself produce a diarrhea. The 
inhibition can only be due to the atropine. If by the twentieth hour the cathartics do not 
act the symptoms of the reduction of the morphine, viz., sneezing, nervousness and pain, 
come on in full force, and the patient begins to suffer. If the cathartics do act well, a second 
dose of morphine or opium should be given of about one-third or one-sixth of what was 
given as the initial dose at the beginning of the treatment. Twelve hours after this second 
dose of morphine or opium the patient should again have four of the vegetable cathartic pills, 
each with ginger and capsicum and ■£% of a drop of croton oil, or four compound cathartic 
pills with the 5 grains of blue mass, and following this the stools will begin to be green. 
After the liquid green stools have occurred following the thirty-second hour cathartic, an 
ounce of castor oil should be administered, and will cause the thick, green stool as described 
under alcoholic treatment. After this movement, the patient feels suddenly relaxed and 
comfortable and the nervousness ceases. Most patients then go to sleep. After the thirtieth 
hour of such treatment, and he well says earlier if the patient is in a weak condition, stimu- 
lation with strychnine, from ^jr"io oi a grain, is advisable. 



966 INTOXICATIONS— SUNSTROKE 

ism is rare; it may result from the acetate of lead when given internally 
or externally, and from impure subnitrate of bismuth; its criminal use 
is very uncommon, (e) Predisposing factors are alcoholism, age (from 
thirty to forty) and sex (75 per cent, are females, Olivier) . Susceptibility 
varies greatly; plumbism may cause death within a week or may not 
develop until after forty-two years of work in the metal (Tanquerel des 
Planches, 1838). Absorption of lead usually occurs (i) by the digestive 
mucosa; most of the metal is precipitated by the albumin of the food 
and eliminated without absorption; (ii) by the respiratory mucosa, 
by inspiration, as dust in white-lead factories; or (iii) by the sound or 
diseased skin (cosmetics) or even the conjunctiva or vagina (lead douches) . 
It is eliminated chiefly by the urine; Putnam found lead in 25 per cent, 
of 150 persons who had no evidence of plumbism; the liver and alimen- 
tary mucosa eliminate smaller quantities. 

I. Acute Poisoning.— This is uncommon ; its symptoms are (a) gastro- 
intestinal; a styptic, burning taste occurs in the mouth, thirst is present, 
there is a lead line on the gums in some cases, though less than in chronic 
poisoning, nausea and vomiting sometimes of white-lead chloride, ab- 
dominal colic, retraction of the abdomen, diarrhea with black (lead 
sulphide) or bloody movements or sometimes constipation. On post- 
mortem examination, the catarrhal gastro-enteritis may be wrongly 
considered a postmortem change; Orfila's white spots may be seen. 
(b) Under circulatory symptoms, the pulse may be slow (50 to 20) and 
irregular; anemia, cyanosis and collapse may occur; (c) nervous symp- 
toms embrace vertigo, stupor, delirium, neuralgia, cramps, convulsions 
and even cerebral and peripheral paralyses; (d) nephritis with suppression 
of urine may develop. 

Treatment. — Treatment consists of full doses of sodium and mag- 
nesium sulphate, in order to precipitate an insoluble lead sulphate, 
and to remove it, demulcent drinks (eggs and mucilages), opium for 
pain and cardiants. 

II. Chronic Poisoning. — Symptoms. — (a) Colic, the most common 
symptom, occurred in 88 per cent, of Tanquerel's 1390 cases. It is due 
to local deposit of lead in the intestines, spasm of the bowel, changes in 
the nerves or angiospasm. It may develop early or late; it may be pre- 
ceded by malaise, lumbago, pain in the legs or alcoholic excesses. It is 
accompanied by constipation (dry colic), rarely by diarrhea; first um- 
bilical, it spreads over the abdomen, perhaps to the legs or scrotum; 
it is relieved by pressure, though sometimes the abdominal wall is hyper- 
esthetic; vomiting and absolute constipation may simulate obstruction, 
and the author observed intussusception as a result of lead poisoning. 
There is no fever, the pulse is small and hard and the urine is scanty. 
Without treatment colic is protracted; its relief is usually marked by a 
bowel movement. Relapses are very frequent, (b) The gingival lead line 
(Burton, 1834), present in over 90 per cent., is a gray-black line, 2 to 
3 mm. wide, seen most clearly on the lower gums and due to deposition 
from the blood of lead sulphide, precipitated by the sulphuretted hydrogen 
of the tartar. The coincident anemia brings it out very clearly. Similar 
deposits may occur under the buccal mucosa opposite the molars. It is 



LEAD POISONING 967 

very frequently mistaken for tartar, which occurs on the teeth, sometimes 
for the black carbon line seen in miners, or rarely for the dark line in 
argyria or bismuth poisoning, (c) Other digestive symptoms are coated 
tongue, fetid breath, parotitis, saturnine dyspepsia and rarely icterus. 
Test meals show lactic acid and no HC1. (d) Anemia is very frequent 
in the "lead cachexia/' The hemoglobin and erythrocytes decrease 
moderately; the red cells show basophile granules (Grawitz) and quite 
commonly nucleation, even in mild cases (Cadwalader, 1905). The 
leukocytes may be increased, (e) Heart and vessels. The heart is very 
often hypertrophied, as evidenced by a loud second aortic tone and aortic 
regurgitation of atheromatous origin; the arteries are often sclerosed, 
occasionally causing angina pectoris, frequently myocarditis, irregular 
heart action and perhaps some of the brain symptoms (v. i.). The 
asthma saturninum is cardiac or uremic. (/) The kidneys are often 
sclerotic, as a result of the elimination of the metal; the change does not 
begin around the vessels but in the tubules, which are the seat of a 
necrosing deposit of carbonate of lime. Nephritis, gout and plumbism 
may coexist, (g) Nervous manifestations. Peripheral degenerative neuritis 
occurs in 7 per cent., usually as a late symptom; one-tenth of these 
cases have not had colic. It is characterized by the paralysis of muscles 
with the same function, by muscular atrophy and cramps, tremor, 
cutaneous hyperesthesia, neuralgia, arthralgia (55 per cent.), myalgia 
and by varying degrees of reaction of degeneration. The musculospiral 
type, iC wrist-drop," is the most common and is bilateral; the supinator 
longus (a flexor) and the small extensor of the thumb escape involvement; 
tenderness and anesthesia are rare. Gubler's tumors are swellings of the 
extensor tendon sheaths, due to backward dislocation of the carpus or 
perhaps to a trophic change; they are hard, ovoid, indolent, seldom 
painful and regress with the paralysis. A second but rare form is the 
brachial, involving the deltoid, biceps, brachialis anticus and supinator 
longus, rarely the pectorals. A third type is the Aran-Duchenne, which 
is especially observed in tailors and involves the small muscles of the 
hand, the thenar and hypothenar eminences; it resembles that of chronic 
anterior poliomyelitis (which indeed has been found in a few cases at 
autopsy). A fourth type, the peroneal, involves the peronei and toe 
extensors; but 13 per cent, of lead palsies affect the leg. Lastly, rare 
types may involve the larynx, vagus and face; generalized paralyses, 
either slow or rapid like Landry's paralysis, are very rare; primary 
muscular atrophy may occur, most often of the Aran-Duchenne type. 

Cerebral forms (encephalopathia saturnina) occur in 5 per cent.; they 
are often preceded by headache, colic and insomnia and are attended by 
amaurosis, limitation of the visual field, retinitis albuminurica or satur- 
nina (with inflammation, engorgement and possibly ultimate atrophy) 
and paralysis of the eye muscles. The most frequent type is the delirious 
encephalopathy, which is variable or mobile in character, and sometimes 
resembles delirium tremens; the next type is the convulsive (epilepsia 
saturnina) which occurs without aura?, is usually generalized, often fatal 
and is always considered when epilepsy develops in an adult; the third 
type is the comatose. Hysteria frequently occurs with plumbic encephal- 



968 INTOXICATIONS— SUNSTROKE 

opathy. Unrecognized cases may become dements (pseudodementia 
paralytica saturnina). Deposit of lead in the brain is the usual cause; 
sometimes the cerebral symptoms are arteriosclerotic (as hemiplegia) 
or uremic. 

Lead poisoning is usually diagnosticated by the etiology, lead line, 
lead in the urine, colic and wrist-drop. In a case of long coma with 
choked disk, in the Cook County Hospital, no cause was found, until 
after a second examination, the lead line was seen. The man was a 
barber, who dyed the hair and probably absorbed the lead through his 
hands. 

Prognosis. — The acute forms are more favorable. Vascular and renal 
changes are largely incurable. Atrophic paralyses are serious. The 
wrist-drop usually regresses, though it is sometimes permanent; 25 per 
cent, of cases with coma, convulsions and other cerebral symptoms die; 
after apparent recovery mental degeneration may develop. 

Treatment. — (a) Prophylaxis. A mask should be worn in white-lead 
factories to avoid inhalation of lead dust; workers are careless and 
poisoning is frequent despite precautions. Painters and others may often 
avoid poisoning by carefully cleaning the hands and nails before eating. 
(b) Lead colic is treated by hypodermics of morphine, nitroglycerin and 
atropine to control pain and spasm. Spts. of chloroform (Tfl,xx) with 
other aromatics may be given by mouth, (c) The constipation and re- 
moval of any lead salts unabsorbed in, or excreted by, the alimentary 
mucosa necessitate catharsis. Full doses of castor oil (5iv or more) 
with paregoric (5j) evacuate the bowels and relieve pain and spasm; 
sodium and magnesium sulphates purge and coincidently precipitate the 
lead as an insoluble sulphate, id) To eliminate the lead from the tissues 
potassium iodide should be given. In acute or severe chronic cases it 
should be given in small doses (gr. iij-v), for it transforms the fixed tissue 
metal into free metal in the circulation; some writers obtain better effects 
from potassium bromide (gr. v-x). Warm baths and pilocarpine (gr. §) 
promote excretion by diaphoresis and plenty of water stimulates the 
renal elimination, (e) Iron (not arsenic) should be given for anemia. 
(J) For treatment of neuritis, see Multiple Neuritis. 

ARSENICAL POISONING. 

Acute poisoning has been considered under Pernicious Anemia. 

Chronic Poisoning. — (a) Criminal poisoning is of great medicolegal 
importance, as in the unfortunate Maybrick case, (b) Poisoning by 
reason of occupation is uncommon, (c) Therapeutic poisoning is not 
common, but may occur in chorea, leukemia and pernicious anemia. 
(d) Most cases are accidental. The dyes in garments, toys, glazed paper 
used in kindergartens, wrappers, artificial flowers and wall paper are 
important sources of intoxication. The action of moulds (pencillium 
and mucor) may liberate volatile arsenical gases. Contaminated glucose, 
used in beer, caused the Manchester epidenlic. Arsenic is absorbed by 
the lungs and alimentary tract and is chiefly eliminated by the kidneys, 
which may degenerate. Putnam found arsenic in the urine of 30 per cent. 



FOOD POISONING 969 

of persons who showed no other symptoms of arsenical poisoning. Arsenic 
is widely found in plants, sea water and springs. Smaller amounts are 
eliminated by the bowel, milk and other secretions. 

Symptoms. — The symptoms are (a) gastro-intestinal, as dry throat, 
vomiting, purging or colic; the "rice-water" stools contain flecks of 
mucus; and (b) respiratory, as dry cough or chronic bronchitis, (c) 
Emaciation, weakness, fever and anemia may occur, (d) Cutaneous 
symptoms, as erythema, keratosis, pemphigus, herpes and brown pig- 
mentation and (e) nervous manifestations, as weak memory, vertigo, 
headache and multiple neuritis may develop. The neuritis has the same 
general features as the saturnine form, but sensory changes are more 
frequent and the legs are more often affected than the arms; paralysis 
of the peronei and foot extensors causes the "steppage" gait. The small 
muscles are less often affected than in plumbic or alcoholic neuritis; 
paralysis, ataxia, trophic disturbances and the reaction of degeneration 
occur as in other neuritides. 

Treatment. — Treatment is that of lead poisoning or neuritis. 

FOOD POISONING. 

Bromatotoxismus (Vaughan) exists in several forms: 

I. Meat Poisoning (Kreatoxismus) . — Sausages and head cheese are 
more dangerous than beef or mutton.- Sausage poisoning (botulism 
or allantiasis) was known in Germany a century ago. Van Ermingem 
isolated an anaerobic organism, the Bacillus botulinus; it contains spores, 
is flagellated and motile and grows only on alkaline media at a low 
temperature (18° to 35° C); it is a saprophyte and causes symptoms by 
its toxins, which are not destroyed by the gastric juice. Paratyphoid 
organisms were found by Durham (1900). Meat may taste and smell 
normal yet contain ptomaines; their nature is still undetermined, though 
Cobert considers them promatropin. Canned meat has often caused 
severe symptoms. In instances botulism was caused by eating salad 
and beans. 

Symptoms. — The symptoms of botulism appear in twelve to forty- 
eight hours, with nausea, vomiting and sometimes diarrhea. In the 
Wellback cases Ballard noted as early symptoms headache, chilliness 
or rigors and pains in the chest or back. Paralysis of the soft palate, 
larynx and esophagus rapidly develop and somewhat later paralysis of 
the bowel, or symptoms like atropine poisoning, mydriasis, ptosis, 
disordered vision, adynamia and weak heart action; the sensorium is 
clear and fever is unusual. The mortality ranges between 20 and 50 per 
cent. ; death occurs in four to ten days and the autopsy shows parenchy- 
matous degenerations and ecchymoses, but especially degeneration of the 
ganglionic cells, as those of the vagus or oculomotorius; if the patient 
survives, convalescence is established only after months. 

The symptoms of other forms of meat poisoning are either toxemic 
(typhoid type) or gastro-intestinal (cholera type) ; the typhoidal symptoms, 
which appear after an incubation of four to six days, are fever, status 
typhosus and even roseolas; the choleriform symptoms, which develoj) 



970 IN TOXIC A TIONS— SUNSTROKE 

in two to twelve hours, are vomiting, incessant purging, watery stools, 
clammy skin, collapse and cyanosis. Acute meningitis may be simulated 
exactly (A. D. Dunn). Mild forms occur in most epidemics. 

Treatment. — Early gastric lavage, colonic flushings and purgation are 
indicated; calomel followed by castor oil is the best aperient. Otherwise 
symptomatic medication, as in cholera or typhoid, is indicated; cham- 
pagne, strychnine, hypodermocylsis and opium may be given. The 
resemblance of botulism to the diphtheria toxins has suggested the 
use of antitoxine; its effects in animals have been remarkable, but to 
the author's knowledge it has not been used in man. 

II. Poisoning by Milk. — Galactotoxismus produces symptoms analog- 
ous to those of the infantile affections of the bowel, as vomiting, bloody 
diarrhea, fever and collapse. In cheese poisoning Vaughan found tyro- 
toxicon and other more frequent toxins, probably albumoses. Similar 
ptomaines were found in refrozen ice-cream and custard. In Norway 
where tyrQtoxismus is most prevalent, the colon bacillus has been re- 
peatedly found. Home-made cheese is more dangerous than the factory 
product. Various forms of toxemia result; some are cholera-like and 
others resemble belladonna poisoning. Treatment is that of kreatoxismus. 

III. Poisoning by Fish (Ichthyotoxismus) and Shell-fish (Mytilo- 
toxismus). — (a) Ichthyotoxismus, described by Comby (1827), may be 
caused by poisonous fish or poisonous glands in certain fish, as the roe 
or testicles, the muscular parte being harmless; the barbel in Europe 
and the tetrodon, diodon and fugu in Asia are poisonous (v. Beriberi). 
The poisoning due to putrefaction is more common. Paralytic symptoms, 
like curare poisoning, are most frequent, (b) Mussel poisoning (mytilo- 
toxismus) may cause dyspeptic symptoms in mild infections and cholera- 
like symptoms or symptoms of belladonna poisoning in severe ^forms. 
Rashes are common. Brieger isolated a mytilotoxin, which is found 
largely in the liver. The danger lies in placing mussel- or oyster-beds 
near river mouths, so that they feed on poisonous excreta. In restaurants 
certain glands near the heads of lobsters, considered toxic, are carefully 
excised. 

IV. Grain Poisoning (Sitotoxismus) . — 1. Ergotism. — Ergotism (Thuil- 
lier, 1830, and Tuczek, 1879) results from eating grain mixed with the ergot 
fungus (claviceps purpurea). Ergotized grain is found largely in bad 
harvests, resulting from wet springs and hot summers. Epidemics have 
occurred in Europe, and sporadic cases are not rare. Acute ergotism, 
with digestive symptoms, colic, cyanosis, weak heart and generally 
lethal outcome is less common than chronic ergotism, of which two forms 
exist; the first is the convulsive form, attended by paresthesia, lightning 
pains, headache, delirium, melancholy, dementia, muscular relaxation, 
generalized epileptiform attacks or local muscular contractures (flexion 
of the arms and extension of the toes and feet) ; it is said to result from 
the alkaloid cornutin. The second form is the gangrenous, due to spha- 
celinic acid and marked by localized gangrene, usually in the phalanges 
and less often in the tips of the ears and nose. Chronic ergotism is 
characterized by a number of symptoms which suggest tabes, as lightning 
pains, ataxia of station and movements, and lost knee-jerks; and in five 



PELLAGRA 971 

autopsies Tiiczek and Siemens found degeneration with, later, sclerosis 
of the posterior columns; degeneration in the anterior cornua, and minute 
foci of softening or hemorrhage also occur. The clinical course is chronic 
and death is frequent from convulsions or cachexia. 

Treatment. — Treatment includes avoidance of diseased grain and 
opium for convulsions and nitroglycerin for gangrene. 

2. Lathyrism (Lupinosis). — Lathyrism is produced by meal made 
from vetches, chiefly the lathyris sativus and cicera. Irving described 
the disease in India and it has been seen also in Algiers and Italy. It 
probably produces a lateral and possibly some posterior sclerosis of the 
cord, though no autopsies are reported. Clinically there is a spastic 
paraplegia with increase of reflexes and some paresthesia. 

V. Potato Poisoning. — Solanin is contained in potatoes in small 
amounts (0.06 per cent.) but larger amounts (0.4 per cent.) occur in 
potatoes which lie for some time in the ground or sprout in cellars (Bact. 
solaniferum). Fever, chills, general or cardiac weakness, vomiting, 
diarrhea and jaundice may develop. 

PELLAGRA. 

A disease with periodic alimentary disturbance, skin lesions and 
changes in the nervous system. 

Etiology. — The older theory ran that maidism was a chronic nutritional 
or toxic affection due to the use of corn or maize, which was unripe, 
decayed or infected with the aspergillus or other moulds. The present 
tendency is to regard it as an infection. The disposing etiology is " peasant 
life, poverty and polenta" (corn). It is endemic in Italy, Roumania, 
France, Spain and Mexico and the United States where there were 
30,000 to 50,000 cases in the six years before 1913. The first authentic 
description dates from Casal, of Spain (1735). The name is derived from 
pelle (skin) and agra (rough). 

Prodromal symptoms develop in the spring and include lassitude, 
vertigo, headache, anorexia, coated tongue, vomiting, epigastric pain and 
diarrhea. There is seldom fever. The vernal erythema appears largely 
on the exposed parts, face, hands and neck, possibly initiated by the 
sun's rays. The circlet of eruption on the neck is very characteristic. 
The hands are most commonly and characteristically involved, the palms 
generally being exempt. The eruption is a dull red, like sunburn, fades 
on pressure and may become macular. The color then deepens to a 
livid blue, ending in desquamation and pigmentation. More rarely 
vesiculation, crustation, Assuring and suppuration develop. Recurrence 
occurs the next spring (in Italy) or the same fall (in the United States) 
and leaves the skin atrophic, 'parchment-like, perhaps ulcerated or 
ecchymotic. 

Nervous Symptoms. — The prodromal symptoms (v. s.) intensify and 
the skin may become so hyperesthetic as to induce suicide. The patellars 
vary. Babinski's sign may be observed. Mental depression occurs in 
most cases; stupor, hallucinations, etc., may develop; 10 per cent, 
become insane. There are severe pains in the back but the most char- 



972 IN TOXICA TIONS—S UN STROKE 

acteristic symptom is the ataxic paraplegia; autopsies reveal a postero- 
lateral sclerosis, sometimes with atrophy of the anterior horns, lepto- 
meningitis and variable brain findings. In some cases mydriasis, cataract, 
paralysis of the eye muscles, optic neuritis and choroiditis develop. 

Digestive symptoms commence in the prodromal stage. Stomatitis, 
the stipple-tongue (with black pigment), vomiting, pyrosis, meteorism 
and severe, even dysenteric, diarrhea increase the discomfort and lead to 
prostration and emaciation. There is slight anemia, with some increase 
of the large mononuclears, very few eosinophiles and no leukocytosis. 
The mortality is 35 per cent. 

The rarer acute cases may resemble typhoid in symptoms and pathology 
(status typhosus and swelling with ulceration of the intestinal lymph 
structures), or meningitis (foci of acute meningomyelitis) . Other findings 
at autopsy are atrophy of the digestive mucosa, parenchymatous de- 
generation and pigmentation, the latter of which is thought to occur 
from adrenal inflammation. 

Treatment. — Treatment is prophylactic (proper storage of the grain); 
change of diet or of locality is indicated and arsenic should be given 
internally. 

BERIBERI. 

Definition. — Beriberi or polyneuritis endemica (Balz, Scheube) is an 
endemic and epidemic affection of the tropics and subtropics, of un- 
known etiology, characterized anatomically by degenerative inflammation 
of the peripheral nerves, and clinically by motor and sensory disturbances, 
anasarca and cardiac disturbance. Beri signifies a sheep's gait, and 
kakke means disturbance of the gait. 

History. — Beriberi is mentioned in the oldest Chinese writings and 
was observed in the Roman legions, 24 B.C., by Strabo and Cassius. 
In the seventeenth century, beriberi was noted in Brazil and the Malay 
archipelago; in recent times it has been described in India, Japan, the 
Dutch Oriental colonies and in this country. 

Distribution. — The main foci of beriberi are (1) the Malay archipelago, 
Sumatra, Borneo and Java; also China, India, the Philippines, Japan 
and even Australia. The mortality was very high among the Chinese 
coolies in the Dutch possessions. (2) Africa, including the mainland 
and adjacent islands. (3) America and the West Indies, Brazil, Hon- 
duras and Cuba. Scheube doubts that the cases in the epidemic at 
Tuscaloosa, Alabama, were beriberi, but they apparently were Oriental 
beriberi. Cases appeared in Dublin (1894-1898, with forty-two deaths), 
in England and in Paris. 

Etiology. — There are two distinct views: (1) That it is an acute in- 
fection (Balz, Scheube); the same telluric conditions promote beriberi 
which promote malaria. In 80,000 cases among the Japanese troops 
in the Russo-Japanese War, Kokubo frequently found a coccus. (2) The 
second view is that beriberi results from food. Polished rice loses its 
pericarp, in which there is some vital substance the loss of which causes 
beriberi; polished or milled rice causes polyneuritis in fowl; and in the 
disease, the feeding of the pericarp is curative. Natives are more often 



BERIBERI 973 

affected than Europeans, and males more frequently than females. 
In 1879 there were 8197 cases in Japan and in 1891, only 1. Poor food, 
overcrowding and lack of hygiene are important factors. 

Symptoms. — The incubation is several months. The symptoms are 
threefold : 

1. Neuritic Symptoms. — A more detailed description of these symp- 
toms has been given under Multiple Neuritis. Anatomically, there is 
the same symmetrical degeneration or inflammation in the distal parts 
of the peripheral nerves, but also often in the phrenic and pneumogastric 
nerves and the cardiac, renal and solar plexuses; the nuclei of the sheath 
multiply; the axis-cylinders degenerate; there is a lumpy degeneration 
in the medullary sheath and later, a connective-tissue hypertrophy. 
In 8 cases there were degenerative changes in the cord, anterior horns 
and posterior ganglia. Clinically, the onset is gradual and the course 
chronic. 

(a) Motor Symptoms. — The muscles of the calves, the knee extensors 
and the abductors and flexors of the thigh are weakened, flaccid, swollen 
and atrophied. The muscles are more frequently tender than the nerve 
trunks. In severe cases the trunk, arms and even the face are involved. 
Anatomically, the muscles are degenerated. Phrenic weakness and vagus 
symptoms, such as rapid heart, vomiting, epigastric oppression or 
digestive disorder are not infrequent; the lungs are sometimes acutely 
emphysematous, from involvement of the pulmonary plexus. Laryn- 
geal, glossopharyngeal, hypoglossal or ocular participation is more rare. 
Cramps and fibrillary contractions are frequent, but ataxia is uncommon, 
although the name beriberi refers specifically to disturbed locomotion. 
The gait is described as like that of one walking in wet clothes or wading 
in water. 

(b) Sensory Symptoms. — Paresthesia is common. Hypesthesia is 
most marked in the distal parts, though the soles are exempt; it is more 
frequent than anesthesia, which is rarely complete. Hyperesthesia may 
occasionally occur over the spine and abdomen. Pains over the joints 
and intercostal spaces are quite common. 

(c) Trophic Symptoms. — These are uncommon. They include joint 
relaxation, herpes or skin atrophy. 

(d) Reflexes. — The skin reflexes are seldom abolished. Reduction 
of the tendon reflexes develops equally with the paralysis. 

(e) Degeneration. — Slight reaction of degeneration is common and may 
be marked in severe cases. It occurs particularly in the leg. 

2. Dropsy. — Dropsy occurs in 97 per cent, of cases and is invariably 
in fatal cases; it may be marked in the legs and face. It is most severe 
in the pericardium, quite severe in the pleurae, and least severe in the 
peritoneum. It is caused by cardiac and perhaps also by vasomotor 
involvement. 

3. Cardiac Insufficiency. — In acute cases, death may result in a 
day, and 65 per cent, of acute cases terminate fatally within two weeks. 
There is palpitation, cardiac or epigastric oppression or pain; tachy- 
cardia, dyspnea and cyanosis develop ; the right ventricle is hypertrophied 
and dilated; the first apical tone is weak; there is splitting of the heart 



974 INTOXICATIONS— SUNSTROKE 

tones, gallop-rhythm, and systolic or even diastolic functional bruits; 
the urine is decreased in amount; the liver is turgid. Anemia is marked 
and the leukocytes may be increased. Acute pulmonary edema is usually 
fatal. The heart muscle is pale, friable, colloid or inflamed. 

The types of beriberi only accentuate the above-named symptoms: 
(1) The rudimentary form may begin with fever and catarrh of the air 
passages and alimentary tract. There is a slight edema of the ankles, 
muscular weakness, especially in the legs, and muscular tenderness, 
paresthesia and palpitation. (2) The atrophic form is marked by atrophic 
paralysis. If edema does not develop, these types are called " dry forms." 
(3) The dropsical form is characterized by much transudation and pro- 
nounced insufficiency of the heart. (4) The acute cardiac or pernicious 
form (v. s.). 

Diagnosis. — The leading points are the multiple neuritis, most marked 
in the legs; vagus neuritis and cardiac insufficiency; and dropsy. 

Prognosis. — In Japan and the Dutch Indies the death-rate is 3 or 4 
per cent.; in Brazil it formerly reached 50 to 75 per cent., and in the 
Malay archipelago, 40 to 50 per cent. Death results primarily from heart 
failure, secondarily from paralysis of respiration, less frequently from 
uremia, pulmonary embolism, aspiration pneumonia, dysentery, tuber- 
culosis or marasmus. Even in recovery, permanent residua are common, 
such as weakness, or obstinate contractures of the legs, absence of knee- 
jerks and cardiac instability and hypertrophy. In 43 per cent, of the 
fatalities there is a sudden death. Recurrences are common. 

Treatment. — In the early stages, purgation and salicylates are bene- 
ficial. In the later stages, electrotherapy and other measures employed 
in multiple neuritis (q. v.) are indicated. Venesection relieves the over- 
laden right heart and dyspnea, and promotes action of the kidneys. 
Digitalis frequently fails when the vagus is degenerated; in dropsical 
forms it is helpful, as is caffeine. The ice-bag over the heart, bromides 
and belladonna may mitigate cardiac unrest and palpitation. 

ILLUMINATING-GAS POISONING. 

Illuminating gas contains H, hydrocarbons and CO. Steam is forced 
through the hot coke in the manufacture of the gas and methane, ethane, 
and benzene are added. Water-gas contains 45 per cent. CO. Alcoholism, 
the increasing difficulty in procuring morphine and other poisons, igno- 
rance and carelessness cause many deaths yearly. 

Symptoms are due to close union of the gas and the hemoglobin, 
abolition of gaseous interchange, a particular action of the poisons on 
the nervous system, and absence of oxidation of the waste substances 
of the body. Respiration: The breathing is rapid, loud, stertorous and 
often of the Cheyne-Stokes's type. W. G. Thompson gives the average 
number of respirations 30; they were G2 in one non-fatal and 80 in a fatal 
cases. The mouth is covered with froth which is often bloody. In 
fatal cases, there is found pulmonary congestion and edema; sometimes 
bronchopneumonia, atelectasis and emphysema. Circulation: The pulse 
is disproportionately rapid (120-140), considering the fever and respi- 



-m 



SUNSTROKE 975 

ration, feeble and often irregular. The cherry-red blood is notorious. 
W. G. Thompson noted leukocytosis, even 50,000; in his fatalities, the 
white cells exceeded 18,000 but patients with higher counts may recover. 
The hemoglobin is decreased to 70 per cent, or lower (20 per cent.). 
G. J. Jones noted reduction of the reds to 1,000,000, often with poly- 
chromatophilia; contrary to Thompson's report, he finds no increase of 
the red cells. 

Nervous Symptoms. — Coma ranks first. In most poisonings it is pro- 
found; enduring over forty-eight hours, the outlook is generally unfavor- 
able, yet Kinnicutt reports recovery after two weeks of coma. Of Thomp- 
son's series, 80 per cent, of comatose cases recovered. The pupils are 
usually small and immobile but may vary or dilate. Muscular twitch- 
ings, convulsions, delirium, opisthotonos, rigidity, increased reflexes and 
incontinence are common. Postmortem findings include intense cerebral 
congestion, cerebral apoplexy, serous leptomeningitis, disseminated 
encephalitis, encephalomyelitis, multiple neuritis and cerebral thrombosis 
with softening in the internal capsule and lenticular nucleus (Kolisko). 
Acute mania and paralyses may regress after days or months. Gangrene 
of the legs may ensue. 

Vomiting is occasional and dryness of the mouth the rule. The skin 
is generally cold, dry, cyanotic but may be clammy; in fatal cases Jones 
observed serous blebs. The temperature, at first subnormal, in nearly 
all cases rises after twelve to eighteen hours to 99° or 103°; high fever is 
usually fatal in one to three days but W. A. Steele records recovery with 
110° and a pulse of 215. Glomerulonephritis is common. The urine is 
high in specific gravity and the nitrogen is increased. 

Therapy. — Fresh air and oxygen inhalations seem rational but actually 
are seldom efficacious. The tongue is held out and occasionally gently 
pulled. Artificial respiration is indicated. Robin advises the sitting 
posture but it is difficult to see how it is practicable. The skin should be 
kept warm. Atropine, gr. t ^q, and adrenalin, TTLxxx, are indicated but 
vasodilators, as nitroglycerin, are always injurious. Venesection fol- 
lowed by normal salt solution, given subcutaneously and repeated in 
urgent cases, is helpful. 

SUNSTROKE. 

The difference between the two forms, (1) sunstroke, and (2) heat 
exhaustion, was first recognized by Dowler, of New Orleans. 

Sunstroke, also known as siriasis, insolation, coup de soliel and thermic 
fever, is due to exposure to the sun. A very frequent factor is alcoholism. 
There is thought to be a paralysis of the bulbar heat centres, leading to 
excessive production of heat and deficient elimination of it. The theory 
of infection has also been advanced. 

Symptoms.— Symptoms may develop very abruptly and cause early 
or even immediate death from asphyxia and paralysis of the heart; 
this type was long confused with apoplexy. In most cases there is an 
interval lasting from a few minutes to an hour, in which there are 
headache, vertigo, visual disturbances, nausea, and perhaps vomiting 
before coma intervenes. 



976 IN TOXIC A TIONS—S UN STROKE 

During the coma which develops rapidly, and in which the physician 
usually sees the patient, the following signs are observed: the face is 
first flushed, later rather cyanotic, and sometimes stained with petechias. 
The preliminary pupillary dilatation passes into myosis and the skin has a 
peculiar odor. The pulse usually exceeds 100, and is bounding. The rectal 
temperature ranges from 107° to 112° and respiration is deep, labored 
and stertorous. Save for the laboring chest, the patient is usually quiet; 
about 25 per cent, of the author's patients struggled during treatment 
by the cold bath and about 20 per cent, of the severe cases had epilepti- 
form convulsions. Lewis and Packard (1901) in 92 cases found con- 
vulsions and unconsciousness in all severe cases; immobile pupils and 
absent knee-jerks were common. Involuntary evacuations are usual and 
the thin feces have a peculiar odor. There is a leukocytosis in about 
75 per cent, of the cases. Recovery is frequent; consciousness returns 
and the fever falls. Despite treatment, the Cheyne-Stokes's breathing 
may develop, the pulse may grow smaller and more rapid, and death may 
follow, usually in a little more than a day. The autopsy shows early 
rigor mortis, fluidity of the blood, great venous hyperemia, particularly 
in the brain and lungs, and dilatation of the. right and contraction of 
the left ventricle. 

After sunstroke the patient becomes extremely susceptible to hot 
weather. Epilepsy, multiple neuritis and mental symptoms are among 
its after-effects. The author saw one case with a temperature of 109° 
in which the fever fell with hydrotherapy but rose to 104°; in a few days 
the trouble was recognized as typhoid. 

Diagnosis. — The diagnosis is easily made. Practically, there is but 
one possible cause of confusion, pontine hemorrhage, but the latter 
never develops nearly as high a temperature and death is almost in- 
stantaneous; should the patient survive, paralysis, usually of the crossed 
type, is obvious. 

Heat exhaustion may result from exposure to the sun or to high tem- 
perature with humidity; the cases seen by the writer came largely from 
laundries, basement stores or engine-rooms; heat exhaustion occurs also 
among stokers on steamers. The symptoms are those of a centric vaso- 
motor paralysis. The skin is cool and livid, rather than red, and the rectal 
temperature is often 3° or 4° subnormal; the pulse is rapid and weak and 
the breathing is rapid but not labored. In short, the symptoms of collapse 
are present. Restlessness, anxiety and sometimes delirium are noted, 
though the sensorium is practically normal in most cases. 

Treatment. — In sunstroke the chief indication is reduction of the 
retained heat, by immersing the patient in a bath gradually cooled by large 
pieces of ice. Shock is averted by this means; cerebral congestion is 
lessened by placing a block of ice under the neck, an ice-bag on the vertex 
and an ice-bladder over the anterior neck; active friction of the body 
and limbs with the open hands brings to the surface the blood, which is 
cooled by the bath and the rubbing with pieces of ice. With this treat- 
ment, few more than one-third of the cases should die. The patient 
should be taken from the bath when his rectal temperature is 102°, 
for the fall usually continues after cessation of treatment. Laxatives 



SUNSTROKE 977 

are generally unnecessary, for the bowels move freely. Heart stimulants 
should be given pro re nata. For convulsions, a little chloroform by 
inhalation and a hypodermic of morphine are indicated. Asphyxia and 
distention of the right heart are relieved by phlebotomy. 

In heat prostration the treatment is diametrically the opposite; a 
warm bath or hot bricks for subnormal registration, diffusive cardiants, 
as ammonia, camphor and strychnine, saline solutions under the skin 
and applications of mustard are indicated; cold and venesection are 
obviouslv contra-indicated. 



62 



I 



1 



INDEX. 



Abdominal pain, causes of, 547, 563 
in pneumonia, 73 
in typhoid fever, 36 
Abortion in diabetes, 732 

in syphilis, 221 

in typhoid fever, 40 
Aboulia, hysterical, 907 
Abscess of brain. See Brain, abscess of 
cold, 148 

extradural, differentiation of, 802 

of liver. See Liver, abscess of. 

of lung. See Lung, abscess of. 

perinephric, 654 

subphrenic, 611 

differentiation of, 465, 472 
Acetanilide, 599, 943 
Acetonuria, diabetic, 728, 730, 735 
Acetphenetidin, 50, 57, 106, 412, 741 
Achlorhydria, 502, 503 
Achondroplasia, 956 
Achylia gastrica, 503 

etiology of, 503 
pathology of, 503 
prognosis of, 503 
symptoms of, 503 
treatment of, 503 
" Acid-fast" bacilli, 165, 411 
Acidosis, diabetic, 728, 730, 735 
Aconite, 268, 412 
Acoria, 533 
Acrodynia, 290 
Acromegaly, 720 

course of, 721 

diagnosis of, 721 

differentiation of, 721 

etiology of, 720 

prognosis of, 721 

symptoms of, 720 

treatment of, 721 
Acroparesthesia, 944 
Actinomycosis, 193 

diagnosis of, 195 

digestive tract, 194 

etiology of, 193 

forms of, 193 

head and neck, 193 

incubation in, 193 

parapleuritis, 195, 462 

respiratory tract, 195 

treatment of, 195 
Acupuncture, 905, 950 
Adams-Stokes's syndrome, 342 
Addison's anemia, 672 



Addison's disease, 701 
course of, 703 
diagnosis of, 703 
differentiation of, 704 
etiology of, 701 
symptoms of, 702 
treatment of, 704 
Adenia, 687 
Adenitis, bronchial, 169 

cervical, 169 
Adenoids, 488 

Adhesions in gastric ulcer, 514 
Adhesive plaster, 466 
Adiamorrhysis, 764 
Adipose ascites, 617 
Adiposis dolorosa, 747 

pathology of, 747 
symptoms of, 747 
treatment of, 748 
Adiposity, 746 
Adrenal glands, diseases of, 701 

insufficiency in typhoid, 41 
Adrenalin, 77, 88, 89, 110, 189, 704, 411, 

430, 702, 704 
Aerophagia, 531 
African lethargy, 246 
Agar-agar, 560 
Agaricin, 188 
Ageusia, 881 
Agraphia, 755, 756 
Ague-cake in malaria, 236 
Ainhum, 947 

Air, fresh, in tuberculosis, 184 
Albumin in urine, 644 
Albuminuria, 644 

albumose, 646 

Bence-Jones, 646 

diabetic, 729 

diagnosis of, 646 

diphtheritic, 83 

etiology of, 645 

genuine, 644 

globulin, 644 

in malaria, 237 

mucin, 646 

in nephritis, 620, 625, 628 

nucleo-albumin, 646 

peptone, 646 

in pneumonia, 70 

prognosis of, 646 

renal, 644 

rheumatic, 285 

scarlatinal, 264 

spurious, 644 

syphilitic, 207 



980 



INDEX 



Albuminuria, tests for, 645 
boiling, 645 
ferrocyanide, 646 . 
Jolles's, 646 
nitric acid, 645 
Spiegler's, 646 
in tuberculosis, 168 
in typhoid fever, 40 
in yellow fever, 293 
Albumose, tests for, 646 
Alcohol, coma from, 959, 772 
injections, 943 
therapeutics of, 56, 76, 943 
Alcoholism, acute, diagnosis of, 959 
symptoms of, 959 
treatment of, 959 
chronic, prognosis of, 960 
symptoms of, 960 
treatment of, 961, 962 
delirium tremens, 961 
differentiation of, 772, 807, 959 
Alexia, 753, 956 

Alkalies. See Sod. bicarbonate. 
Alkaptonuria, 651 
Allantiasis, 969 
Allergy, 88 

Allocheiria, tabetic, 852 
Aloes, 562 
Alum, 416 
Amaurosis, 875 

with idiocy, 866 
Amblyopia, 874, 875 
Ameba dysenterise, 120 
Amebiasis, 120 

Amebic dysentery. See Dysentery. 
Ammonia, aromatic spirits, 336, 535 
Ammoniemia, 653 
Ammonium acetate, 268 
carbonate, 76, 377, 422 
chloride, 415, 422 
in urine, 569, 728 
Amyl nitrite, 189, 399, 400-, 452 
Amyloid degeneration of kidneys, q. v. 
of liver, q. v. 
of spleen, q. v. 
• in tuberculosis, 168 
Amyotonia, 951 

congenita, 951 
Anaphylaxis, 88 
Anarthria, 754 
Anemia, aplastic, 676 
classification of, 667 
in family jaundice, 590 
in heart disease, 366 
in ictero-anemia, 590 
infantum pseudoleukemica, 690 
lienalis, 687 
lymphatica, 687 
pernicious, 672 
course of, 675 
diagnosis of, 676 
differentiation of, 523, 676, 677 
etiology of, 672 
prognosis of, 675 
symptoms of, blood, 672 
circulation, 674 « 
digestion, 674 
hemolymph glands, 674 



Anemia, pernicious, symptoms of, metab- 
olism, 673 
nervous, 675 
skin, 673 
subjective, 673 
treatment of, 677 
pseudopernicious, of children, 690 
secondary, parasitic, 311 

posthemorrhagic, acute, 678 
etiology of, 678 
prognosis of, 679 
symptoms of, 678 
treatment of, 679 
chronic, etiology of, 679 
differentiation of, 677 
symptoms of, 680 
treatment of, 680 
splenic, 690 
splenica infettiva dei bambini, 690 
Anesthesia, dissociated, 831, 836, 847, 848 

dolorosa, 831 
Aneurysm, abdominal, 408 
diagnosis of, 409 
prognosis of, 409 
signs of, 408 
symptoms of, 408 
treatment of, 408 
of aorta, 400 
of brain, 211, 782 
celiac, 409 
gastric, 409 
of heart, 330 
hepatic, 409 
intracranial, 211, 782 
diagnosis of, 783 
etiology of, 782 
pathology of, 783 
symptoms of, 783 
treatment of, 783 
of lung, 424 
mesenteric, 409 

miliary, in cerebral hemorrhage, 765 
renal, 409 
splenic, 409 
syphilitic, 208, 211 
thoracic, 400 

death, mechanism of, 407 
diagnosis of, 406 
differentiation of, 407, 460 
etiology of, 208, 211, 400 
pathology of, 401 
physical signs of, 402 

heart changes, 403 
respiratory changes, 404 
sympathetic, 406 
vascular changes, 404 
prognosis of, 407 
symptoms of, 401 
treatment of, 408 
Angina abdominalis, 335, 398 
cruris, 335, 397 
erysipelatous, 59 
Ludovici, 84, 482 
pectoris, 333 

diagnosis of, 335 
differentiation of, 335 
etiology of, 333 
pathology of, 333 



INDEX 



9S1 



Angina pectoris, prognosis of, 335 
symptoms of, 333 
treatment of, 335 
phlegmonosa, 484 
Angina, scarlatinal, 263 
syphilitic, 203 
in typhoid fever, 34 
ulceromembranosa, 484 
Vincent's, 484 
Angioneurotic crisis, 693 

edema, 945 
Angiosclerosis, 392 
Anguillula intestinalis, 316 
Ankylostoma duodenale, 311 
Anopheles, 232 
Anorexia, 533 
Anosmia, 873 
Anthracosis of lungs, 440 
Anthrax, 127 

bacteriology of, 127 
etiology of, 127 
external, 128 

diagnosis of, 128 
differentiation of, 45, 60, 128 
prognosis of, 129 
symptoms of, 128 
treatment of, 129 
internal, 129 
intestinal, 129 

diagnosis of, 45, 129 
symptoms of, 129 
respiratory, 130 

symptoms of, 130 
treatment of, 130 
septicemia, 130 
Antiformin, 140 
Antimony, 420, 422 
Antitoxin in diphtheria, 87 

in tetanus, 136 
Anuria, renal colic causing, 659 
Aorta, aneurysm of, 400 

arteriosclerosis of, 394, 397 
atheroma of, 394, 397 
dilatation of, intermittent, 409 
embolism of, 410 
inflammation of, 410 
rupture of, 410 
syphilis of, 208 
thrombosis of, 410 
tuberculosis of, 181 
Aortic insufficiency, 351 

diagnosis of, 355, 361 
etiology of, 351 
mechanism of, 352 
physical signs of, 352 

auscultation, 354 
inspection, 352 
palpation, 353 
percussion, 354 
prognosis of, 370 
treatment of, 371 
stenosis, 356 

diagnosis of, 357 
differentiation of, 357, 361 
etiology of, 356, 380 
mechanism of, 356 
physical signs of, 356 

auscultation, 356 



Aortic stenosis, physical signs of, inspec- 
tion, 356 
palpation, 356 
percussion, 356 
prognosis of, 370 
treatment of, 370 
Aortitis, acute, 208, 410 
chronic, 394, 401 
syphilitic, 208, 351 
Aphasia, amnestic, 755 
auditory, 755 
conduction, 755 
localization, 754 
motor, 754 
optic, 753 
sensory, 755 
visual, 756 
Aphthae epizooticee, 301 
Aphthous fever, 301 
Apneumatosis of lungs, 441 
Apocynum, 377 
Apomorphine, 422, 959 
Apoplectiform attacks in paretic demen- 
tia, 805 
bulbar paralysis, 780, 811 
seizures in multiple sclerosis, 844, 848 
Apoplexy, 765. See Cerebral Hemorrhage, 
cardiac, 332, 772 
habitus, 765 
Appendicitis, 544 

actinomycotic, 194 
in aged, 547 

bacteriology of, 544, 547 
in children, 547 
complications of, abscess, 546 
chronic changes, 547 
necrosis, 546 
peritonitis, 546 
ulceration, 546 
diagnosis of, 547 

differentiation of, 73, 172, 194, 515 
etiology of, 544 
pathology of, 544 
prognosis of, 547 
symptoms of, 544 
early, 544 
late, 546 
remote, 547 
treatment of, 548 
tuberculous. 172, 176 
typhoid, 73\ 
Appendix vermiformis, cancer of, 554 
foreign bodies in, 544 
inflammation of , 544 
typhoid ulcers of, 35, 36 
Appetite, disturbance of sense of, 533 
Aprosexia, 488 

Argyll-Robertson pupil, 853, 855, 877 
in paretic dementia, 805 
Argyria, 704 
Arrhythmia, 339 

Arsenic, 188, 228, 229, 377, 430, 687, 691, 
932 
action and administration, 677, 678 
Arsenical poisoning, 968 
Arterial tension, 395, 396, 399 
Arteries, diseases of, 392 

syphilitic endarteritis of, 208, 211 



982 



INDEX 



Arteritis, 392, 410 

pneumococcic, 71 
syphilitic, 208, 211 
in typhoid fever, 32 
Arteriocapillary fibrosis, 392 
Arteriosclerosis, 392 

diagnosis of, 395, 398 

differentiation of, from syphilitic 

endarteritis, 211 
etiology of, 392 
pathogenesis of, 393 
pathology of, 393 
prognosis of, 398 
symptoms of, 395 
syphilitic, 208, 211 
treatment of, 399 
Artery of hemorrhage, 765 
Arthritis deformans, 951 
diagnosis of, 954 
differentiation of, 954 
etiology of, 951 
pathology of, 951 
symptoms of, 951 
treatment of, 955 
types of, 952 

diffuse, acute, 952 

chronic, 952 
Heberden's nodes, 953 
juvenile, 953 
monarticular, 953 
vertebral, 953 
divitum, 738 
gonorrheal, 137 
pauperum, 738 
pneumococcic, 71 
rheumatic, 282 
in scarlatina, 265 
in syphilis, 218 
in tuberculosis, 182 
in typhoid fever, 41 
Arthropathies, syringomyelic, 847 

tabetic, 854 
Asafetida, 55, 502, 564 
Ascaris lumbricoides, 307 
Ascites, adipose, 617 

in cancer of liver, 579 
chyliform, 617 
chylous, 617 
in cirrhosis of liver, 568 
diagnosis of, 614 

differentiation of, 173, 614, 615, 616 
etiology of, 613 
in heart disease, 369 
in pericarditis adhesiva, 389, 586 
symptoms of, 613 
treatment of, 618 
Aspergillosis, 165, 197 
Aspidium, 303 
Aspiration, abdominal, 616 
thoracic, 388, 458, 467 
Aspirin, 288 
Assam fever, 245 

Associated movements in apoplexy, 771 
Association, centres for, 754 
Astasia-abasia, hysterical, 909 
Asthenic bulbar paralysis, 810' 
Asthma, bronchial, 427 

diagnosis of, 429 



Asthma, bronchial, differentiation of, 429, 
368 
etiology of, 427 
pathogenesis of, 428 
prognosis of, 429 
symptoms of, 427 
treatment of, 429 
cardiac, 368 
Millar's, 718 
thymic, 718 
Ataxia, cerebellar, 762, 856, 866 
cortical, 753 
crus lesion causing, 760 
Friedreich's, 865 
hereditary, 865 
cerebellar, 866 
diagnosis, of 865 
etiology of, 865 
pathology of, 865 
prognosis of, 865 
symptoms of, 865 
locomotor, 849 
poliomyelitic, 100 
pons lesions causing, 760 
in tabes, 851 
Atelectasis of lungs, acquired, 441 

congenital, 441 
Ateliosis, 723 
Atheroma, 392 

of aorta, 394, 397 
Athetosis, in cerebral infantile paralysis, 
789 
posthemiplegic, 772 
Athyrea, 709, 712 
Atophan, 741 

Atrophia hepatis fusca, 565 
Atrophy, hemifacial, 882 

progressive spinal, 882 
Atropine, therapeutics of, 77, 88, 188, 269, 

342 
Aura, epileptic, 920 
Autoserotherapy, 468 
Autumnal fever, 24 



Babinski's sign, 630, 770, 858, 859 
Baccelli's sign in pleurisy, 458 

hi pneumonia, 69 
Bacilluria, treatment of, 57 

in typhoid fever, 40 
Bacillus, acid-fast, 165, 411 

aerogenes encapsulatus, 391 
in pneumothorax, 469 

anthracis, 127 

botulinus, 496, 969 

coli, 21 

comma, 141 

diphtheriae, 78 

dysenterise, 119 

enteritidis, 496 

fusiformis, 485 

influenza, 102 

Klebs-Loefner, 78 

leprae, 140, 190 

mallei, 130 

Oppler-Boas, 523 



INDEX 



983 



Bacillus, pertussis, 107 

plague, 115 

pseudotuberculosis, 165 

smegma, 140 

tetani, 133 

tuberculosis, 139 

typhosus, 25 
Bacterial latency, 20 
Bacteriemia, septic infections, 17, 19, 32 
Balantidium coli, 247 
Balne's cough, 488 
Balsam of Peru, 422 
Bamberger's sign in pericarditis, 385 
Banting's cure, 746 
Banti's disease, 571, 690 
Barlow's disease, 697 

diagnosis of, 697 
etiology of, 697 
prognosis of, 697 
symptoms of, 697 
treatment of, 697 
Basedow's disease, 709 
Basham's mixture, 635 
Baths in typhoid fever, 50 
Baume's law, 221 
Becker's sign, 710 
Bednar's plaques, 478 
Bed-sores in typhoid fever, 57 
causes of, 57, 840 
treatment of, 57, 840 
Beef-tea 52 

Belladonna, 110, 124, 188, 268, 269, 338, 
378, 412, 430, 502, 518, 535, 538, 558, 
562, 711 
Bence- Jones's albumose, 646, 691 
Benzene, 311 
Benzoic acid, 422 
Benzoin, 188 
Benzol, 687 
Beriberi, 972 

diagnosis of, 974 

etiology of, 972 

prognosis of, 974 

symptoms of, 973 

treatment of, 974 
Beta-naphtol, 535 
Beta-oxybutyric acid, 728 
Bichloride. See Hydrargyrum. 
Biernacki's sign, 852 
Bile ducts. See Gall ducts. 
Bile, flow of, 536 
Bilharzia disease, 316 
Bilirubin, test for, in stools, 537 
Biot's breathing, 92, 151 
Bismuth, 55, 124, 497, 518, 535 
Black death, 115, 117 

smallpox, 252 

vomit, 292, 293 

water fever, 240 
Bladder, tuberculosis of, 179 
Blastomycosis, 165, 196 
"Bleeders," 698 
Blindness, mind-, 753 

color-, 753 
Blood, bacilli in, 17, 19, 32 

cultures in pneumonia, 69 
in sepsis, 19 
in typhoid, 32 



Blood, diseases of, 667 
Blood-pressure, 395, 396, 399 
Bloodvessels, syphilis of, 208, 211 

tuberculosis of, 184 
Blue mass, 225, 376 
Bones, diseases of, 956 
* syphilis of, 217 
tuberculosis of, 181, 182 
Boric acid, therapeutics of, 268 
Bothriocephalus latus, 304 
Botulism, 969 
Boulimia, 533 
Bowels. See Intestines. 
Brachycardia, 341 
Bradycardia, 341 
etiology of, 342 
prognosis of, 343 
symptoms, 342 
treatment of, 343 
Brain, abscess of, 799 

diagnosis of, 801 
differentiation of, 796, 801, 802 
etiology of, 799 
pathology of, 799 
prognosis of, 802 
symptoms of, 800 
treatment of, 802 
actinomycosis of, 195 
anemia of, 763 
aneurysms of, 211, 782 
arteriosclerosis of, 211, 397, 779 
atrophy of, 780 
cancer of, 212, 789 
circulatory diseases of, 763 
congestion of, 763 
cysts of, 790 
degeneration of, 788 

lacunar, 782 
diseases of, 749 
edema of, 764 

embolism. See Cerebral embolism, 775 
glioma of, 790 
gumma of, 212, 213, 790 
hemorrhage of. See Cerebral hemor- 
rhage, 765 
in syphilis, 211 
hyperemia of, 763 
inflammation of. See Encephalitis 

also, 782 
lesions of, in diphtheria, 83, 84 
localization of. See Cerebral locali- 
zation, 749 
sarcoma of, 212, 790 
sclerosis of, 788, 804 
"softening" of, 779, 782, 802 
syphilis of, 211 

arterial disease, 211 
differentiation of, 211, 212, 213, 

790, 796, 803, 846 
gumma, 212, 213, 790 
meningitis, 212 
softening, 211 
thrombosis, 211 
thrombosis. See Cerebral thrombosis. 
See Brain, syphilis of. 
See Sinus thrombosis, 
tuberculosis of, 175, 789 
tumors of, 789 



984 



INDEX 



Brain, tumors of, classification of, 789 
course of, 796 
diagnosis of, 795 
differentiation of, 781, 795, 796, 

807, 811 
etiology of, 789 
. localization of, 792, 796 
pathology of, 789 
prognosis of, 796 
symptoms of, 791 
treatment of, 797 
Brand bath in typhoid fever, 51, 52 
Breasts, syphilis of, 218 
tuberculosis of, 180 
Breathing, Biot's, 92, 151 

Cheyne-Stokes's, 92, 151, 631, 772 
metamorphosing, 159 
Bright's disease. See Nephritis. 
Brill's disease, 278 
Briquet's syndrome, 910 
Broadbent's sign, 389 
Broca's convolution, 755 
Brodie's joints, 906, 909 
Bromatotoxismus, 969 
Bromides, 57, 110, 338, 924. See Potass. 

bromide. 
Bromism, differentiation of, 807 
Bromoform, 110 
Bronchi, dilatation of, 423 
diseases of, 418 
foreign bodies in, 426 
inflammation of, 418 
stenosis of, 426 
stones in, 427 
syphilis of, 210 
Bronchial adenitis, 108, 168 
asthma, 427 
breathing in pleurisy, 458 

in pneumonia, 68, 69, 73, 74 
in tuberculosis, 158 
casts, 66, 423 
glands, anthracosis of, 440 

tuberculosis of, 108, 168 
stenosis, 426 

diagnosis of, 427 
etiology of, 426 
symptoms of, 426 
treatment of, 427 
ulcers, syphilitic, 210 
Bronchiectasis, 423 

complications of, 425 
diagnosis of, 425 
differentiation of, 425 
etiology of, 423 
pathology of, 423 
physical signs of, 424 
symptoms of, 424 
treatment of, 425 
Bronchitis, acute, 418 

etiology of, 419 
symptoms of, 419 
treatment of, 420 
capillary, 434 
chronic, 421 

diagnosis of, 195, 422 
etiology of, 421 
pathology of, 421 
prognosis of, 422 



Bronchitis, chronic, symptoms of, 421 
treatment of, 422 
fibrinous, 423 

diagnosis of, 423 
etiology of, 423 
prognosis of, 423 
symptoms of, 423 
treatment of, 423 
in heart disease, 368 
in influenza, 104, 105 
in measles, 272 
mucinosa, 423 
pseudomembranacea, 423 
putrid, 421 

differentiation of, 425 
syphilitic, 210 
tuberculous, 153, 165 
in typhoid fever, 39 
in whooping-cough, 108 
Bronchophony, 69, 73, 74, 159, 458 
Bronchopneumonia, 434 
bacteriology of, 435 
capillary, 436 
diagnosis of, 437 
differentiation of, 148, 161, 437 
diphtheritic, 84, 85 
disseminated, 436 
etiology of, 434 
generalized, 436 
in influenza, 104 
issues of, 437 
measles as cause of, 272 
pathology of, 435 
physical findings of, 436 
prognosis of, 437 
symptoms of, 435 
treatment of, prophylactic, 437 

symptomatic, 437 
types of, special, 436 
in typhoid, 39 
in whooping-cough, 108 
Bronchorrhea, 421 
Brown mixture, 422 
Brown-Sequard's paralysis, 835 
Bryson's sign, 710 
Brudzinski's sign, 91 
Bruit d' arain in pneumothorax, 471 
de diable, 668 
de pot fele, 159 
Bubonic plague, 115 

Bulbar paralysis, apoplectiform, 811, 780 
asthenic, 810 
chronic, 808 

diagnosis of, 809 
etiology of, 808 
pathology of, 808 
prognosis of, 810 
symptoms of, 808 
treatment of, 810 
syringomyelia, 848 
Bundle of His, 320, 342 ■ 
Burr bath, in typhoid fever, 51 
Bursitis, syphilitic, 218 



Cachexia Henalis,_687 
lymphatica, 687 



INDEX 



985 



Cachexia, scorbutic, 695 
strumipriva, 714 
thyreopriva, 714 
Cacodylates, 671, 678 
Caffeine, 76, 376 
Caisson paralysis, 834 
Calcium lactate in hemorrhages, 189, 452 

salicylate, 537 
Calculus. See Gall-stones and Kidney 

calculus, etc. 
Calmette tuberculin test, 164 
Calomel, 225, 562, 637 
Caloric feeding, 53, 54 
Camphor, 77, 110, 412 
Camphor-chloral, 943 
Camphoric acid, 188 
Cancrum oris, 479 
Cannabis indica, 939 
Capsule, internal, localizing signs, 756 
Caput Medusae, 569 
Carbohydrates, physiology of, 725 
Carbolic acid. See Phenol. 
Carbuncle, differentiation of , 116, 117, 128 
Cardiac insufficiency of stomach, 531 

spasm, 492, 531 
Cardialgia, 532 
Cardiogmus, 337 
Cardiolysis, 390 
Cardiopalmus, 337 
Cardiospasm, esophagus, 492, 531 
Carlsbad water, 517 
Carphologia in typhoid fever, 33 
Cascara, 562 
Castor oil, 562 

Casts in pneumonia, bronchial, 66 
fibrin, 66, 423 
urinary, 620, 625, 629 
Cat's tongue, scarlatinal, 264 
Catarrhus sestivus, 412 
Catechu, 535 
Cathartics, 561 
Catheter, nasal, 52 
Cauda equina, lesions of, 825 
Cavity, signs of, 159 
Cecum, actinomycosis of, 194 

tuberculosis of, 176 
Cellulitis, differentiation of, 60 
Centrum ovale, localizing symptoms, 756 
Cercomonas, 247 
Cerebellar ataxia, 762 
Cerebellum, localizing symptoms of, 761 
Cerebral embolism, 775 

diagnosis of, 778 
differentiation of, 781 
etiology of, 775 
localization of, 777 
basilar, 778, 811 
cerebral, anterior, 778 

posterior, 778 
internal carotid, 778 
Sylvian artery, 777 
vertebral, 778 
pathology of, 775 
prognosis of, 778 
symptoms of, 776 
treatment of, 779 
hemorrhage, 765 
cerebellar, 733 



Cerebral hemorrhage, cortical, 733 
crus, 733 
diagnosis of, 772 
of coma, 722 
of hemiplegia, 773 
of location, 773 
differentiation, 633, 781, 783, 908 
etiology of, 765 
localizations of, 766 
medulla, 773, 811 
pathology of, 765 
pons, 773 
prognosis of, 773 
symptoms of chronic, 770 
hemiplegia, 769 
individual, 769 
insult, 768 
permanent, 768 
prodromes, 768 
reflexes, 770 
sensation, 770 
stroke, 768 
* treatment of chronic stage, 775 
of insult, 774 
of reaction, 775 
ventricular, 773 
localization, 749 

centrum ovale, 756 
cerebellum, 761 
cerebral peduncle, 759 
corpora quadrigemina, 758 
corpus striatum 758 
crus, 759 

frontal cortex, 754 
internal capsule, 756 
motor cortex, 749 
occipital cortex, 753 
optic thalamus, 758 
parietal cortex, 753 
pons, 760 

temporal cortex, 753 
thrombosis, 779 

diagnosis of, 781 
differentiation of, 781, 811 
etiology of, 779 
localization of, basilar, 780 
cerebral anterior, 780 

posterior, 780 
Sylvian artery, 780 
vertebral, 780 
pathology of, 779 
prognosis of, 782 
symptoms of, 779 
treatment of, 782 
Cerebrasthenia, 913 
Cerebrospinal fever, 89 

meningitis, epidemic, 89 
Cerium oxalate, 497 
Cervical adenitis, 169 

rib, 900 
Cervix, syphilis of, 217 
Cestodes, diseases caused by, 302 
Chalicosis of lungs, 440 
Chalk, 502, 535 
Chancre, 199 
Chancroid, 200 
Charcot-Leyden crystals, 429 
Charcot's disease, 854, 858 



986 



INDEX 



Cheese poisoning, 970 

Cheyne-Stokes's breathing, 92, 151, 631, 

772 
Chiasm, optic, 873 
Chicken-breast, 489 

rhachitic, 743 
Chicken-pox, 259 

complications of, 260 
diagnosis of, 260 
differentiation of, 254, 260 
etiology of, 259 
sequels of, 260 
symptoms of, 259 
Chills, treatment of, 242 
Chloral, 110, 136, 400, 638, 917, 932 
Chlorides, absence of, in pneumonic 

urine, 70 
Chloroform, 55, 62, 110, 188, 336, 422 
Chloroma, 686 
Chlorosis, 667 

complications of, 669 
course of, 669 
diagnosis of, 670 
differentiation of, 156, 670, 677 
etiology of, 667 
prognosis of, 669 
symptoms of, 667 
treatment of, 670 
Choked disk in brain tumor, 791, 796 
Cholangitis, catarrhal, 598 

differentiation of, 594, 595 
suppurative, 598 
Cholecystitis, 597 

differentiation of, 594, 595 
etiology of, 597 
following typhoid fever, 38 
prognosis of, 598 
symptoms of, 598 
treatment of, 598 
Cholecystotomy, 597 
Cholelithiasis. See Gall-stones, 591 
Cholemia, 566, 570, 589 
Cholera, Asiatic, 111 

bacteriology of, 111 
complications of, 112 
diagnosis of, 112 
dissemination of, 111 
prognosis of, 114 
symptoms ofj 112 
treatment of, 114 
infantum, 541 
nostras, 113 
Cholorine, 113 

Chondrodystrophia fetalis, 956 
Chorea, acute, 926 

course of, 929 
diagnosis of, 929 
etiology of, 927 
pathology of, 927 
prognosis of, 929 
symptoms of, 927 
treatment of, 931 
types of, 929 
in cerebral infantile paralysis, 789 
chronic, 930 
electric, 930 

endocarditis from, 348, 929 
habit, 930 



Chorea, Huntingdon's, 930 

posthemiplegic, 771, 789 

rheumatic, 285 
Choreiform affections, 926 
Choroidal tubercles, 150, 152 
Choroiditis, syphilitic, 215 
Chromaffin cells, 702 
Chvostek's sign, 717 
Chyle in urine, 314, 649 

vessels, disease of, 564, 649 
Chyliform ascites, 617 

pleurisy, 473 
Chylothorax, 473 
Chylous ascites, 617 
Chyluria, 649 

parasitic, 314 
Circulation, diseases of, 319 
Cirsomphalos, 569 
Claudication intermittente, 334, 397 
Climate in tuberculosis, 185 
Cocaine, 106, 411, 558 
Coccidia, 247 
Coccidioides, 196 
Coccygodynia, 942 
Codeine, 110, 420, 736 
Cod-liver oil, 188 
Colchicum, 741, 742 
Colectasia, 556 
Colic, biliary, 592 

, renal, 659 
Colica mucosa, 538 

etiology of, 538 
symptoms of, 538 
treatment of, 538 

pictonum, 965, 966 
Colitis, membranacea, 538 

mucosa, 538 
Collapse in diphtheria, 82 

in pneumonia, 69 

in typhoid fever, 28, 31, 38, 48 
Collar of brawn in scarlatina, 265 
Collargol, 23 
Colles's law, 221 
Colon bacillus. See Septic infections. 

dilatation of, 556 

prolapse of, 556 
Coloptosis, 556 
Coma, alcoholic, 772, 959 

apoplectic, 632, 772, 773, 776, 780, 
781 

diabetic, 729, 730 

epileptic, 921 

gas-poisoning, 975 

influenzal, 103 

opium, 772 

in pernicious malaria, 240 

uremic, 630, 631, 632, 772 

vigil in typhoid fever, 33 
Comma bacillus, 111 

Common bile duct, gall-stones in, 593, 606 
Concato's disease, 612 
Concretio pericardii, 389 
Conjugate deviation, 761, 769, 878 
Constipation, 558 

in colica mucosa, treatment of, 538 

etiology of, 558 

spastic, 561 

symptoms of, 559 



INDEX 



987 



Constipation, treatment of, cathartics, 
561 
diet, 560 
enemata, 561 
exercise, 561 
massage, 561 
Constitutio lymphatica, 719 
Constitutional diseases, 725 
Consumption, 152 
Contractures in apoplexy, 771 

hysterical, 909 
Conus medullaris, lesions of, 825 

stenosis, 207, 330 
Convulsions in brain tumor, 791, 795 
in cerebral embolism, 777, 781 
hemorrhage, 769, 781 
thrombosis, 781 
epileptic, 920, 923 
hysterical, 907, 923 
infantile, 926 

etiology of, 926 
symptoms of, 926 
treatment of, 926 
Jacksonian, 751, 752, 792, 795, 923 
in syphilis, 212 
in typhoid fever, 33 
in uremia, 630 
in whooping-cough, 108, 109 
Coproliths, 569 
Cor bovinum, 325, 352 

villosum, 382 
Cornea, syphilis of, 214 
Coronary disease, arteritis, 207, 330 
Corpora oryzoidea, 182 

quadrigemina, localizing symptoms, 
758 
Corpulence, 746, 747 
Corpus striatum, localizing symptoms, 

758 
Corrigan's disease, 351 
Corset liver, 584 

Cortex, cerebral, localization, 749 
Coryza, 411 

in diphtheria, 81 
in influenza, 104 
syphilitic, 222 
in typhoid fever, 39 
Cough, therapy of, 187 
Courvoisier's law, 593 
Cracked-pot resonance, 

cavities, 159 
Craniotabes, rhachitic, 743 
Cranium progenium, 721 . 
Crede's collargol, 23 

silver, 23 
Creolin, 61 
Creosote, 187, 425 
Crepitant rale, 68 

diseases where present, 68 
in pneumonia, 68 
Cretinism, 712 

diagnosis of, 713 
etiology of, 712 
symptoms of, 713 
Crie hydrencephalique, 91, 151 
Crises, tabetic, 854 
Croton oil, 270, 774 
Croton-chloral, 943 



in tuberculous 



Croup, differentiation of, 85 

diphtheritic, 81 

false, 415 

differentiation of, 85, 108, 415 
Crus, localizing symptoms, 759 
Cryptococcus, 196 
Crystals, Charcot-Leyden, 429 
Culex, 232, 289 
Cyanosis in heart disease, 368, 380 

with polycythemia, 691 

with splenomegaly, 691 
Cyclaster scarlatinalis, 261 
Cycloplegia, 877 
Cynanche gangrceneuse, 482 
Cysticercus, of brain, 302, 790, 796 

cellulosse, 304 
Cystitis differentiation of, 178, 653 

in typhoid fever, 40 
Cytodiagnosis, 460 

in lumbar puncture, 94 
Cytorrhyctes vacciniae, 256 

variola?, 248 



D 



Damoiseatj's curve in pleurisy, 456 
Dandy-fever, 289 
Deafness, 888 

cortical, 753, 754 
Death, sudden, 207, 371, 449, 464, 468, 

708, 718, 719 
Degeneratio renum poly cystica, 664 
De la Camp's sign, 170 
Delhi boil, 245 
Delirium cordis, 340, 367 

in fevers, treatment of, 57 
in pneumonia, 71 
tremens, diagnosis of, 961 
etiology of, 961 
prognosis of, 961 
symptoms of, 961 
treatment of, 962 
Dementia paralytica, 802 
diagnosis of, 806 
differentiation of, 807 
etiology of, 802 
pathogenesis of, 802 
pathology of, 802 
prognosis of, 807 
symptoms of, 804 
treatment of, 808 
paretic, 802 
senile, 807 
Dengue, 289 

complications of, 290 
diagnosis of, 290 
differentiation of, 290 
etiology of, 289 
prognosis of, 290 
sequels of, 290 
symptoms of, 290 
treatment of, 290 
Dercum's disease, 747 
Dermatitis, differentiation of, 60, 266 
Dermatomyositis, 949 
D'Espine's sign, 170 
Dextrocardia, 380 
Diabete bronze, 572, 732 



988 



INDEX 



Diabetes, bronzed, 572, 732 
coma from, 730 
decipiens, 728 
insipidus, 737 

cerebral syphilis, 212, 737 
diagnosis of, 737 
etiology of, 737 
prognosis of, 738 
symptoms of, 737 
treatment of, 738 
mellitus, 725 

cerebral syphilis, 212 
complications of, 730 
amaurosis, 731 
arteries, 731 
blood, 731 
coma, 730 
cystitis, 732 
dyspnea, 730 
heart, 731 
gangrene, 733 

of lungs, 731 
genital, 732 
infectious, 732 
intestines, 732 
liver, 732 
mental, 730 
neuralgia, 730 
neuritis, 730 
pregnancy, 732 
renal, 732 
retinitis, 731 
skin, 732 
stomach, 731 
tuberculosis of lungs, 731 
course of, 733 
diagnosis of, 733 
etiology of, 725 
physiology of, 725 
prognosis of, 733 
symptoms of, glycosuria, 727 
tests for, 727 
polydipsia, 729 
polyphagia, 729 
urine, acetone, 728 
albuminuria, 729 
ammonium, 729 
iS-oxybutyric acid, 729 
diacetic acid, 729 
pneumaturia, 729 
quantity, 728 
sugar, 727 
treatment, complications, 735 
diet, 733 
general, 735 
types, 736 
phosphatic, 650 
Diacetone, diabetic, 729 
Diaphragmatic hernia, 472, 550 
Diarrhea, 558 

in cholera Asiatica, 112 
in dysentery, 119, 121, 123 
etiology of, 540, 558 
infantile, 540 

cholera infantum, 541 
chronic dyspepsia, 542 
fermental, 540 
ileocolitis, 541 



Diarrhea, infantile, treatment of acute 
colitis, 543 
dyspepsia, 542 
enteritis, 543 
of cholera infantum, 543 
of chronic dyspepsia, 543 
dietetic/ 542 
nervous, 558 
in pneumonia, 69 
treatment of, 114, 123 
in typhoid fever, treatment of, 55 
Diazo reaction, in malaria, 237 
in measles, 273 
in pneumonia, 70 
in tuberculosis, 168 
in typhoid fever, 40 
Dibothriocephalus, 304 
Dicrotic pulse in typhoid fever, 30 
Diet in constipation, 560 
in diabetes, 733 
in gastric catarrh, 501 
in gastric dilatation, 508 
in gastric ulcer, 518 
in gout, 741 
Karen's, 372 
in obesity, 746 
in nephritis, 633 
in tuberculosis, 186 
in typhoid, 52 
Dietl's crisis, 644 
Dietrich's heart stenosis, 207, 330 
Digestive tract, diseases of, 477 
Digitalis, physiological action, 373 
preparations, 375 
therapeutics of, 76, 189, 269, 336, 375, 

376, 377 
toxicity, 374 
Diphtheria, 78 

bacteriology of, 78 
complications of, 82 
alimentary, 84 
glands, 84 
heart, 82 
nephritis, 83 
paralysis, 83 
respiratory, 84 
skin, 84, 82 
course of, 85 
diagnosis of, 85 

differentiation of, 85, 263, 415, 486 
dissemination of, 79 
etiology of, 78 

bacillus diphtheria), 78 
Klebs-Loeffler bacillus, 78 
laryngeal, 81 

localization of, special, 80 
ear, 82 
eye, 82 
genitalia, 82 
larynx, 81 
nose, 81 
skin, 82 
nasal, 81 
pathology, 79, 80 
pharyngeal, 80 
prognosis of, 85 
sequela? of, 82 
S} r mptoms of, 80 



INDEX 



989 



Diphtheria, symptoms of, classifications 
of, 80 
treatment of, 86 
general, 88 
local, 86 
prophylactic, 86 
serotherapy, 87 
symptomatic, 88 
types of, 78, 80 
catarrhal, 80 
chronic, 80 
general infection, 81 
latent, 80 
pharyngitic, 80 
septic, 81 
simple, 80 
tonsillitic, 80 
Diphtheritic croup, 81 
enteritis, 539 
ophthalmia, 82 
otitis, 82 

vulvovaginitis, 82 
Diphtheroid, 78 
Diplegia, in cerebral infantile paralysis, 

787 
Diplococcus intracellularis meningitidis, 

89 
Diplopia, 878 
Dipsomania, 959 
Disinfection, 49 

by formaldehyde, 258 
Distoma of kidney, 316 
of lung, 316 
pulmonale, 316, 317 
Distomiasis, 316 

Dittrich's mycotic plugs, 421, 424 
Diuretin, 377, 635 
Diver's paralysis, 834 
Dobell's solution, 411 
Doehle's bodies, 264 
Dover's powder. See Opium. 
Drachontiasis, 315 
Dracunculus medinensis, 315 
Dropsy. See Edema. 
Drug eruptions, 266, 272 
Driisenfieber, 298 
Dubini's disease, 930 
Duct. See Gall ducts. 
Ductless glands, diseases of, 701 
Ductus Botalli, patency, 379 
Duke's disease, 275 
Dumdum fever, 245 
Dunbar's serum, 413 

Duodenal ulcer. See Stomach ulcer, 509 
Duroziez's murmur, 355 
Dysacusis, 888 
Dysarthria, 754, 761 
Dysbasia intermittens, 397 
Dyschesia, 561 
Dysentery, 118 

classification of, 119 
amebic, 120 

complications of, 122 
etiology of, 120 
issues of, 122 
pathology of, 122 
symptoms of, 121 
treatment of, 123 



Dysentery, classification of, indeterminate 
types, 123 
catarrhal, 123 
croupous, 123 
gangrenous, 123 
parasitic, 123 
liver abscess in, 122, 576 
Shiga's bacillary, 119, 541 
diagnosis of, 120 
pathology of, 120 
prognosis of, 120 
symptoms of, 119 
treatment of, 123 
Dyspepsia, acute, 496 

in children, acute, 540 
chronic, 498 
intestinal, 534, 536 
nervosa, 527, 533 
Dysphagia, 491, 761, 890 
Dyspnea in heart disease, 368 

Kussmaul's, in diabetes, 730 
Dystrophy, muscular, 862 



S 



Ear, diphtheria of, 82 

syphilis of, 216 

tuberculosis of, 180 
Ebstein's cure, 746 
Echinococcus disease, 305 

of brain, 790 

of heart, 336 

of liver. See Liver, cysts of. 

of lungs, 306 

of pleura, 466 

renal, 666 
Eclampsia in contracted kidney, 630 

in kidney of pregnancy, 622 
Eczema, differentiation of, 60 
Edema, angioneurotic, 945 

cardiac, 370 

of glottis, 417 

in heart disease, 370 

hereditary, 946 

of larynx, 417 

of lungs, 450 

renal, 620, 626, 632, 636 

in scarlatina, 265 

in trichiniasis, 310 
Egophony, 69, 159, 458 
Ehrlich's diazo reaction, 40, 70, 168, 273 

side-chain theory, 87, 134 
Eiselsberg's sign, 509 
Elastic fibers, 154 
Elaterin, 636 
Elephantiasis, 315 
Embolism. See Aorta, etc. 

in sepsis, 20 
Emetin, 124 

Emphysema of lungs, 430 
Empyema, 460, 468 

necessitatis, 461 

pneumococcic, 70, 460 

pulsans, 460 

streptococcic, 460 
Encephalitis, 797 

acute hemorrhagic, 798 



990 



INDEX 



Encephalitis, acute, ophthalmoplegic, 798 
in aged, 782 
etiology of, 797 
in influenza, 103 
pathology of, 797, 798 
poliencephalitis, 798 
inferior, 798 
superior, 798 
poliencephalomyelitis, 798 
prognosis of, 798 
suppurative, 799 
symptoms, 798 
syphilitic, 211 
treatment of, 799 
Encephalomalacia, atheromatous, 779 
embolic, 775 
syphilitic, 211, 840 
Encephalomyelitis, disseminated, 841 
Encephalopathia, saturnina, 967 
Endarteritis deformans, 392 

syphilitic, 208 
Endocarditis, 343 
acute, 344 

benign, 348 

diagnosis of, 46, 47, 349 
etiology of, 263, 283, 348 
localization of, 349 
pathology of, 348 
prognosis of, 349 
symptoms of, 349 
treatment of, 349 
malignant, 344 

bacteriology, 347 
diagnosis of, 21, 46, 47, 347 
etiology of, 344 
pathology of, 344 
prognosis of, 348 

septic, 346 
symptoms of, 345 
treatment of, 349 
types of, 345 
typhoidal, 345 
verrucose, 348 
visceral, 346 
chorea, relations of, 248, 927, 928, 929 
chronic, 350. See Aortic insuffi- 
ciency, etc. 
etiology of, 350 
pathology of, 350 
prognosis of, 370 
symptoms of, 351, 366 
treatment of, 371 
differentiation of, 46, 47, 283, 286, 386 
pneumococcic, 70 
rheumatic, 283, 286 
scarlatinal, 263 
syphilitic, 207 
tuberculous, 160, 181 
Endocardium, diseases of, :>43 
Enemata, nutrient, 516 

oil, 561 
English sweats, 299 
Enstrongylus, 316 
Entameba dysenteriae, L20, 121 
I Interalgia, 563 
Enterij i-. acl inomycotic/ 194 
acute, 534 

diagnosis of, 45, 535 



Enteritis, acute, etiology of, 534 
pathology of, 534 
symptoms of, 534 
treatment of, 535 
chronic, 536 

pathology of, 536 
prognosis of, 537 
symptoms of, 536 
treatment of, 537 
croupous, 539 
diphtheritic, 539 
mucous, 538 
phlegmonous, 539 
Enterocolitis, 535 
Enterodynia, 563 
Enterokinase, 536 
Enteroliths, 552 
Enteroptosis, 555 
etiology of, 555 
symptoms of, 556 
treatment of, 557 
Enterospasm, 563 
Enterostenosis, 551 
Eosinophilia, 310, 313, 581 
Ephemeral fever, 298 
Epididymitis in mumps, 280 

in tuberculosis, 179 
Epilepsy, 919 

in cerebral infantile paralysis, 787, 

789 
convulsions in cerebral syphilis, 211, 

213 
course of, 923 
diagnosis of, 922 
differentiation of, 923, 630, 795 
etiology of, 919 

Jacksonian, 751, 752, 792, 795, 923 
pathology of, 919 
prognosis of, 923 
symptoms of, 919 
syphilitic, 211, 213 
treatment of, 924 
types of, 921 
Epileptiform attacks in paretic dementia, 

805 
Epinephrin, 702 
Epistaxis, etiology of, 414 
treatment of, 414 
in typhoid fever, 39, 57 
Erb-Goldflam syndrome, 810 
Erb's sign, 716 
Ergot, therapeutics of, 57 
Ergotism, 970 
Eructations, gastric, 531 
Erysipelas, 58 

bacteriology of, 58 
complications of, 59 
circulatory, 59 
genito-urinary, 60 
nervous, 59 
respiratory, 59 
septic, 60 
course of, 59 
as curative agent, 62 
diagnosis of, 60 
differentiation of, 60, 61 
etiology of, 58 

streptococcus erysipelatis, 



INDEX 



Goitre, exophthalmic, symptoms of, 
constitutional, 711 
exophthalmos, 709 
goitre, 710 
tachycardia, 709 
tremor, 710 
treatment of, 711 
general, 711 
medicinal, 711 
organotherapy, 712 
thyroidectomy, 712 
Gonococcus. See Septic infections, 21 

localizations, 137, 347 
Gonorrheal infection, 137 
arthritis, 137 

classification, 138 
course, 138 
pathology, 138 
symptoms, 138 
treatment, 138 
regional, 137 
septicopyemia, 137 
Gout, 738 

acute, symptoms of, 739 

treatment of, 741 
chronic, 742 

symptoms of, 739 
complications of, 740 
diagnosis of, 740 
etiology of, 738 
pathology of, 739 
prognosis of, 741 
Grafe's, von, sign, 710 
Grain poisoning, 970 
Grancher's sign, 170 
Grape-sugar for hemorrhage, 56 
Graphospasmus, 932 
Graves's disease, 709 
Greene's sign in pleurisy, 455 
Grindelia, 430 
Grippe. See Influenza, 102 
Grocco's sign in pleurisy, 456 
Ground-itch, 311, 312 " 
Guaiac, 484, 487 
Guaiacol, 188, 955 
Guinea-worm disease, 315 
Gumma. See Syphilis. 
Gums, tuberculosis of, 175 
Gutta cadens, 471 



H 



Habitus enteroptoticus, 556 

"Half-moon" space, 456, 470 

Hanford's tender toes in typhoid fever, 

32, 34 
Hanot's disease, 573 
Hay fever, 412 

etiology of, 412 
symptoms of, 412 
treatment of, 412 
Haygarth's nodosities, 952 
Head, actinomycosis of, 193 
Seadache, in brain tumor, 791 . 795 
difM^tiation of, 938 

reaument of, 57 
^90, 91, 95 



Headache, migraine, 937 
sick, 937 

in typhoid fever, 33 
Head's maximal points, 942, 940] 
Hearing, centre for, 753 
Heart. See also MyocardiumJ 
dium. 
aneurysm of, 330 
arrhythmia, 339 
arteriosclerosis of, 207, 208," 
atrophy of, 327 
block, 320, 342 
bovine, 325, 352 
bundle of His, 320, 342 
dilatation of, 320 

diagnosis of, 322, 668 
differentiation of, 322, 387, 389 
etiology of, 320 
pathology of, 321 
prognosis of, 323 
signs of auricular dilatation, 322 
of left ventricle dilatation, 

321, 396 

of right ventricle dilatation, 

322, 432 
symptoms of, 322 
treatment of, 323 
in typhoid fever, 30 

disease cells, 368 
congenital, 378 

aortic atresia, 380 
dextrocardia, 380 
interauricular defects, 379 
interventricular defects, 379 
patent ductus Botalli, 379 
persistent isthmus aortas, 

379 
prognosis of, 381 
pulmonary stenosis, 378 
symptoms of, general, 380 
transposition of vessels, 380 
treatment of, 381 
tricuspid stenosis, 380 
valvular anomalies, 380 
valvular, combined lesions, 365 
diagnosis of, 365 
prognosis of, 370 
course of, 370 
prognosis of, 370 
signs of. See Individual 

lesions, 
symptoms of, 366 
cardiac, 367 
constitutional, 366 
edema, 370 
embolism, 370 
gastro-intestinal, 369 
joints, 370 
kidney, 369, 639 
liver, 369, 585 
nervous, 367 
respiratory, 368 
spleen, 369 
treatment of, 371 

cardiants, 373, 375 
\ «**- ited lesiri 






INDEX 



lisease, valvular, treatment of, 
exercise, 372 
hygiene, 372 
Oertel method, 323 
purgative, 372 
rest, 372 

Schott method, 323 
symptomatic, 376 
uncompensated lesions, 

372 
venesection. 372 
fess, 322 
JHTbolism, 345 
'failure, diphtheritic, 82 
fatty, 327 

diagnosis of, 328 
etiology of, 327 
pathology of, 327 
prognosis of, 328 
signs of, 328 
symptoms of, 328 
treatment of, 328 
fragmentation of, 82 
functional tests, 323 
gallop-rhythm, 321 
hypertrophy of, 324 
diagnosis of, 326 
etiology of, 324 

in interstitial nephritis, 396, 629 
pathology of, 325 
prognosis of, 326 
signs of left ventricle hyper- 
trophy, 325, 396 
of right ventricle hyper- 
trophy, 326, 358, 432 
symptoms of, 325 
treatment of, 327 
intermittence of, 339 
irritable, 337 

murmurs, anemic diastolic, 347, 355, 
668, 674 
Flint's, 354 

functional diastolic, 347, 355, 
668, 674 
systolic, 347, 357, 359, 363, 
668, 674 
neuroses of, 337 
palpitation of, 337 
diagnosis of, 338 
etiology of, 337 
signs of, 338 
symptoms of, 337 
treatment of, 338 
pang, 333 
parasites of, 336 
physiology, 319 

retraction of apex of, 389 
rupture of, 330, 332 
diagnosis of, 333 
etiology of, 332 
pathology of, 332 
symptoms of, 332 
treatment of, 333 
sino-auricular node, 319 
■izc of, 322 
fcyphilis of. 207 
[{ hrombosis^LJ337 



Heart, tumors of, 336 
Heat exhaustion, 976, 977 
Heberden's nodes, 953 
Hematemesis, diagnosis of, 527 

differentiation of, hemoptysis, 452 

etiology of, 526 

in gastric cancer, 517, 521 
ulcer, 512, 515, 517 

in pneumonia, 71 

in portal cirrhosis, 570 

symptoms of, 527 
, treatment of, 518 
Hematomyelia, 829, 833 
Hematoporphyrinuria, 651 
Hematorrhachis, 829 
Hematuria, 647 

angioneurotic, 647 

diagnosis of, 647 

endemic, 316 

etiology of, 647 

renal stone causing, 659, 660 
tumor causing, 662 

symptoms of, 647 

treatment of, 648 

tuberculosis causing, 178 
Hemianesthesia, hysterical, 906 

lesions in, crus, 760, 778 

internal capsule, 757, 770, 771 
optic thalamus, 758 
pons, 760 
spine, 835, 836 
Hemianopsia, 753, 757, 758, 760, 770, 

778, 874, 875 
Hemiathetosis, 758, 772, 789 
Hemiatrophy, facial, 882 
Hemichorea, 758, 771, 789 
Hemichromatopsia, 753, 874 
Hemicrania, 937 
Hemifacial atrophy, 882 

hypertrophy, 882 
Hemi hypertrophy, facial, 882 
Hemiopia. See Hemianopsia. 
Hemiplegia in aged, 782 

alternating, 759, 760, 811 

in apoplexy, 768, 769, 770, 773, 7S1 

cerebral, 757, 793 

collateral, 77 r ' 

cortical, 750 

in crus, 759 

in diphtheria, 84 

double, 760, 761, 787, 811 

embolism, 777, 781 

etiology of, 773, 781 

hysterical, 908 

infantile paralysis, 786 

internal capsule lesion in, 757, 758 

in meningitis, 92 

in pachymeningitis, 815 

in pleurisy, 468 

in pons, 760 

spinal, 831, 835 

thrombosis, 780, 781 

in typhoid, 34 

uremic, 630-633, 772 
Hemochromatosis, 572, 732, 704 
Hemoglobinuria, 648 

epidemic, 648, 694 
iology of, 648 



INDEX 



995' 



j oglobinuria in malaria, 240 

in nephritis, 619, 622, 648 

paroxysmal, 648 

symptoms of, 648 

syphilitic, 207 

treatment of, 649 
Hemopericardium, 392 

differentiation of, 387 
Hemophilia, 698 

diagnosis of, 699 

etiology of, 698 

prognosis of, 699 

renal, 647, 698 

symptoms of, 698 

treatment of, 699 
Hemoptoe. See Hemoptysis. 
Hemoptysis, 154, 450 

aneurysm causing, 406 

bronchiectasis causing, 423 

cause of tuberculosis, 154 

differentiation of, 452 

endemic, 317 

etiology, 423, 451 

forms of, 154, 155 

frequency of, 154, 451 

in heart disease, 368 

prognosis, 452 

symptoms of, 154, 451 

treatment of, 188, 452 

in tuberculosis, 154 
Hemorrhagic diseases, 692 

classification of, 692 
hemophilia, 698 
infantile scurvy, 697 
of newborn, 694 
purpura, 692 
scurvy, 695 
Hemorrhoids, 557 
Hemothorax, 473 
Henoch's purpura, 694 
Hepar adiposum, 582 

migrans, 584 

mobile, 584 
Hepatargia, 566, 570, 589 
Hepatic fever, intermittent, 571, 593 

insufficiency, 566, • K ' 7r >. 589 

vein cirrhosis of 567 ■ 

vessels, diseases t _/86, 588 
Hernia, diaphragmatic, 472, 550 
differentiation of, 472 

external, 550 

internal, 550 

of linea alba, 515 
Heroine, 377, 415, 420, 422 
Herpes in malaria, 47, 236 

in meningitis, 47, 93 

in pneumonia, 69 

in tuberculosis, 47 

in typhoid fever, 30 

zoster, 881, 901, 942 
Herpetic fever, 298 
Herxheimer reaction, 201 
Hexamethylenamina, 57, 101, 102 
Hiccough, 897 
Hippocratic facies, 38, 608 

fingers, 168, 425, 574 

ligature, 452 

succussion, 471 



Hirschsprung's disease, 556 
His's bundle, 320, 342 
Hodgkin's disease, 687 
Hormones, 701 
Hormonol, 563 
Horseshoe kidney, 643 
Hour-glass stomach, 508 
Hunger, disturbance of sense of, 533 
Huntingdon's chorea, 930 
Hutchinson's facies, 879 
mask, 852 
teeth, 223 
triad, 214, 222, 223 
Hydatid cysts. See Liver, cysts of. 

thrill, 580 
Hydatids, 305 

Hydrargyri chloridum mite, 224, 225 
corrosivi, 225, 226 
iodidum, 225, 487 
massa, 225, 376 
tannicum, 225 
unguentum, 225, 226 
Hydrarthrosis, intermittens, 946 
Hydrencephalic state, 541, 763 
Hydrencephaloid, 541, 763 
Hydrobilirubin, test for, in stools, 537 
Hydrocephalus, acute, 811 
chronic, acquired, 813 

diagnosis of, 813 
etiology of, 813 
symptoms of, 813 
treatment of, 813 
congenital, 812 
course of, 813 
etiology of, 812 
pathology of, 812 
symptoms of, 812 
Hydrochinon in urine, 651 
Hydrochloric acid, action of, 502 

tests for, in stomach, 499 
Hydrocyanic acid, 497 
Hydrogen peroxide, 80, 125, 538 
Hydromyelus, 846 
Hydronephrosis, 655 
diagnosis of, 656 

differentiation of, 656, 657, 663, 665 
etiology of, 655 
pathology of, 655 
prognosis of, 657 
symptoms of, 656 
treatment of, 657 
Hydropericardium, 391 

differentiation of, 387 
Hydroperitoneum, 613 
Hydrophobia, 294 
course of, 296 
diagnosis of, 296 
differentiation of, 296 
etiology of, 295 
incubation in, 295 
pathology of, 296 
prognosis of, 296 
stages of, 295 
symptoms of, 295 
treatment of, 296 
inoculation, 296 
late, 297 
primary wound, 297 



996 



INDEX 



s 



Hydrophobia, treatment of, prophylactic, 

296 
Hydrops articulorum intermittens, 946 

pericardii, 391 

renum cysticus, 664 
Hydrotherapy in typhoid fever, 51 
Hydrothorax, 472 4 

diagnosis of, 473 

differentiation of, from pleurisy, 465 

etiology of, 472 

symptoms of, 473 
Hymenolepis, 305 
Hyoscine, 57 

Hyoscyanius, 377, 430, 562 
Hyperaciditas hydrochlorica, 528 
Hyperacusis, 885, 888 
Hyperchlorhydria, diagnosis of, 528 

differentiation of, 517, 528 

etiology of, 528 

in gastric ulcer, 513 

prognosis of, 528 

symptoms of, 528 

treatment of, 516, 529 
Hyperesthesia of stomach, 532 
Hyperdiamorrhysis, 764 
Hyperglycemia, 725, 727 
Hyperkinesis cordis, 337 

gastric, 531 
Hypernephroma, 663 
Hyperorexia, 533 
Hyperosmia, 873 
Hyperostosis cranii, 722 
Hyperpituitarism, 720 
Hypersecretion, gastric, 529 
Hypersusceptibility, 88 
Hyperthyroidism, 709 
Hypertrophy, hemifacial, 882 
Hypnotism, 911 
Hypochlorhydria, 530 
Hypochondriasis, 807, 916 
Hypodermatoclysis, 77, 637 
Hypophysis, diseases of, 719 
Hypopituitarism, 720 
. Hyposecretion, gastric, 530 
Hysteria, 905 

course of, 910 

diagnosis of, 911 

differentiation of, 109, 296, 840, 846, 
908 

etiology of, 905 

prognosis of, 910 

symptoms of, 905 

treatment of, 911 



Icing liver, 369, 612, 616 
Icterus, 588 

acute catarrhal, etiology of, 598 
prognosis of, 598 
symptoms of, 598 
treatment of, 598 
febrile, '299 
in cancer of liver, 579 
in cirrhosis of liver, 571, 573, 587 
diagnosis of, 587, 590 
differentiation of, 587, 590 



Icterus, epidemic, 299 
etiology of, 588 
family icterus, 590 
gravis, 566 
in heart disease, 369 
hematogenous, 588 
ictero-anemia, 590 
malarial, 240 
neonatorum, 589 
pneumonic, 71 
prognosis of, 591 
symptoms of, 589 
syphilitic, 205, 207 
treatment of, 591 
in typhoid fever, 38 
urobilin, 369, 588, 590 
in yellow fever, 293 
Ichthyotoxismus, 970 
Idiocy, amaurotic family, 866 
Ileocolitis in children, acute, 541 

dysenteric, 541 
Ileus, dynamic, 552 
hysterical, 552 
Illuminating-gas poisoning, 974 
Incoordination. See Ataxia. 
Indicanuria, 651 
Infantile convulsions, 926 
diarrhea, 540 
paralysis, cerebral, 786 

diplegic form, 787 
hemiplegic form, 786 
Infantilism, 722 
Infarcts. See Kidney, etc. 
Influenza, 102 

bacteriology of, 102 
diagnosis of, 105 
differentiation of, 105 
etiology of, 102 
prognosis of, 106 
symptoms of, 103 
alimentary, 105 
circulatory, 105 
classification of, 103 
duration of, 103 
fever, 103 
genito-urinary, 105 
joint, 105 
muscle, 105 
nervous, 103 
respiratory, 104 
skin, 105 
types of, 102, 103 
treatment of, 106 
varieties of, 102, 103 
Infusions, saline, 77 
Insane, paralysis of, 802 
Insolation, 975 

Intermittent limping, 334, 397 
Internal capsule, localizing symptoms, 756 
Intestinal dyspepsia, 534, 536 

obstruction, 548 
Intestines, actinomycosis of, 194 
amyloidosis of, 168, 204 
anthrax of, 129 
arteriosclerosis of, 398 
cancer of, 553 

complications of, 554 
diagnosis of, 554 



: 



INDEX 



997 



Intestines, cancer of, differentiation of, 
555 
etiology of, 553 
pathology of, 553 
symptoms of, 554 
treatment of, 555 
congestion of, 369 
diseases of, 534 
diverticula, 563 
foreign bodies in, forms of, 551, 552, 

559 
hemorrhage of, 557 
diagnosis of, 557 
etiology of, 557 
symptoms of, 557 
treatment of, 557 
in typhoid, 36, 55 
inflammation of, 534, 536, 538, 

539 
neuroses of, 563 

obstruction of, diagnosis of, 552 
differentiation of, 552, 602 
dynamic, 552 
foreign bodies, 551 
gall-stones causing, 551, 552, 

596 
intussusception, 548 
invagination, 548 
knots, 550 
strangulation, 549 
stricture, 551 
treatment of, 553 
tumors, 553 
twists, 550 
volvulus, 550 
perforation of, typhoid, 37, 56 
syphilis of, 204 
typhoid fever, hemorrhage, 36 

perforation, 37, 56 
tuberculosis of, 167, 176 
tumors of; benign, 555 
cancer of, 553 
sarcoma of, 555 
ulceration of, 539 

dysenteric, 120, 122, 123 
syphilitic, 204 
in tuberculosis, 167, 176 
in typhoid, 35 
uremic, 631 
Intoxications, 17, 959 
Intubation in diphtheria, 89 
Intussusception of bowel, 548 
etiology of, 548 
issues of, 549 
pathology of, 548 
symptoms, 549 
varieties of, 548 
'.odides. See Potas. iodide. 
Iodine, 54, 484 
■odoform, 61 
pecac, 124, 420 
jidoplegia, 877 
iritis, syphilitic, 214 
ron, therapeutics of, 62, 86, 338, 377, 

635, 670, 671 
schialgia, 903 

sthmus aortae, persistent, 379 
tching, treatment of, 599 



Jaboulay's sign in hour-glass stomach, 
509 ' 

Jacksonian convulsions. See Epilepsv. 

Jalap, 636 

Jaundice. See Icterus. 

Jellinek's sign, 710 

Joffroy's sign, 710 

Joints, diseases of, 951 

rheumatic, 281 

syphilis of, 217, 218 

tuberculosis of, 181, 182 
Jungle fever, 240 
Justus's test in syphilis, 209 



Kahler's disease, 646 
Kakke, 972 
Kala azar, 245 
KarelTs diet, 372 
Keratitis, syphilitic, 214, 223 
Kernig's sign, 91 
Ketonuria, 728 
Kidneys, absent, 642 

amyloid degeneration of, 639 

differentiation of, 640, 641 
etiology of, 639 
pathology of, 639 
symptoms of, 642 
syphilitic, 207 
tuberculous, 168 
anomalies of secretion, 644 

of structure, 642 
arteriosclerosis of, 397, 627 
ascending infection of, 652 
calculus of, 657 

chemistry of, 658 
complications of, 660 
diagnosis of, 660 
differentiation of, 660 
etiology of, 657 
pathology of, 658 
prognosis of, 660 
symptoms of, 658 
treatment of, 660 
cancer, complications of, 662 
diagnosis of, 662 
differentiation of, 663 
etiology of, 661 
pathology of, 661 
prognosis of, 662 
symptoms of, 661 
treatment of, 664 
congestion of, passive, 369, 638 
diagnosis of, 639 
differentiation of, 640, 641 
etiology of, 638 
pathology of, 638 
symptoms of, 639 
contracted, arteriosclerotic, 627 
ascending, 653 
embolic, 639 
primary, 627, 640, 641 
secondary, 625, 640, 641, 653 
cystic, 664 



998 



INDEX 



Kidneys, cystic, diagnosis of, 665 

etiology of, 664 

pathology of, 664 

symptoms of, 664 

treatment of, 665 
degeneration of, cystic, 664 
diseases of, 619 
dislocation of, acquired, 643 

congenital, 643 
distoma of, 316 
echinococcus of, complications of, 666 

symptoms of, 665 

treatment of, 666 
embolism of, 370, 639 
enstrongylus of, 316 
floating, 643 
functional tests, 635 
horseshoe, 643 
hypernephroma, 663 
infarction of, 370, 639 
large, red, 624 

variegated, 624 

white, 624 
malformations of, 642 
movable, 643 

complications of, 644 

diagnosis of, 644 

etiology of, 643 

prognosis of, 644 

symptoms of, 643 

treatment of, 644 
of pregnancy, eclampsia in, 622 
rudimentary, 642 
sarcoma of, 663 
stone of, 657 
supernumerary, 643 
"surgical," 654 
syphilis of, 207 
tuberculosis of, 177 
tumors of, 661 
Klebs-Lceffler bacillus, 78 
Kopftetanus, 135 
Koplik's spots, 271 
Korsakow's psychosis, 871 
Kreatotoxismus, 969 
KussmauPs breathing, 730 
Kyphosis, rhachitic, 743 



Labioglossopharyngeal paralysis, 808 
Labyrinth, inflammation of, 95 
Lachrymal glands, symmetrical hyper- 
trophy of, 482, 691 
Lactic acid in gastric cancer, 522 
Lactosuria, 726 

La Grippe. See Influenza, 102 
Landry's paralysis, 842 
Lane's kink, 559 
Langerhans's islands, 725 
insufficiency, 725 
Laryngismus stridulus, 108, 415, 716, 892 
Laryngitis, acute catarrhal, 414 

diagnosis of, 415 

etiology of, 414 

symptoms of, 415 

treatment of, 415 



Laryngitis, acute, in children, 415 
fibrinous, 416 
nodose, 416 
submucous, 416 
suppurative, 416 
chronic catarrhal, 416 

etiology of, 416 
symptoms of, 416 
treatment of, 416 
hypertrophic, 417 
pachydermia, 416 
tuberosa, 416 
diphtheritic, 81 
rheumatic, 484 
stridulous, 108, 415, 716, 892 
syphilitic, 209, 180 
Larynx, diseases of, 414 
edema of, 417 
erysipelas of, 60 
paralysis of, 404, 891-893 
perichondritis of, 39, 417 
symptoms of, 417 
treatment of, 418 
spasm of, 716, 892 
stenosis of, 415, 416, 418 
syphilis of, 180, 209 
tuberculosis of, 180 
tumors of, 418 
typhoid, 39 
ulcerations of, 418 
Lasegue's sign, 282, 903 
Lathyrism, 971 
Lead, acetate, 55, 416, 741 

colic, differentiation of, 966, 807 
poisoning, acute, 965, 966 
chronic, 965, 966, 871 
Leishmaniasis, 245 
Leontiasis ossea, 722 
Leprosy, 190 

bacteriology of, 190 
course of, 192 
diagnosis of, 192 
differentiation of, 849 
distribution of, 190« 
pathology of, 191 
prognosis of, 192 
symptoms of, 191 
treatment of, 192 
Leptomeningitis. See Meningitis. 
Leukanemia, 686 
Leukemia, 680 

classification of, 680 
lymphatic, acute, 680 

diagnosis of, 681 
symptoms of, 681 
chronic, 682 

course of, 683 
diagnosis of, 683 
symptoms, iSS'2 
myeloid, 683 

complications of, 685 
diagnosis of, 685 
differentiation of, 686 
prognosis of, 686 
symptoms of, 683 
treatment of, 687 
Leukocythemia, 680 
Leukocytosis in pneumonia, 69 



: 



- 



i 



INDEX 



999 



Leukocytosis, v. s. Leukemia. 

in sepsis, 19 
Leukoderma, 202 
Leukopenia in typhoid fever, 32 
Leukoplakia, syphilitic, 203 

of tongue, 480 
Levulose, 736 

Leyden-Curschmann spirals, 429 
Licorice. See Glycyrrhiza. 
Lien mobile, 706 
Lientery, 535, 606 
Life assurance, syphilis and, 221 
Linitis plastica, 509 
Lips, tuberculosis of, 175 
Lipuria, 650 
Liquor antisepticus, 52 
Lithuria, 650 
Litten's sign in pneumonia, 68 

in pleurisy, 455 
Little's disease, 788, 789 
Liver, abscess of, 575 
amebic, 576 

diagnosis of, 577 
differentiation of, 46, 47, 206, 

547, 578, 587 
pathology of, 576 
symptoms of, hepatic, 576 
icterus, 577 
rupture, 577 
septic, 576 
treatment of, 578 
cholangitic, 576 
differentiation of, 206, 465, 577, 

578, 580, 587 
dysenteric, 122, 575 
etiology of, 575 
pylephlebitic, 575 
septic, 575 
solitary, 575, 576 
tropical, 575, 576 
in typhoid fever, 38 
varieties of, 575 
actinomycosis of, 195 
amyloid, 168, 204, 583 
diagnosis of, 583 
differentiation of, 587 
etiology of, 168, 583 
pathology of, 583 
symptoms of, 583 
anomalies of, 584 
atrophy of, acute yellow, 565 
course of, 566 
diagnosis of, 566 
differentiation of, 566, 

587 
etiology of, 565 
pathology of, 565 
symptoms of, 565 
treatment of, 567 
cancer of, 578 

diagnosis of, 580 
differentiation of, 206, 580, 587 
primary, 578, 580 
secondary, 578, 580 
symptoms of, ascites, 579 
cachexia, 579 
icterus, 579 
liver, 578 



Liver, cancer of, treatment, 578 
cirrhosis of, 567 
alcoholic, 567 
atrophic, 567 
biliary, 573 

diagnosis of, 574 
differentiation of, 574, 587 
etiology of, 573 
symptoms of, 573 
digestive, 573 
icterus, 573 
liver, 573 
nutrition, 574 
spleen, 573 
urine, 574 
treatment of, 575 
capsular, 567 

cardio tuberculosa, 167, 177 
classification of, 567 
Glissonian, 567 
Hanot's, 573, 567 
hepatic vein, 567 
in heart disease, 367 
Laennec's, 567 
malarial, 237 
mixed, 567 
Pick's pseudo cirrhosis, 571, 611, 

616 
pigmentary, 572 
portal, 567 

classification of, 567 
complications of, 570 
cardiac, 570 
febrile, 571 
hematemesis, 570 
hemorrhages, 570 
icterus, 571 
nephritis, 570 
peritonitis, 570 
pulmonary, 570 
course of, 571 
diagnosis of, 571 
differentiation of, 571, 572, 

574, 587, 616, 637 
etiology of, 567 
pathology of, 567, 574 
prognosis of, 571 
symptoms of, 568 
general, 568 
liver, 568 
treatment of, medical, 572 
surgical, 573 
tuberculous, 167, 177 
congestion of, arterial, 585 
passive, 367, 585 

differentiation of, 585, 587 
etiology of, 585 
pathology of, 585 
symptoms of, 367, 585 
corset, 584 
cysts of, echinococcus, 580 

complications of, 5S1 
diagnosis of, 581 
differentiation of, 581, 587 
multilocular, 307 
prognosis of, 581 
rupture of, 581 
symptoms of, 580 



1000 



INDEX 



Liver, cysts of, echinococcus, treatment 
of, 582 
unilocular, 580 
hydatid, differentiation of, 581, 

587 
non-parasitic, 581 
diseases of, 565 

differential table of, 587 
echinococcus, 580 
enlargement of, differentiation of, 

from pleurisy, 581 
fatty, 582 

differentiation of, 587 
etiology of, 582 
pathology of, 582 
symptoms of, 582 
floating, 584 
flukes, 317 
gumma of, 206 
icing liver, 612, 616, 571 
insufficiency, 566, 570 
large, causes of, 571 
lobulated, 206 

nut-meg, in heart disease, 367 
perihepatitis, 369 
sarcoma of, 578 
small, causes of, 572 
syphilis of, 205 

differentiation of, 206, 587 
gummatous, 206 
interstitial, 205 
tuberculosis of, 167, 177 
tumors of, 578 
wandering, 584 
zuckerguss, 612, 616, 571 
Lobelia, 430 
Lock-jaw, 133 
Locomotor ataxia, 849 

system, diseases of, 949 
Lceffler's solution, 86 
Ludwig's angina, 84, 482 
Lues venerea, 197 
Luetin, 219 
Lumbago, 950 
Lumbar puncture, 57, 93, 94, 637 

and injections, 95 
Lumpy- jaw, 194 
Lungs, abscess of, 442 

bacteriology of, 442 
diagnosis of, 443 
differentiation of, 443 
etiology of, 442 
pathology of, 442 
pneumonic, 71 
prognosis of, 443 
symptoms of, 443 
treatment of, 443 
in typhoid fever, 39 
actinomycosis of, 195 
anthracosis of, 440 
anthrax of, 130 
arteriosclerosis of, 398 
atelectasis of, 441 
acquired, 441 

etiology of, 441 
pathology of, 441 ; 
symptoms of, 441 
treatment of, 441 



Lungs, atelectasis of, congenital, 441 
etiology of, 441 
pathology of, 441 
symptoms of, 441 
treatment of, 441 
calculi of, 427 
cavities of, differentiation of, 472 

signs of, 159 
chalicosis of, 440 
circulatory affections of, 448 
cirrhosis of, 438, 464 
congestion of, active, 448 

passive, 368, 448 

treatment of, 449 

in typhoid fever, 39 
diseases of, 430 
echinococcus of, 306 
edema of, 450 

etiology of, 450 

in heart disease, 368 

pathology of, 450 

symptoms of, 450 

treatment of, 450 
embolism of. See Infarct of. 
emphysema of, 430 

diagnosis of, 433 

differentiation of, 433 

etiology of, 431 

interstitial, 433 

pathogenesis of, 431 

pathology of, 431 

prognosis of, 433 

symptoms of, 431 

treatment of, 433 
erysipelas of, 60 
fever, 62 
flukes, 317 
gangrene of, bacteriology of, 444 

complications of, 445 

course of, 446 

diagnosis of, 446 

differentiation of, 446 

etiology of, 444 

pathology of, 444 

physical signs of, 445 

pneumonic, 71 

prognosis of, 446 

symptoms of, 445 

treatment of, 446 

in typhoid fever, 39 
hemoptysis, 450 
hemorrhage of, 154, 450 
hypertrophy of, 433 ■ 
hypostasis of, 39, 57, 448, 449 
induration of, 162, 438, 464 

brown, 368, 448 

pneumonic, 71 
infarct of, 449 

diagnosis of, 73, 449 • 

etiology of, 449 

pathology of, 449 

symptoms of, 449 

in typhoid, 39 
interlobar fissures of, 463 
parasites of, 316 

distoma, 316, 317 

echinococcus, 306 
pneumokoniosis, 440 



INDEX 



1001 



Lungs, senile, 433 
siderosis of, 440 
stones, 427 
syphilis of, q. v. 
tuberculosis of, q. v. 
tumors of, 446 
cancer, 446 

etiology of, 446 
physical signs of, 447 
symptoms of, 447 
differentiation of, 407, 465 
lymphosarcoma, 448 
sarcoma, 448 
Lupus, 183 
Lymphadenitis, anthracosis, 440 

glands, tuberculosis of, 169, 109, 689 
Pfeiffer's, 298 
Lymphangitis, differentiation of, 60 
Lymphatism, 719 
Lymphemia, acute, 680 

chronic, 682 
Lymphoma, malignant, 687 
Lymphosarcomatosis, 690 
Lyssa, 298 



M 



Magnesium carbonate, 502, 518 
oxide, 501 
sulphate, 137, 636 
Maidism, 971 
Maladie de Roger, 379 

de Woillez, 448 
Malaria, 229 

cachexia of, 238 

chronic, 238 

diagnosis of, 240 

differentiation of, 46, 47, 239, 240, 

241 
etiology of, 230 

Plasmodium, 230 

forms of, estivo-autumnal, 
231 
half-moons, 232 
quartan, 230 
tertian, 231 
latency, 238 
pernicious, 239 

etiology of, 239 
forms of, 239 
algid, 240 
alimentary, 240 
biliary, 240 
cerebral, 240 
comatose, 240 
convulsive, 240 
hemoglobinuric, 240 
hemorrhagic, 240 
meningeal, 240 
typhoid, 239 
prognosis of, 241 
relapses of, 238 

relation of, to other diseases, 238 
spontaneous recovery from, 241 
symptoms of, 233 
blood, 235 
circulatory, 236 
digestive, 237 



Malaria, symptoms of, fever, 233 
estivo-autumnal, 235 
quartan, 234 
tertian, 235 
genito-urinary, 237 
nervous, 238 
respiratory, 237 
skin, 236 
spleen, 236 
treatment of, 241 

prophylactic, 241 
specific, 242 
symptomatic, 242 
Mai perforant de pied, 192, 730, 806, 854 
Male fern, 303 
Mallein, 131 
Malta fever, 125 

complications of, 126 
course of, 126 
diagnosis of, 126 
etiology of, 125 
prognosis of, 126 
symptoms of, 125 
treatment of, 126 
types of, 126 
Mammae, syphilis of, 218 

tuberculosis of, 180 
Mania, 807 
Mania a potu, 961 
Marriage after syphilis, 224 
Mastitis, syphilitic, 218 
Measles, 270 

clinical course of, 270 

diagnosis of, 274 

differentiation of, 106, 249, 254, 255, 

273 
etiology of, 270 

German. See German measles, 
prognosis of, 274 
stages of, 270 
symptoms of, 271 
digestive, 273 
eruption, 271 
fever, 272 
general course, 270 
genito-urinary, 273 
nervous, 273 
respiratory, 272 
treatment of, 274 

of complications, 274 
Meat poisoning, 969 
Meat-juice, 52 
Meckel's diverticulum, 549 
Mediastinal hemorrhage, 476 v 
pleurisy, 462 
tumors, 474 
Mediastinitis, acute, 475 

chronic, 389 
Mediastinopericarditis, 389 
Mediastinum, diseases of, 474 
Medulla, diseases of, 761 
Megalogastria, 507 
Megalomania, 804 
Melanemia in malaria, 236 
Melanoderma, 701, 702 
Melanoglossia, 481 
Melanotrichia lingua 1 , 481 
Melanuria, 579 



1002 



INDEX 



Melasma suprarenale, 702 
Meniere's disease, diagnosis of, 889 
etiology of, 888 
symptoms of, 889 
treatment of, 889 
Meninges, carcinoma of, 212 
cerebral, diseases of, 814 
hemorrhage into, 816 
inflammation of, 89 
spinal, diseases of, 829 

hemorrhage, 829 
pachymeningitis, 829 
tumors of, 830 

differentiation of, 213, 
832 
tuberculosis of, 175 
tumors of, 830 
sarcoma of, 212 
Meningismus, 34, 95 
Meningitis, carcinomatous, 212 
chronic, 818 

epidemic cerebrospinal, 89 
bacteriology of, 89 
clinical forms of, 93 
complications of, 93 
diagnosis, 93 
differentiation, 46, 47, 93, 94, 

95, 101 
etiology of, 89 
pathology of, 89 
prognosis of, 93 
sequelae of, 93 
symptoms of, 89 
treatment of, 95 
in influenza, 103 
pachymeningitis, 814 
pneumococcic, 71, 94 
sarcomatous, 212 
serous, 818 

differentiation of, 93, 94 
symptoms of, 818 
suppurative, 846 

differentiation of, 46, 47, 94, 95, 

240 
pathology of, 817 
symptoms of, 818 
syphilitic, 212 
tuberculous, 150 

differentiation of, 14, 46, 47, 94, 

95, 148, 149 
etiology of, 150 
pathology of, 150 
symptoms of, 151 
in typhoid fever, 33 
Meningococcus intracellularis, 89 
Meningomyelitis, 837 
Menthol, 86, 412, 538 
Meralgia paresthetica, 901 
Mercury, 223, 224, 225, 226, 227, 228, 229 
intoxication by, 478. See Hydrargy- 
rum. 
Merycismus, 532 

Mesenteric glands, suppuration of, in 
typhoid fever, 38 
tuberculosis of, 170 
vessels, dilatation of, 564 
embolism of, 564 
periarteritis of, 410 



Mesenteritis, 173, 564, 610, 616 
Mesentery, diseases of, 564 
embolism of, 564 
hemorrhage of, 564 
inflammation of, 564 
suppuration of, 564 
tumors of, 564 
Metabolism, diseases of, 725 
Metastasis, 20 
Metatarsalgia, 942 
Metazoan diseases, 302 
Meteorism in typhoid fever, 35, 55 
Methyl blue, 653 
Micrococcus catarrhalis, 419 

melitensis, 125 
Microgastria, 509 
Micromania, 805 
Micromelia, 713, 721 
Migraine, 937 

diagnosis of, 938 
etiology of, 937 
ophthalmoplegic, 877 
prognosis of, 938 
symptoms of, 937 
treatment of, 939 
Mikulicz's disease, 482, 691 
Miliaria, differentiation of, 260 
in pneumonia, 69 
in typhoid fever, 30 
Miliary fever, 299 

tuberculosis, 46, 47, 146 
Milk diet, 52, 634 
poisoning, 970 
sickness, 300 
Millar's asthma, 718 
Mimetic movements of expression, 

758 
"Mind-blindness," 753, 754 
Mitral insufficiency, 357 

diagnosis of, 358, 361 
etiology of, 357 
mechanism of, 357 
physical signs of, 357 
prognosis of, 370 
treatment of, 371 
stenosis, 359 

diagnosis of, 361 
differentiation, 332, 361 
etiology of, 359 
mechanism of, 359 
physical signs of, 359 
prognosis of, 370 
treatment of, 371 
Mobius's sign, 710 
Mogigraphia, 932 
Moller's disease, 697 

Monoplegia, in cerebral thrombosis, 
780 
cortical, 750 

internal capsule, lesion in, 759 
Morbilli, 270 
Morbus coeruleus, 380 
coxae senilis, 953 
maculosus neonatorum, 694 
Werlhofii, 693 
Moro's test, 164 

Morphine, 56, 57, 77, 110, 377, 429 
Morphinism, 963 









INDEX 



1003 



Morphinomania, 963 
Morvan's disease, 848 
Mosquito, conveyance of malaria by, 230, 
232, 241 
yellow fever, 289 
Motor cortex, 749 
tracts, 819 

degeneration of, 822 
Mountain fever, 300 
Mouth, diseases of, 477 
syphilis of, 203 
washes, 52, 477, 478 
Movements, associated, 771 
forced, 762 
mimetic, 758 

resisted, in heart disease, 323 
Muguet, 479 
Multiple neuritis, 869 

sclerosis, 843 
Mumps, 279 

complications of, 280 
diagnosis of, 280 
etiology of, 279 
prognosis of, 281 
sequels of, 280 
symptoms of, 279 
treatment of, 281 
Muscles, diseases of, 949 

motor cortex, v. cerebral localiza- 
tion tracts, 819 
syphilis of, 218 
tuberculosis of, 167, 183 
Muscular atrophy, arthritic, 861 
neuritic, 862 
progressive spinal 860 

diagnosis of, 861 
differentiation of, 100, 

841, 861, 864 
etiology of, 860 
pathology of, 860 
prognosis of, 861 
symptoms of, 860 
treatment of, 861 
dystrophy, 862 

diagnosis of, 864 
differentiation of, 100, 864 
infantile atrophic, 863 
juvenile, 864 
pseudohypertrophic, 862 
treatment of, 864 
Musset's sign, 352 
Myalgia, 950 

capitis, 950 
Myasthenia, gravis, 810 

differentiation of, 810 
pseudoparalytica, 810 
Myasthenic reaction, 810 
Mycosis intestinalis, 129 
Mycotic plugs, 421 
Mydriasis, syphilitic, 215 
Myelasthenia, 913 
Myelemia, 683 
Myelitis, acute, 836, 837 
course of, 838 
diagnosis of, 840 
differentiation of, 101, 840, 872 
disseminated, 841 
etiology of, 837 



Myelitis, acute, localization of, 839 
pathology of, 837 
prognosis of, 838 
symptoms of, 838 
transverse, 837 
treatment of, 840 
annular, 837 
chronic, 841 
cortical, 837 
Myeloma, multiple, 690 
Myelomalacia, 214, 833 
Myocarditis, acute, 328 
diagnosis of, 329 
etiology of, 328 
pathology of, 328 
symptoms of, 329 
treatment of, 329 
chronic fibrous, 329 

diagnosis of, 331 
differentiation of, 331 
etiology of, 329 
pathogenesis of, 330 
pathology of, 329 
prognosis of, 332 
symptoms of, 331 
treatment of, 333 
in diphtheria, 82 
rheumatic, 283 
segmentary, 82, 329 
syphilitic, 207 
in typhoid fever, 31 
Myocardium, diseases of, 319. 
Heart, 
fragmentation, 82, 329 
myofibrosis, 329 
myolysis, 82, 329 
myomalacia cordis, 330 
parasites of, 336 
segmentation, 82, 329 
syphilis, 207 
tuberculosis, 181 
tumors of, 336 
Myoclonia, 930 
Myofibrosis, myocarditis, 329 
Myoidema, 167 
Myolysis in diphtheria, 82 

myocardial, 329 
Myomalacia, cordis, 330 
Myopathies, 862 
Myositis, 949 

fibrositic, 949 
ossificans, 950 
rheumatic, 284 
syphilitic, 218 
trichinae, 310 
Myotonia, 933 

etiology of, 933 
symptoms of, 933 
treatment of, 934 
Myrrh, 268, 477 
Myrtol, 188 
Mytilotoxismus, 970 
Myxedema, 712 
of adults, 713 
of children, 712 
differentiated, 709, 713 
operative, 714 
treatment of, 714 



See 



1004 



INDEX 



N 



Nasal feeding in typhoid fever, 52 
Nasopharynx, tuberculosis of, 180 
Nauheim baths in heart disease, 323, 324 
Neck, actinomycosis of, 193 
rigidity, meningitic, 90 
Neck sign, 91 

Negri bodies in hydrophobia, 296 
Nematodes, diseases caused by, 307 
Nephrectomy, 657, 661, 664 
Nephritis, acute, 619 
cholera, 622 
course of, 622 
diagnosis of, 622 
differentiation of, 622, 640, 641 
etiology of, 619 
hemoglobinuric, 622 

kidney of pregnancy, 622 
pathology of, 619 
prognosis of, 622 

recurrent, 622 
symptoms of, albuminuria, 620 
anasarca, 620 
anemia, 621 
casts, 620 
heart, 620 
urine, 620 
treatment, 623 
types of, 622 
chronic, 624 

interstitial, 627 

complications of, 630, 632 
diagnosis of, 632 

of cardiac symptoms, 

632 
of uremia, 632 
of urinary findings, 632 
differentiation of, 632, 640, 

641 
etiology of, 393, 627 
pathology of, 627 
prognosis of, 633 
symptoms of, 628 

cardiovascular, 396, 629 
digestive, 631 
hemorrhages, 632 
inflammations, 632 
retinitis, 629 
uremia, 630 
urinary, 628 
treatment of, 633 
parenchymatous, 624 

complications of, 626 
death in, causes of, 626 
diagnosis of, 626 
differentiation of, 640, 641 
etiology of, 624 
pathology of, 624 
prognosis of, 627 
symptoms of, 625 
anemia, 626 
cardiovascular, 626 
edema, 626 
urinary, 62,5 
treatment of, 633 
treatment of, climate, 633 
diet, 633 



Nephritis, chronic, treatment of, diuretics, 
635 

edema, 636 

heart stimulants, 637 

incisions, 637 

rest, 633 

sweating, 636 

vasodilators, 637 

venesection, 637 

water, 635 
in cirrhosis of liver, 570 
diphtheritic, 83 
gouty, 740 
in malaria, 237 
in pneumonia, 70 
scarlatinal, 264 
suppurative, 652, 654 
syphilitic, 207 
tuberculous, 168 
typhoid, 40 
Nephrolithiasis, 657 
Nephrolithotomy, 661 
Nephrorrhaphy, 644 
Nephrotomy, 654, 657, 661 
Nerves. See also Paralysis, 
anterior crural, 901 
auditory, paralysis of, 887 
brachial plexus, 900 
circumflex, 898 
cranial, diseases of, 873 
diseases of, 867 
eighth, disease of, 887 
eleventh, disease of, 894 
facial, paralysis of, central, 885 

peripheral, 883 
spasm of, 887 
fifth, paralysis of, 880, 881 

spasm of, 882 
fourth, disease of, 875 
glossopharyngeal, 890 
hypoglossal, disease of, 896 
lumbar plexus, 901 
median, 899 
musculospiral, 898 
ninth, 890 
obturator, 901 
olfactory, 873 
optic, 873 
peroneal, 902 
phrenic, 897 
popliteal, 902 
posterior thoracic, 898 
recurrent laryngeal, paralysis of, 890, 
893 

spasm of, 891, 892 
sacral plexus, 902 
sciatic, 902 

seventh, disease of, 885 
sixth, disease of, 875 
spinal accessory, paralysis of, 895 

spasm of, 895 
superior gluteal, 902 
suprascapular, 898 
syphilis of, 214 
tenth, 890 

third, disease of, 875 
twelfth, disease of, 896 
ulnar, 899 



INDEX 



1005 



Nerves, vagus, 890 
Nervous fever, 24 

diseases, 749 
Neuralgia, 939 

cervicobrachial, 941 

cervico-occipital, 940 

diabetic, 730 

etiology of, 939 

in influenza, 104 

intercostal, 942 

lumbar, 942 

in malaria, 238 

phrenic, 941 

sacral, 942 

symptoms of, 940 

treatment of, 943 

trifacial, 940 

visceral, 942 
Neurasthenia, 912 

course of, 916 

diagnosis of, 916 

differentiation of, 807, 916 

etiology of, 913 

prognosis of, 916 

symptoms of, 913 

treatment of, 916 

types of, 913 
Neuritis, 867 

brachial, 900 

diabetic, 730 

diagnosis of, 869 

in diphtheria, 83 

etiology of, 867 

facial, 883 

hypertrophic, 868 

in influenza, 104 

lead poisoning causing, 967 

in leprosy, 191 

multiple, 869 

diagnosis of, 871 

differentiation of , 100, 101, 848, 

871, 872 
etiology of, 869 
pathology of, 870 
prognosis of, 871 
symptoms of, 870 
treatment of, 872 ' 

optic, 92, 873 

pathology of, 867 

rheumatic, 285 

sciatic, 903 

symptoms of, 867 

treatment of, 869, 872 

in typhoid fever, 32, 34 
Neuroma; 872 
Neurones, 819 

motor, 752, 819 

sensory, 823 
Neuroses, 905 

"fatigue, 932 

occupation, 932 

traumatic, 918 

trophic, 944 

vasomotor, 944 
Nigrities linguae, 481 
Nitroglycerin, therapeutics of, 269, 336, 

399, 400, 429, 939 
Nitromuriatic acid, 58 



Nocardiosis, 196 

Nodes, rheumatic, 284, 286 

Noma oris, 479 

Nose, diphtheria of, 81 

diseases of, 411 

saddle-back, 209 

syphilis of, 209 

tuberculosis of, 180 
Nucleo-albumin, tests for, 646 
Nystagmus, 880 

in multiple sclerosis, 844 



Oatmeal diet, 736 
Obermeir's spirillum, 243 
Obesity, 746 

etiology of, 746 
Frolich's type, 720, 722 
symptoms of, 746 
treatment of, 746 
Ochronosis, 651 
Oertel's cure, 747 

treatment of heart disease, 323 
Oidiomycosis, 196 
Oidium albicans, 479 
Oleum olivae, 518 
ricini, 562, 943 
tiglii, 270, 774 
Oligocardia, 341 
Oligochromemia, 668 
Ophthalmia, diphtheritic, 82 

neuroparalytic, 881 
Ophthalmoplegia, progressive nuclear, 879 

syphilitic, 215 
Ophthalmoreaction, 164 
Opisthotonos, 91, 134 
Opium, coma from, 772 
poisoning, acute, 963 

chronic, 963 
therapeutics of, 55, 77, 124, 188, 225, 
268, 415, 420, 422, 429, 558, 736. See 
also Morphine, Codeine, Heroine. 
Oppler-Boas bacillus, 423 
Optic atrophy, multiple sclerosis, 845 
syphilitic, 215 
tabetic, 853 
typhoid, 41 
centre, 753, 874 
chiasm, 873 
nerve, 873, 874 
neuritis, 873 

in brain abscess, 800 
in meningitis, 92 
syphilitic, 215 
in typhoid fever, 41 
thalamus, localizing symptoms, 758, 

794 
tract, 874, 875 
Orchitis, in mumps, 280 
syphilitic, 216 
in typhoid fever, 41 
Oriental sore, 245 
Osmic acid injection, 943 
Osteitis deformans, 722 
Osteo-arthropathie hypertrophiante p/icu- 
monique, 168, 425, 722 



1006 



INDEX 



Osteoarthropathy, hypertrophic, 168, 425, 

722 
Osteochondritis, syphilitic, 223 
Osteomalacia, 956 
Osteomyelitis. See Septic infections, 22 

in typhoid fever, 41 
Otitis, diphtheritic, 82 

media, brain abscess from, 799 
sinus thrombosis from, 784 

measles, 274 

scarlatinal, 265 
Ovary, syphilis of, 217 
Oxaluria, 651 
Oxycephaly, 957 
Oxygen, therapeutics of, 77 
Oxyuris vermicularis, 308 
Ozena, 413 



Pachydermia, 203, 713 
Pachymeningitis, cervical hypertrophic, 
829 
external, 814 

hemorrhagic, diagnosis of, 815 
differentiation of, 807, 815 
etiology of, 803, 814 
pathology of, 803, 814 
prognosis of, 815 
symptoms of, 815 
treatment of, 815 
internal, 814 
Paget's disease, 722 
Pain, abdominal, 36, 547, 563 

centre for, 754 
Palate, tuberculosis of, 175 
Palpitation of heart, 337 
Palsy, shaking, 934 
Pancreas, calculi of, 604 

cancer of, differentiation of, 606 

symptoms, 605 
cysts of, 604 

diagnosis of, 604 
etiology of, 604 
pathology of, 604 
symptoms of, 604 
treatment of, 605 
diseases of, 601 
hemorrhage, from 603 
inflammation of, acute, 601 

chronic, 603 
necrosis, 601 
syphilis of, 205 
tumors of, 605 

differentiation of, 606 
symptoms of, 605 
treatment of, 606 
Pancreatitis, acute, diagnosis of, 601, 602 
differentiation, 602 
etiology of, 601 
prognosis of, 602 
symptoms, 601 
treatment of, 603 
chronic, etiology of, 603 
pathology of, 603 
prognosis of, 603 
symptoms of, 603 
treatment of, 603 



Paracentesis, abdomen, 616 

chest, 388, 458, 467 
Paradysentery, 119 
Paragonimus Westermanni, 317 
Paralysis. See Monoplegia, Hemiplegia, 
Paraplegia, and Nerves, 
agitans, 934 

diagnosis of, 936 
differentiation of, 845, 936 
etiology of, 934 
pathology of, 934 
prognosis of, 936 
symptoms of, 934 
treatment of, 936 
alternating, 759, 760 
anterior crural, 901 
of auditory nerve, 887 
Bell's, 883 
brachial plexus, 900 
Brown-Sequard's, 835 
bulbar, apoplectiform, 100, 780, 811 
asthenic, 810 
chronic, 808 
caisson, 834 
circumflex, 898 
combined, of arm nerves, 900 
compression, spinal, 831 
conjugate, 760 
cortical, 750, 793 
crossed, 759, 760 
diphtheritic, 83 
diver's, 834 
facial, 883 

diagnosis of, 885 
etiology of, 883 
localization of, 760, 885 
pathology of, 883 
1 prognosis of, 886 
symptoms of, 883 
in tetanus, 135 
treatment of, 886 
of fifth nerve, 880 
of fourth nerve, 877 
Gublers's, 760 
hemiplegia, q. v. 
hypoglossal, 808, 896 
' ' hysterical, 908 

infantile cerebral, 96, 786 
diplegic, 787 

diagnosis of, 789 
etiology of, 787 
pathology of, 787 
symptoms of, 788 
treatment of, 789 
hemiplegic, 786 

diagnosis of, 787 
etiology of, 786 
symptoms of, 786 
treatment of, 789 
of insane, 802 
labioglossopharyngeal, 808 
Landry's, 100, 842 
laryngeal, 891 

recurrent, 404, 891, 893 
lead, 967 

lumbar plexus, 901 
in malaria, 240 
median, 899 



INDEX 



1007 



Paralysis in meningitis, 92 

monoplegia, q. v. 

musculospiral, 898 

ninth, 890 

obturator, 901 

ocular, 759, 760, 798, 853, 875, 879 

oculomotor, 759, 760, 798, 853, 875, 
876, 877, 878 

paraplegia, q. v. 

periodic family, 213, 858, 936 

peroneal, 902 

phrenic, 897 

popliteal, 902 

posterior thoracic, 898 

progressive, of insane, 802 

pseudo-, 697 

pseudobulbar, 810 

pupil, 877 

recurrent, 877 

sacral, 902 

sciatic, 902 

seventh, 883 

sixth nerve, 877 

spinal accessory, 894 

superior gluteal, 902 

suprascapular, 898 

of sympathetic nerves, 879, 944 

third nerve, 876 

ulnar, 899 

uremic, 630, 631, 632, 633, 772 

vagus, 809, 890 

of vocal cords, 891, 893 

Weber's, 759 
Paramyoclonus multiplex, 930 
Paramyotonia, ataxic, 934 

congenital, 934 
Paranephritis, 654 
Paraplegia, ataxic, 866 

in cerebral infantile paralysis, 787, 
788 

cerebral, 749 

dolorosa, 826, 831 

hysterical, 840, 908 

spastic spinal, 857 
Paraplegic state, 841 
Parapleuritis, 462 

Parasites, diseases due to animal, 302 
Parathyroid glands, 715 
Paratyphoid fever, 26, 45, 46 
differentiation of, 46 
microorganisms of, 46 
symptoms of, 46 
Paregoric. See Opium. 
Paresie andlgesique avec panaris, 848 
Parkinson's disease, 934 
Parorexia, 533 
Parosmia, 873 
Parotitis, acute, 481 

chronic, 482 

epidemic, 279 

postoperative, 281 

secondary, 281 

in typhoid fever, 34 
Parrot's disease, 697 

ulcers, 478 
Pasteur treatment, 296 
Pastia's sign, 262 
Pavor nocturnus, 488 



Peliosis rheumatica, 692 
Pellagra, 971 

differentiation of, 971 
Pelletierine, 303 
Pelvis, rhachitic, 744 
Penis, syphilis of, 216 
Pentosuria, 733 
Pepsin, test for, in stomach, 500 

therapy of, 502 
Periarteritis nodosa, 410 
Pericarditis, 381 
adhesive, 389 

diagnosis of, 390 
prognosis of, 390 
symptoms of, 389 

cardiac insufficiency, 389 
diastolic collapse of veins, 
389 
recoil, 389 
inspiratory swelling of veins, 

389 
paradoxical pulse, 389 
retraction of apex, 389 
of chest wall, 389 
treatment of, 390 
differentiation of, from pleurisy, 386, 

465 
effusive, 382 

course of, 388 
diagnosis of, 386 

character of exudate, 387 
dulness, 386 
friction-rub, 386 
pathology of, 382 
physical signs of, 383, 385 
prognosis of, 388 
symptoms of, 383 
treatment of, 388 
etiology of, 381 
externa, 386 
fibrinous, 382 

physical findings of, 382 
symptoms of, 382 
pneumococcic, 71 

pseudocirrhosis of liver in, 571, 616 
rheumatic, 283, 286 
syphilitic, 208 
tuberculous, 171, 387 
Pericardium, diseases of, 381 
tuberculosis of, 171, 387 
Perichondritis, laryngeal, in typhoid fever, 
39 
of larynx, 209, 417 
Perihepatitis, 369, 612, 616 

differentiation of, 616 
Perinephric abscess, 654 
diagnosis of, 655 
etiology of, 654 
symptoms of, 654 
Perinephritis, 195, 654 
Periostitis, rheumatic, 284 
syphilitic, 217 
in typhoid fever, 41 
Peripleuritis, 195, 462 
Perisplenitis, 612, 706 
Peristaltic unrest, 531 
Peritoneum, cancer of, 613 

differentiation of, 616 






1008 



INDEX 



Peritoneum, diseases of, 607 

tuberculosis of, 172 
Peritonitis in cirrhosis of liver, 570 
diffuse, acute, 607 

course of, 607 
diagnosis of, 609 
differentiation of, 610 
etiology of, 607 
perforative, 609 
pneumococcic, 609 
puerperal, 22, 609 
symptoms of, abdominal, 
607 
general, 608 
local, 607 
treatment of, 610 
types of, 609 
chronic, 610 

differentiation of, 615, 616 
deforming, 610 
hemorrhagic, chronic, 612 
localized, 611 

adhesive, 612 

perihepatitis, 612 
suppurative, 611 

pyopneumothorax, sub- 

phrenicus, 611 
subphrenic abscess, 611 
tuberculous, 172, 173, 174, 616 
typhoid perforation causing, 37 
Peritonsillar abscess, 487 
Perityphlitis, 194, 544 
Perles, asthma, 429 

Pernicious anemia. See Anemia, per- 
nicious. 
Pertussis. See Whooping cough. 
Peru, balsam of, 422 
Pest. See Plague. 
Pesticemia in plague, q. v. 
Petechias in typhus fever, 277 
Petit mal, 922 
Pharyngitis, acute, 485 
chronic, 485 
diphtheritic, 80 
phlegmonous, 485 
ulcerative, 485 
Pharynx, disease of, 483 
erysipelas of, 59, 61 
paralysis of, 890 
spasm of, 891 
syphilis of, 203 
tuberculosis of, 175 
typhoid ulcers of, 35 
ulceration of, 485 
Pfeiffer's fever, 298 
Phenacetin. See Acetphenetidin. 
Phenol, 55, 137, 268, 412, 484, 497 
Phenylhydrazin test, 728 
Phenylis salicylas, 50, 57, 288, 535, 538 
Phlebitis, pneumococcic, 71 
portal vein, 586 
septic, 20 
syphilitic, 208 
typhoid, 31 
PhlebosclerOsis, 395 
Phlebotomy, 77, 372, 637, 774 
Phlegmon, differentiation of, 60 
Phosphates in urine, 650 



Phosphaturia, 650 
Phosphorus poisoning, 745 

therapy of, 745 
Phrenocardia, 337 
Phthisis, 152 

aneurysmal, 405 
fibroid, 162, 438 
ventriculi, 503 
Pick's pseudocirrhosis, 571, 616 
Pigeon-breast, 489, 743 
Pigmentation in Addison's disease, 701 
Piles, 557 
Pilocarpine, 637 
Pirquet's test, 164 
Placenta, syphilis of, 222 
Plague, 115 

diagnosis of, 118 
etiology of, 115 
prognosis of, 118 
symptoms of, 116 
treatment of, 118 
Plasmodium malarise, 229, 240 
Pleura, diseases of, 453 

tuberculosis of, 162, 171, 454, 460, 

461 
tumors of, 474 
Pleurisy, 453 

bacteriology of, 454 
in children, 462 
chyliform, 461 
course of, 466 
cytodiagnosis in, 460 
diagnosis of, 464 

diaphragmatic, 461 
differentiation of, 73, 74, 464, 465, 

581, 611 
empyema, 454, 460 
necessitatis, 460 
pneumococcic, 70, 460 
pulsans, 460 
streptococcic, 460 
treatment of, 468 
etiology of, 453 
fibrinous, 460 
forms of, 459 
hemorrhagic, 461 
in influenza, 104 
interlobar, 462 
issues of, 462 
mediastinal, 462 
parapleuritis, 462 
peripleuritis, 462 
physical signs of, 454 

auscultation, 457 
diagnostic puncture, 458 
inspection, 454 
palpation, 455 
percussion, 455 
pneumococcic, 70, 460 
polymorphous, 458 
prognosis of, 466 
purulent, 454, 460 
putrid, 461 
rheumatic, 284 
serous, 454, 459 
streptococcic, 460 
suppurative, 454, 460 
symptoms of, 454, 459 



INDEX 



1009 



Pleurisy, treatment of, 466 
aspiration, 467 
in tuberculosis, 162, 171, 453, 454, 

460, 461 
in typhoid fever, 40 
x-ray findings, 458 
Pleuritic friction, 386, 457, 464 
Pleurodynia, 950 
Pleuropericardial friction, diagnosis of, 

386 
Pleuropneumonia, 62 
Plumbism, 965 
Pneumatosis peritonei, 609 
Pneumaturia, 649, 729 
Pneumobacillus, 63 
Pneumococcemia, 62, 69 
Pneumococcic pharyngitis, 483, 486 
Pneumococcus. See Septic infections 
and Pneumonia, 21. 
endocarditis, 347 
meningitis, 94 
peritonitis, 609 
Pneumokoniosis, 440 
etiology of, 440 
pathology of, 440 
symptoms of, 440 
treatment of, 441 
Pneumomalacia, 444 
Pneumonia, 62 

aspiration, 434 
bacteriology of, 62 

pneumobacillus, 63 
pneumococcus, 62 
bronchopneumonia, 434 
central, 67, 73 
cerebral, 73, 74 

clinical types and variations of, 72 
complications of, 70 
abscess of lung, 71 
alimentary, 71 
arteritis, 71 
arthritis, 71 
delirium tremens, 71 
empyema, 70 
endocarditis, 70 
gangrene of lung, 71 
icterus, 71 

induration of lung, 71 
joint, 71 
lung, 71 
meningitis, 71 
nervous, 71 
pericarditis, 71 
peritonitis, 609 
pleurisy, 70 
thrombophlebitis, 71 
course, 63 
crossed, 67 

death, mechanism in, 70 
diagnosis of, 73 
differentiation of, 44, 73, 74, 148, 160, 

161 
erysipelatous, 60 
etiology of, 62 
frequency of, 62 
hepatization in, gray, 67 

red, 67 
immunity from, 63 
64 



Pneumonia, indurative, 438 
diagnosis of, 439 
etiology of, 438 
pathology of, 439 
physical findings of, 439 
prognosis of, 439 
symptoms of, 439 
treatment of, 440 
interstitial, 438 
Litten's sign in, 68 
lobar, in influenza, 104 

in typhoid fever, 39, 44 
lobular. See Bronchopneumonia, 
massive, 67, 73, 74 
migratory, 72 
pathology of, 67 
physical signs of, 67 
plague pneumonia, 117 
pleurogenous, 439 
prognosis of, 74 
rheumatic, 284 
"schluck," 434 
secondary, 72 
symptoms of, 64 
chill, 64 
circulatory, 69 
digestive, 69 
fever, 64 
nervous, 70 
prodromes, 64 
respiratory, 65 
skin, 69 
sputum, 66 
urine, 70 
syphilitic, 210 
total, 67 
treatment of, 75 
hygienic, 75 
prophylactic, 75 
symptomatic, 75 
white, syphilitic, 210 
Pneumonitis, 62 
Pneumopericardium, 391 
Pneumoperitoneum, 609 
Pneumorrhagia, 450 
Pneumothorax, 468 
artificial, 189, 452 
diagnosis of type of, 471 
differentiation of, 472, 611 
etiology of, 469 
pathology of, 469 
physical signs of, 470 
prognosis of, 472 
symptoms of, 469 
treatment of, 472 
in tuberculosis, 166, 189 
Podagra. See Gout. 
Pododynia, 942 
Podophyllin, 562 
Poisoning. See Arsenical, etc. 
Poliencephalitis, inferior, 798 

superior, 798 
Poliencephalomyelitis, 798 
Poliomyelitis, acute, 96 

diagnosis of, 100 
differentiation of, 100, 101, 787 

871 
etiology of, 96 



1010 



INDEX 



Poliomyelitis, acute, pathology of, 96 
prognosis of, 101 
symptoms of, acute stage, 98 
chronic stage, 99 
degenerative stage, 99 
localization, 99 
treatment of, 101 
types, 98, 100 

chronic, 841 

subacute, 841 
Pollakiuria, 178, 628, 728 
Pollantin, 413 

Polyarthritis, rheumatic, 281 
Polycardia, 340 
Polycythemia with splenic tumor, 691 

in heart disease, 367, 380 
Polydipsia, 729, 737 
Polyesthesia, tabetic, 852 
Polyglobulism, 691 
Polymyositis, 949 
Polyneuritis endemica, 972 
Polyorrhomenitis, 612, 616 
Polyphagia, 533, 729, 737 
Polyuria in cerebral syphilis, 212 

diabetic, 728, 737 

in nephritis, 628 

in pyelitis, 652 

in renal tuberculosis, 178 
Pomegranate, 303 
Pons, localizing symptoms, 760 
Porencephalia, 788 
Portal vein phlebitis, 205, 586 
thrombosis, 205, 586 
Postmortem tubercles, 183 
Postures, forced, 762 
Potassium acetate, 269 

bromide, 924, 925 

chlorate, 477, 478 

iodide, 164, 188, 195, 220, 227, 228, 
332, 335, 377, 399, 413, 422, 430, 
484, 708 

permanganate, 413 
Potato poisoning, 971 
Pregnancy, effect of syphilis on, 221 

in heart disease, 371 

tuberculosis and, 168, 190 

typhoid and, 40 
Prison fever, 276 
Proctitis, 535 
Prof eta's law, 221 
Progeria, 723 
Prosopalgia, 940 
Prosoplegia, 883 
Prostitution, regulation of, 224 
Pseudoangina, 335 
Pseudocirrhosis. Pick's pericardiac, 521, 

612, 616 
Pseudodiphtheria, 78, 79 
Pseudoleukemia, 687 

allied affections, 689 

course of, 689 

diagnosis of, 689 

differentiation of, 171, 689 

etiology of, 687 

pathology of, 688 

symptoms of, 688 
blood, 688 
bone, 688 



Pseudoleukemia, symptoms of, fever, 689 
lymph glands, 688 
skin, 688 
spleen, 688 
treatment of, 691 
Pseudomeningitis, 34, 95 
Pseudoparalysis, 697 
Pseudorheumatism, 182, 282, 287 
Pseudosclerosis (multiple), 843, 846 
Pseudotabes, 871 
Pseudotetanus, 135 
Pseudotuberculosis, 141, 165 
aspergillus, 141, 165 
protozoan, 141 
streptothrix, 141, 165 
Psittacosis, 302 
Psychasthenia, 916 
Psychoses, influenzal, 103 
Korsakow's, 871 
in typhoid fever, 33 
Ptosis, 876 
Ptyalism, 481 

Puerperal fever. See Septic infections, 17 
erysipelatous, 22 
lymphangitis, 22 
peritonitis, 22 
sapremia, 22 
thrombophlebitis, 22 
Pulmonary artery, syphilis of, 208 
insufficiency, 362 
etiology of, 362 
mechanism of, 362 
symptoms of, 362 
stenosis, 362, 378 

congenital, 362, 378 
diagnosis of, 362 
etiology of, 362, 378 
mechanism of, 362 
signs of, 362, 378 
Pulse, alternating, 340 
bigeminus, 339, 367 
celer, 353 
collapsing, 353 
dicrotic, q. v. 
differens, 395, 404 
durus, 395 

liver, positive, 363, 364 
paradoxical, 389, 390 
"pistol," 353 
Quincke's capillary, 352 
retarded, 404 
tardus, 341 
venous, negative, 363 

positive, 340, 363, 364 
"water-hammer," 353 
Pulsus paradoxus, 389, 390 
Pupil, Argyll-Robertson, 805, 853, 855, 
877" 
reflexes of, 826 

Wernicke's hemianopsic reaction, 875 
Purpura, fulminans, 694 
hemorrhagica, 693 
diagnosis of, 693 
etiology of, 693 
prognosis of, 693 
symptoms of, 693 
treatment of, 693 
Henoch's, 694 



INDEX 



1011 



Purpura, renal, 647, 698 

rheumatica, 692 

diagnosis of, 692 
prognosis of, 692 
symptoms of, 692 
treatment of, 692 

simplex, 692 

symptomatic, 692 

variolous, 252 

visceral crises in, 693 
Pus in urine, 649 

Pustule, malignant. See Anthrax. 
Pyelitis, 652 

complications of, 653 

diagnosis of, 653 

etiology of. 652 

pathology of, 652 

prognosis of, 653 

symptoms of, 652 

treatment of, 653 

in typhoid fever, 40 
Pj^elonephritis, 652 
Pyemia, 17 
Pyknocardia, 340 
Pylephlebitis, 205, 586 

diagnosis of, 586 

etiology of,. 575, 586 

suppurative, 575, 586 

symptoms of, 586 

treatment of, 586 
Pylethrombosis, 205, 586 
Pylorectomy, 508, 526 
Pylorus, hypertrophy of, 504, 507 

insufficiency of, 532 

spasm of, 504, 507, 515, 531 

stenosis of, 504, 507 
Pyocyaneus. See Septic infections. 
Pyonephrosis, 656 
Pyopneumothorax subphrenicus, 465, 472, 

611 
Pyothorax subphrenicus, 611 
Pyramidal tracts, 749, 766, 819-823, 827 
Pyuria, 649 

diagnosis of, 649 

etiology of. 649 

renal calculus causing, 659 

symptoms of, 649, 652 

treatment of, 649 

tuberculosis causing, 178 



Quincke's lumbar puncture, 93 

pulse, 352 
Quinine in malaria, 242 

administration of, 62, 109, 110, 
124, 188 
Quinquad's sign, 960 



R 



Rabic tubercles in hydrophobia, 296 
Rabies, 294 

Rag-sorters' disease, 130 
Rat-bite fever, 301 
Ray fungus, 193 



Raynaud's disease, 945 
Reaction of degeneration, 868 
Rectal feeding, 516 
Rectum, cancer of, 555 

syphilis of, 204 
Recurrent fever, 243 

convalescence in, 245 
diagnosis of, 245 
etiology of, 243 
prognosis of, 245 
symptoms of, 243 
treatment of, 245 
Reflexes in spinal cord, 82 
Relapsing fever, 243, 689 
Ren arcuatus, 643 

Renal calculus. See Kidney, calculus of. 
Rennet, test for, 500 
Resorcinol, 479, 502 
Respiratory tract, diseases of, 411 
Rest cure, 917 

Retina, arteriosclerosis of, 398 
Retinitis, 873 

albuminuric, 629 
diabetic, 731 
leukemic, 685 
syphilitic, 215 
Retropharyngeal abscess, 484 
Rhachitis. See Rickets. 

acute. See Barlow's disease, 697 
Rhatany, 479 
Rhubarb, 562 
Rheumatic fever, 281 
Rheumatism, acute articular, 281 
course, 281 
diagnosis of, 286 

anomalous forms, 283 
in childhood, 236 
gonorrheal, 287 
pseudorheumatism, 287 
scarlatinal, 287 
differentiation of, 287 
etiology of, 281 
frequency of, 281 
prognosis of, 286 
symptoms of, 281 
arthritis, 282 
blood, 285 
bone, 284 
circulatory, 283 
digestive, 285 
eye, 285 
fever, 282 
general, 281 
genito-urinary, 285 
muscle, 284 
nervous, 285 
prodromal, 282 
pseudorheumatism, 

187, 282, 287 
respiratory, 284 
skin, 284 
treatment of, 287 
atypical, 283 
cerebral, 282, 285 
chronic, 951 

endocarditis from, 283, 2o3, 348 
masked, 283 
muscular, 950 



1012 



INDEX 



Rheumatism, relations of chorea to, 285, 
927-929 

pericarditis, 381, 283 

scarlatinal, 265 

spinal, 285 

syphilitic, 217, 218 

tonsillitis, 485 

tuberculous, 182 

visceral, 287 
Rheumatoides, 287 
Rhinitis, acute, 411 

etiology of, 411 
symptoms of, 411 
treatment of, 411 

chronic, 413 

atrophic, 413 
hypertrophic, 413 
treatment of, 413 

diphtheritic, 81 

fibrinous, 81, 413 

syphilitic, 222 
Rickets, 742 

acute, 697 

complications of, 745 

course of, 745 

diagnosis of, 745 

differentiation of, 745, 811 

etiology of, 742 

pathology of, 744 

prognosis of, 745 

symptoms of, 743 

tardy, 742 

treatment of, 745 
Riga's disease, 478 
Risus sardonicus, 134 
Rocky Mountain fever, 300 
Romberg's sign, 851 
Rosary, rhachitic, 743 
Rose cold, 412 

spots. See Roseola. 
Roseola, in measles, 271 

in typhoid fever, 29 

in typhus fever, 277 
Rosin's sign, 710 
Rotheln, 275 
Rubella, 275 
Rubeola, 270 

notha, 275 
Rumination, 532 
Rumpel-Leede sign, 262 



St. Anthony's fire, 58 
St. Vitus's dance, 926 
Salicylates, action of, 287 

administration, 288, 289, 741, 932 ' 
Saline infusions, 77, 637 
Salivary calculi, 482 

glands, diseases of, 481 

inflammation of. See Parotitis, 
symmetrical hypertrophy of, 482, 

691 

tuberculosis of, 175 

Salivation, etiology of, 481 

symptoms of, 481 

treatment of, 481 



Salol. See Phenylis salicylas. 

Salt, 635 

Salt-free diet, 635 

Salvarsan, 228, 229 

Sanatoria in tuberculosis, 185 

Santal oil, 422 

Santonin, 308 

Sapremia, 17 

Saturnism, 965 

Scarlatina. See Scarlet fever, 260 

Scarlet fever, 260 

diagnosis of, 265 

differentiation of, 249, 263, 266, 

273, 796, 807, 845, 846, 856 
endocarditis from, 263, 348 
etiology of, 260 
prognosis of, 267 
sequels of, 265 
symptoms of, 261 
blood in, 264 
bones and joints, 265 
cardiac, 263 
digestive, 264 
eruption, 262 
fever, 262 
kidney, 264 
lymphatic glands, 265 
respiratory, 263 
special senses, 265 
stages, 261 
throat, 263 
tongue, 264 
treatment of, 267 
Scarlet-red ointment, 57 
Schistosoma hematobium, 316 
Schlesinger's sign, 716 
Schott's treatment of heart disease, 323 
Schroth treatment of pleurisy, 466 
Sciatic neuritis, 903 
Sciatica, 903 

diagnosis of, 904 
etiology of, 903 
pathology of, 903 
prognosis of, 904 
symptoms of, 903 
treatment of, 904 
Scleredema, 541 
Sclerema adiposum, 541 
Sclerodactylia, 947 
Scleroderma, 946 
Sclerose en plaques, 843 
Sclerosis, amytrophic lateral, 858 
diagnosis of, 860 
etiology of, 859 
pathology of, 859 
prognosis of, 860 
symptoms of, 859 
treatment of, 861 
disseminated, 843 
insular, 843 
multiple, 843 

course of, 845 

diagnosis of, 845 

differentiation of, 796, 807, 845, 

846, 856 
etiology of, 843 
pathology of, 843 
prognosis of, 845 



INDEX 



1013 



Sclerosis, multiple, symptoms of, 843 
treatment of, 847 
scorbutic, 696 
Scotoma, 845, 875 
Scorbutus, 695 
Scrofula, 168, 169, 182, 183 
Scrofuloderma, 183 
Scurvy, 695 

course of, 696 
diagnosis of, 696 
etiology of, 695 

infantile. See Barlow's disease, 697 
prognosis of, 696 
symptoms of, 695 
treatment of, 696 
Secretin, 536 
Secretion, internal, 701 
Semilunar space, 456 
Senega, 422 
Senna, 562 
Sensation, cortical representation, 753 

spinal localization, 823, 824 
Sensory crossway, 757 
Sepsis. See Septic infections, 17 
Septic infections, 17 
atrium, 18 

colon bacillus, sepsis, 21 
diagnosis of, 23 

differentiation of, 23, 46, 47, 266 
from malaria, 46, 47 
from meningitis, 46, 47 
from Malta fever, 126 
from miliary tuberculosis, 

46, 47 
from rheumatism, 23 
from typhoid, 46, 47 
from syphilis, 206 
endocarditis, ulcerative, 20, 46, 

47, 346 
etiology of, 18 
gonococcic infection, 21, 137 
groups of, 17 
osteomyelitis, 21, 22 
otogenous sepsis, 22 
pathology of, 18 
peritonitis, 22 
pneumococcic infection, 21 
prognosis of, 23 
puerperal fever, 22 
pyocyaneus infection, 22 
sore throat, 286 
staphylococcic infection, 21 
streptococcic infection, 21, 486 
symptoms of, 18 
general, 18 
special, 21 
treatment, 23 
typhoid infection, 20 
diphtheria, 81 
Septicemia, 17 
Septicopyemia, 17 

gonorrheal, 137 
Serotherapy, in diphtheria, 87 
in dysentery, 123 
in erysipelas, 62 
in meningitis, 95 
in plague, 118 
in scarlatina, 270 



Serotherapy in sepsis, 23 

in tetanus, 136 
Serous membranes, tuberculosis of, 171 
Serum disease, 88 
Flexner's, 95 
normal, 56, 189, 699 
Shaking palsy, 934 
Sheep-stools, 561 
Shick's test, 88 

Shiga's bacillary dysentery. See Dysen- 
tery, Shiga's. 
Sialodochitis fibrinosa, 482 
Sialolithiasis, 482 

pancreatica, 604 
Sialorrhea, 481 
Side-chain theory, 87, 134 
Siderosis of lungs, 440 
Silver, 106, 125, 502, 518, 529 
Singultus, 897 

Sinus irregularity of heart, 339 
thrombosis, 783 

of cavernous sinus, 785 

diagnosis of, 785 

differentiation, 786 

etiology of, 669, 783 

of lateral sinus, 785 

pathology of, 783 

prognosis of, 786 

of superior longitudinal sinus, 

785 
symptoms of, 785 
treatment of, 786 
Sitotoxismus, 970 
Situs viscerum inversus, 380, 584 
Skin, bronzing of, 701, 702 
diphtheria of, 82 
tuberculosis of, 183 
Skoda's note in pleurisy, 456 

resonance in pneumonia, 68 
Sleeping sickness, 246 
Smallpox, 247 
black, 252 

complications and sequelae of, 253 
diagnosis of, 254 
differentiation of, 254, 27S 
etiology of, 248 
prognosis of, 255 
symptoms of, 249 

purpura variolosa, 252 
variola confluens, 251 

pustulosa hemmorrhagica, 

252 
discreta, 249 
varioloid, 252 
treatment of, 256 

prophylactic, 256, 258 
symptomatic, 258 
vaccination 256 
Smegma bacillus, 140 
Smell, centre for, 754 
Sodium benzoate, 110, 376 

bicarbonate, 110, 516, 562, 735 
borate, 52 

bromide, 110, 338, 925 
chloride, 635 

salicylate, 287, 741, 932, 939 
sulphate, 124, 562 
Sokudu, 301 



1014 



INDEX 



Soor, 479 

Spartein, 188, 376, 400 
Spasm, cardio-, 492, 531 
of facial nerve, 887 
of fifth nerve, 882 
habit, 930 
masticatory, 882 
mobile, 772 
ocular, 880 
phrenic, 897 

of spinal accessory nerve, 895, 896 
of vagus, 891, 892 
of vocal cords, 892 
Spasmophilia, 716 
Speech, centres for, 754 
disturbances of, 754 
scanning, 844 
Spina ventosa, syphilitic, 217 

tuberculous, 182 
Spinal atrophy, progressive muscular, 860 
cord, abscess of, 840 
anatomy of, 819 
anemia of, 833 
compression of, 831 
degeneration of, ascending, 825 
descending, 822 
in pernicious anemia, 675 
embolism, 833 
functions of, 819 
hemorrhage of, 833 
inflammation of, 836 
localization of, 819, 824 
physiology of, 819 
reflexes of, 824, 826 
segments, 824 
symptomatology of, 819 
syphilis of, 213 
tracts of, motor, 819-823 

sensory, 823 
thrombosis, 833 
transverse lesion of, 835 
trauma of, 835 
tumors of, 830 

diagnosis, 832 
localization, 831 
pathology, 830, 831 
prognosis, 832 
symptoms, 831 
treatment, 833 
irritation, 914 
meninges, diseases of, 829 
paraplegia, spastic, 857 
Spinalgia, 170 

Spirals, Leyden-Curschmann, 429 
Spirillum Obermeyeri, 243 
Spirochete darticola, 485 
pallida, 198 
refringens, 198 
Splanchnomegaly, 721 
Splanchnoptosis, 555 
Spleen, abscess of, 705 

amyloid, 168, 204, 706 

cysts of, 707 

diseases of, 705 

embolism of, 705 

endothelioma of, 707 

enlargement of, differentiation of, 657 

in erythremia, 691 



Spleen, extirpation of, 707 
floating, 706 
in ictero-anemia, 590 
movable, 706 
neoplasms of, 707 
rupture of, 706 
syphilis of, 205 
tuberculosis of, 177 
tumor, acute, 705 
chronic, 705, 707 
Splenectomy, 691, 706, 707 
Splenitis, acute, 705 
chronic, 705 
suppurative, 706 
Splenomegaly, 707 
infantile, 245 
Leishman's, 245 

with polycythemia and cyanosis, 691 
primary, 707 
Splenopex3 r , 707 
Spondylitis, ankylosing, 953 

luetic, 217 
Spondylose rhizomyelique, ,953 
Sporotrichosis, 196 
Spotted fever, 93 
Sputum, disinfection of, 183 
Squills, 376, 422 

Staphylococcus. See Septic infections, 21 
endocarditis, 347 
spray, 86 
Status lymphaticus, 719 

thymicus, 719 
Steatorrhea, 589, 606 
Stegomyia, 291 
Stellwag's sign, 710 
Stenocardia, 333 

Stenosis. See Aorta, Bronchi, etc. 
Stereognostic sense, 753 
Still's disease, 953 
Stokes-Adams's syndrome. 342 
Stomach, abscess of, 497 
amyloid, 168 
analysis of contents, 499, 500, 503, 

506, 513, 522 
anomalies of, 508 
arteriosclerosis of, 398 
atony of, 505 
atrophy of, 503 
cancer of, 519 

complications of, 520 

diagnosis of, 524 

differentiation of, 517, 524, 525, 

532 
etiology of, 514, 519 
histology of, 520 
localization of, 520 
pathology of, 519 
prognosis of, 525 
symptoms of, 521 
anemia, 523 
ascites, 524 
cachexia, 523 
digestive, 521, 522 
general, 521 

hematemesis, 517, 521, 526 
metastases, 524 
pain, 521 
toxemia, 523 



INDEX 



1015 



Stomach, cancer of, symptoms of, tumor, 
522 
urine, 523 
vomiting, 521 
treatment of, medical, 525 
surgical, 526 
cardia of, cancer of, 524 
catarrh of. See Gastritis, 
cirrhosis of, 503, 509 
congestion of, 369 
dilatation of, acute, 71, 504 
etiology of, 504 
prognosis of, 504 
symptoms of, 504 
treatment of, 504 
chronic, 504 

complications of, 507 
diagnosis of, 507, 532 
etiology of, 504 
signs of, 506 
symptoms of, 505 
treatment of, 507 
dimensions of, 506 
diseases of, 496 
form, changes in, 508 
hemorrhage from. See Hemateme- 

sis, 526 
hemorrhagic erosions of, 515 
hour-glass, 508 

inflammation of. See Gastritis, 
inflation of, 506 
insufficiency of, motor, 504 
lavage of, 497, 501, 508 
location of, 508 
motility of, tests, 506 
neuroses of, 527 
mixed, 533 
motor, 531 
secretory, 528 
sensory, 532 
pain in, 496, 499, 511, 514, 515, 517, 

521, 528, 529, 532 
perforation of, in cancer, 520 

in ulcer, 514 
prolapse of, 556 
round ulcer of, 509 

complications of, 514 
course of, 513 
diagnosis of, 514 
differentiation of, 515, 517, 

532 
etiology of, 510 
frequency of, 510 
localization of, 490, 514 
pathology of, 510 
prognosis of, 516 
symptoms of, 510 
general, 510 
hematemesis, 512 
hyperchlorhydria, 513 
pain, 511 
vomiting, 513 
treatment of, diet, 518 
gastric rest, 516 
hyperacidity, 516 
medicinal, 518 
pain, 516 
rest, 516 



Stomach, round ulcer of, treatment of, 
surgical, 519 
symptomatic, 518 
types of, 513 

size of, 506, 508 

syphilis of, 204 

tuberculosis of, 167, 175 

tumors of, 519, 525 

ulcer. See Stomach, Round ulcer. 

ulceration of, syphilitic, 204 
typhoid, 34, 35 

volvulus of, 507 
Stomatitis, aphthous, 478 

catarrhal, 477 

epidemic, 301 

gangrenous, 479 

parasitic, 479 

ulcerative, 477 
Stomatomycosis o'idica, 479 
Stones, fecal, 551, 552, 596 

of kidneys, q. v. 
Strabismus, 878 
Stramonium, 430 

Strawberry tongue, scarlatinal, 264 
Streptococcus. See Septic infections, 21 

in diphtheria, 79, 81 

endocarditis, 347 

in erysipelas, 58 

in rheumatism, 281 

in scarlatina, 261 

sore throat, 486 
Streptothricosis, 165 
Streptothrix, pseudotuberculosis, 165 
Strongyloides intestinalis, 316 
Strophanthus, 76, 336, 375 
Struma lipomatoses aberrans renis, 663 
Strumitis, 708 
Strychnine poisoning, diagnosis of, 135 

therapeutics, 56, 58, 76, 188, 269, 376, 
562 
Subphrenic abscess, 611 

differentiation from pneumo- 
thorax, 472 
from pleurisy, 465 

pyopneumothorax, 611 
Subsultus tendinum in typhoid fever, 33 
Succussio Hippocratis, 471 
Sudor anglicus, 299 
Sugar, therapeutics, 56 
Sulphonal, 377, 917 
Sulphuric acid, 124 
Summer catarrh, 412 
Sunstroke, diagnosis of, 976 

etiology of, 975 

symptoms of, 975 

treatment of, 976 
Suprarenal glands, degenerations of, 704 
diseases of, 701 
physiology of, 702 
tuberculosis of, 701 
tumors of, 704 
Suralimentation, 186 
Sweats, therapy of, 636 
Sympathetic nerves, irritation of, 944 

paralysis of, 944 
Synechia pericardii, 389 
Synovitis, sj^philitie, 218 
Syphilis, 197 



1016 



INDEX 



Syphilis, accidental, 199 
acquired, 198 

associated conditions, 221 
bacteriology, 198 
course of, abnormal, 220 
etiology of, 198 

accidental, 199 

sexual intercourse, 198 
life assurance in, 221 
symptoms of, 201 

aorta, 208, 401 

blood, 208, 219 

bloodvessels, 209 

bone, 217 

brain, 211, 790 

arterial disease, 211 
differentiation, 211, 212, 

790, 796 
gumma, 213, 790 
meningitis, 212 
nerves, cerebral, 212 

chancre, 199 

characteristics, 199 
course of, 200 
differentiation of, 200 
extragenital, 199 
female, 199 
histology of, 200 
male, 199 
perigenital, 199 

circulatory, 207, 401 

ear, 216 

eruptions, 201 

eye, 214 

choroid, 215 
conjunctiva, 214 
cornea, 214 
iris, 214 
muscles, 215 
orbit, 216 
retina, 215 

fever, 201, 206 

gastro-intestinal, 203 
esophagus, 204 
intestine, 204 
mouth, 203 
pancreas, 205 
rectum, 204 
stomach, 204 

genitalia, 216 
cervix, 217 
ovaries, 217 
penis, 216 
testes, 216 
tubes, 217 
vagina, 216 
vas deferens, 216 
vulva, 216 

gummata of aorta, 208, 401 
of bones, 217 
of brain, 213, 790 
of bronchi, 210 
of ear, 216 
of esophagus, 204 
of eye, 214 
of heart, 207 
of intestines, 204 
of joints, 218 



Syphilis, acquired, symptoms of, gummata 
of kidney, 207 
of larynx, 209 
of liver, 206 
of lungs, 210 
of mammae, 218 
of meninges, 212 
of mouth, 203 
of muscles, 216 
of nose, 209 
of ovary, 217 
of penis, 216 
of peritoneum, 205 
of pharynx, 204 
of rectum, 204 
of skin, 202 
of spleen, 205 
of stomach, 204 
of tendons, 218 
of testis, 216 
of trachea, 209 
of tubes, 217 
of uterus, 217 
of vagina, 216 
of vessels, 208, 211 
of vulva, 216 

heart, 207 

immunity, 220 

joints, 217, 743, 954 

kidney, 207 

liver, 205 

lymphadenitis, 200 

lymphangitis, 200 

mammas, 218 

muscles, 216 

nervous, 210 

onychia, 203 

primary lesion, 199 

respiratory, 209 
bronchi, 210 
larynx, 180, 209 
lungs, 210 
nose, 209 
trachea, 209 

secondary, 201 

enanthem, 201 
exanthem, 201 
lymphadenitis, 200 

skin, 201 

spleen, 205 

syphilides, 201 

tertiary, 198, 201 
treatment of, 224 

initial stage, 224 

local, 224 

prophylactic, 224 

secondary, 224 

tertiary, 227 
of bones, differentiation of, 745 
of brain, 211, 213, 790, 796, 803, 846 
of bronchi, 210 
cachexia, 221 
congenital, 221 
diabetes insipidus in, 212 

mellitus in, 212 
diagnosis, 219 ; 

ex juvantibus, 227 
luetin test, 219 



INDEX 



ior 



Syphilis, diagnosis, treponema, 219 

Wassermann, 219, 229 
hemorrhagica neonatorum, 223, 694 
hereditary, 221 

diagnosis of, 223 

influence on child, 221, 222 

parental, 221 

symptoms of, 222 
incubation of, 199 
of larynx, 180, 209 
leukoderma, 202 
leukoplakia, 203 
of liver, differentiation of, 205, 206, 

587 . 
of lungs, 210 
lymph glands, 200, 203 
malignant, 220 
nerves, 214 
of nose, 209 
parasyphilis, 198 
polyuria in, 212 
primary, 198, 199 
prognosis, 221 
secondary, 198, 201 
of spinal cord, 213 
spirochete, 198 
stages of, 198, 201 .' 
tertiary, 198, 201 
of trachea, 209 
treponema, 198 
Syringomyelia, 846 
arthropathies, 847 
bulbar, 848 
diagnosis of, 848 
differentiation of, 848 
etiology of, 846 
felons, 847 
pathology of,. 846 
prognosis of, 849 
symptoms of, 847 
treatment of, 849 
System diseases, 849, 857, 864 



Tabes dorsalis, 849 

complications of, 855 
course of, 855 
diagnosis of, 855 
differentiation of, 855, 871 
etiology of, 849 
pathology of, 850 
prognosis of, 855 
stages of, 850 
symptoms of, 850 

ataxia, 851 

crises, 854 

eyes, 853 

gait, 851 

motor, 851 

reflexes, 853 

Romberg's sign, 851 

sensory, 852 

trophic, 854 
treatment^ of, 856 
mesaraica, 171 
Tache bleudtre in typhoid fever, 30 



Tache cerebrale, 93 
Tachycardia, 340 

diagnosis of, 341 

etiology of, 340 

exophthalmic, 709 

prognosis of, 341 

treatment of, 341 
Taka-diastase, 502 
Talma-Drummond operation, 573 
Tannic acid, 55, 114, 124, 416, 484, 558 
Tannigen, 535, 543 
Tannin, 124 
Tape-worms, 302 
Taste, nerve of, 881, 885 
Teeth, Hutchinson's, 222 
Telangiectases, 414, 699 
Tender toes of Hanford in typhoid fever, 

32, 34 
Tendons, syphilis of, 218 
Tenia cucumerina, 305 

echinococcus, etiology of, 305 
localization of, 306 
multilocular form, 307 
pathology of, 305 
symptoms of, 305 

elliptica, 305 

mediocanellata, 304 

nana, 305 

saginata, 304 

solium, 302 
Terminal infections, 18 
Terpine hydrate, 188, 415, 422 
Test meal, 499, 506 
Testicles, syphilis of, 216 

tuberculosis of, 179 
Tetanus, 133 

in children, 135 

diagnosis of, 135 

differentiation of, 135, 296 

etiology of, 133, 257 

facialis, 135 

head, 135 

incubation in, 134 

neonatorum, 135 
trismus, 135 

prognosis of, 135 

puerperal, 136 

symptoms of, 134 

treatment of, 136 
Tetany, 715 

diagnosis of, 717 

etiology of, 715 

in gastric dilatation, 507, 508 

prognosis of, 717 

symptoms of, 716 

thyroid operation causing, 716 

treatment of, 508, 717 
Thalamic syndrome, 794 
Theocin, 377, 635 
Thiosinamin, 553 
Thomsen's disease, 933 
Thoracocentesis, 388, 458, 467 
Thrombophlebitis in chlorosis, 669, 784 

in septic infections, 20. See also 
Phlebitis. 
Thrush, 479 
Thymol, 314 
Thymus asthma, 718 



1018 



INDEX 



Thymus gland, abscess of, 718 
cyst of, 718 
diseases of, 718 
functions of, 718 
hemorrhage of, 718 
hypertrophy of, 718 
persistence of, 718 
tumors of, 718 
Thyroid extract, 714, 715 
gland, aberrant, 708 
accessory, 708 
cancer of, 708 
chondroma of, 708 
cysts of, 708 
diseases of, 707 
echinococcus of, 708 
goitre, 707 

exophthalmic, 709 
hypertrophy of, 708 
inflammation of, 708 
myxoma of, 708 
overactivity of, 709 
perversion of, 709 
strumitis, 708 
tumors of, 708 
Thyroidectomy, 708, 712 
Thyroidism, 709 
Tic, complex, 931 
convulsif, 887 
douloureaux, 940 
simple, 930 

with explosive utterances, 931 
Tinnitus aurium, 888 
Tobacco leukoplakia, 480 

pseudo- angina, q. v. 
Toe phenomenon, 770, 858, 859 
Toes, tender, Hanford's, 32, 34 
Toluol, 86 

Tongue, actinomycosis, 194 
cat's, 264 
diseases of, 480 
eczema of, 480 
glossitis, 480 
ichthyosis of, 480 
keratosis of, 480 
leukoplakia of, 480 
psoriasis of, 480 
scarlatinal, 264 
strawberry, 264 
syphilis of, 203 
tuberculosis of, 175 
in typhoid fever, 34 
Tonsillar hypertrophy, 488 
Tonsillitis, acute follicular, 485 

complications of, 486 
diagnosis of, 486 
etiology of, 485 
symptoms of, 486 
treatment of, 487 
chronic, 488 

diagnosis of, 489 
etiology of, 488 
symptoms of, 488 
treatment of, 489 
diphtheria, 80, 85 
in influenza, 104 
rheumatic, 282, 485 
septic, 486 



Tonsillitis, suppurative, etiology of, 487 
symptoms of, 487 
treatment of, 487 
Tonsils, diseases of, 485 
tuberculosis of, 175 
Tophi arthritici, 739, 740 
Tormina ventriculi, 531 
Torticollis, 895 
Tourette's disease, 931 
Toxemia, 17 
Trachea, diseases of, 418 

stenosis of, etiology of, 426 

symptoms of, 426 
syphilis of, 209 
tumors, 426 
Tracheal tugging, aneurysmal, 404 
Tracheitis in influenza, 104 
Tracheotomy in diphtheria, 89 
Transudates, character of fluid, 615 
Traube's space, 456 

tones, 355 
Traumatic neuroses, 918 
Trematodes, diseases caused by, 316 
Trembles, 300 
Tremor, exophthalmic, 710 
intention, 844, 845 
varieties of, 934, 936 
Treponema gambiense, 246 
pallidum, 198 
pertenue, 247 
Trichina spiralis, diagnosis of, 46, 308, 310 
etiology of, 308 
prognosis of, 310 
symptoms of, 309 
treatment of, 311 
Trichinosis, 308 

differentiation of, 46, 310 
Trichocephalus dispar, 315 
Trichomonas, 247 
Trichuris trichura, 316 
Tricuspid insufficiency, 363 
diagnosis of, 363 
etiology of, 363 
mechanism of, 363 
signs of, 363 
stenosis, 365 

congenital, 380 
Trismus, 134, 135, 882 
Trophedema, hereditary, 946 
Trophic neuroses, 744 
Trousseau's sign, 716 
Trypanosoma fever, 246 
Trypanosomiasis, 246 
Tubercle bacilli, 139 
Tubercles, postmortem, 183 
Tuberculin injections, 163, 164 

ophthalmoreaction, 164 
Pirquet's, 164 
Tuberculosis, 139 

of alimentary tract, 143, 175 
of aorta, 181 

arthritis, differentiation, 182, 954 
atrium of, 142 

by digestive tract, 143 
by direct inoculation, 143 
by respiratory tract, 142 
bacillus, 139 

chemistry, 140 



INDEX 



1019 



Tuberculosis, bacillus, cultures, 140 
morphology, 139 
staining, 140 
of bladder, 179 
of bloodvessels, 180 
of bones, 181, 182 
of brain, 175, 789, 796 
of bronchial glands, 109, 169 
choroidal, 150, 152 
congenital, 143 
of ear, 180 
of esophagus, 175 
etiology of, 139 
extension of, mode of, 146 
of eye, 175 

of Fallopian tubes, 180 
of genitalia, 179, 180 
of genito-urinary tract, 177 
of gums, 175 
of heart, 181 
herpes in, 150 

histopathology of tubercle, 145 
influenza, as cause of, 104 
of intestines, 176 
of joints, 181, 182, 954 
of kidney, 177 

etiology of, 177 
pathology of, 178 
symptoms of, 178 
general, 179 
local, 178 
urinary, 178 
of larynx, 180 

etiology of, 180 
forms of, 181 
pathology of, 181 
symptoms of, 180 
treatment of, 181 
latent, 141 
of lips, 175 
of liver, 167, 177 
of lungs, 152 

in aged, 163 
in children, 162 
complications of, 165 

amyloid degeneration, 168 
circulatory, 166 
digestive, 167 
genito-urinary, 168 
muscular, 167 
nervous, 167 
respiratory, 165 
skin, 168 
course of, 160 
in diabetes, 731, 736 
diagnosis of, 126, 163, 206, 423, 

425 
extension of, 152 
forms of, acute, 160 

disseminated, 161 
galloping, 160 
miliary, 162, 146 
pneumonic, 74, 160 
ulcerative, 162 
chronic, 162 

fibrous phthisis, 162 
pleuritic, 162 
ulcerative, 162 



Tuberculosis of lungs, pathology of, 152 
prognosis of, 165 
stages of, confirmed, 160 
consummated, 160 
incipient, 160 
symptoms of, 153 
general, 155 
physical signs, 156, 159 
respiratory, local, 153 
treatment, 183 
lymphadenitis, differentiation from 

pseudoleukemia, 171, 689 
of lymph glands, 168 

bronchial adenitis of, 169 

diagnosis of, 109, 170, 

689 
issues of, 170 
signs of, 170 
symptoms of, 170 
cervical adenitis, 169 

atrium of, 169 
pathology of, 169 
symptoms of, 169 
characteristics, 169 
etiology of, 168 
generalized adenitis, 171 
mesenteric adenitis, 170 
pathology of, 169 
treatment of, 171 
of mammae, 180 
of meninges, 149, 150, 175 
meningitis. See Meningitis, tuber- 
culous, 149, 150 
of mesenteric glands, 170 
miliary, acute, 146 

diagnosis of, 46, 47 
etiology of, 146 
prognosis of, 150 
remissions of, 150 
symptoms of, 147 

choroidal tubercles, 

150, 152 
circulatory, 149 
digestive, 149 
fever, 148 
nervous, 149 
respiratory, 149 
types, 147 
chronic, 150 

differentiation of, 46, 47, 104, 
148, 149 
mixed infection, 141 
of muscles, 183 
of nasopharynx, 175, 180 
of nose, 180 
of palate, 175 
of pericardium, 171, 387 
of peritoneum, 172 
course of, 174 
diagnosis of, 174 
differentiation of, 172, 173, 174, 

616 
etiology of, 172 
symptoms of, 173 
adhesions, 173 
ascites, 173 
exudation, 173 
fever, 172 



1020 



INDEX 



Tuberculosis of peritoneum, symptoms of, 
friction, 174 
gastro-intestinal, 174 
meteorism, 173 
pain, 172, 174 
pelvic effusion, 174 
retraction, 173 
treatment of, 174 
types of, 172 
of pharynx, 175 
of placenta, 143 

of pleura, 171, 453, 454, 460, 461 
prevalence of, in animals, 141 

in man, 141 
prognosis of, 165 
of prostate, 179 
pseudotuberculosis, 141, 165 
quiescent, 141 
roseolae in, 150 
of salivary glands, 175 
of serous membranes, 171 
of skin, 150, 183 
of spleen, 177 
of stomach, 175 
of suprarenal glands, 701 
of testicle, 179 
of tongue, 175 
of tonsils, 175 
treatment of, 183 
expectant, 187 
cough, 187 

digestive disorders, 189 
dyspnea, 189 
fever, 187 
hemoptysis, 188 
insomnia, 189 
pain, 189 

sexual symptoms, 190 
sweats, 188 
hygienic, 184 
food, 186 
fresh air, 184 
rest, 186 
prophylactic, 183 

antibacillary, 183 
governmental, 184 
individual, 184 
specific, 186 
tuberculin, 186 
in typhoid fever, 40 
of ureter, 179 

vaccination as cause of, 257 
Tuffnell treatment, 408 
Tumor albus, syphilitic, 218 
Turpentine, 55, 188, 189, 416, 422 
Tussis hepatica, 577 
Tympanites, treatment of, 55 
Typhlitis, tuberculous, 176 
Typhoid fever, 24 
in aged, 43 

anomalous courses of, 41 
bacillus, 25 
carriers, 25, 49 
in children, 42 
chills in, 28, 44 
clinical types of, 26, 41 
convalescence of, 27, 44 
diagnosis of, 44 



Typhoid fever, differentiation of, from 
anthrax, 45 

from endocarditis, 46, 47, 
345 

from enteritis, 45 

from gastritis, 45 

from influenza, 105 

from malaria, 46, 47, 239 

from meningitis, 46, 47 

from miliary tuberculosis, 
46, 47, 147 

from paratyphoid, 45 

from pneumonia, 44 

from sepsis, 46, 47 

from syphilis, 206 

from trichinosis, 46 

from typhus fever, 278, 279 
etiology of, 25 

bacillus typhosus, 25 

predisposing, 26 
exacerbations of, 43 
gall-stones in, relation of, 38 
hemorrhage, 36 
immunity from, 26 
incubation of, 26 
onset of, 26 
paratyphoid, 26 
perforation, 37 
prognosis of, 47 
recrudescences of, 43 
relapses of, 43 
"scarlet-typhoid," 264 
second attacks of, 26 
spine in, 41 
state, 33, 44 
sudoral type of, 28, 30 
symptoms of, 26 

bone, 41 

cardinal, 44 

circulatory, 30 

contra-indicating, 44 

dermal, 29 

digestive tract, 34 

fever, 27 

genito-urinary, 40 

joint, 41 

muscle, 41 

nervous, 33 

pulse, 30 

respiratory, 39 

secondary, 44 

special senses, 41 

splenic tumor, 28 

thyroid gland, 41 
treatment of, 48 

antipyresis, 50 

antiseptic, 50 

of bacilluria, 57 

of bed-sores, 57 

caloric feeding, 53 

care of skin, 57 

of circulatory symptoms, 56 

of convalescence, 57 

of diarrhea, 55 

diet, 52 

of epistaxis, 57 

expectant, 54 

of hemorrhage, 55 



INDEX 



1021 



Typhoid fever, treatment of, hygienic, 50 
of nervous symptoms, 57 
of perforation, 56 
prophylactic, 48 
of respiratory symptoms, 57 
specific, 50 
symptomatic, 54 
of thrombophlebitis, 57 
of tympany, 55 
vaccines, 50 
vomiting, 54 
types, 26, 41 
Typhoidette, 42 
Typhus fever, 276 

differentiation of, 274, 278, 279 
etiology of, 276 
exanthematous, 276 
prognosis of, 279 
symptoms of, 276 
treatment of, 279 
icteroides, 293 

recurrens. See Recurrent fever. 
Tyrotoxismus, 970 



U 



Ulcus perforans of stomach, 509 

rotundum of stomach, 509 
Uncinaria duodenalis, 311 
Uncinariasis, 311 
Urates in urine, 650 
Uremia, 630 

coma from, 631, 772 

convulsions from, 630 

diagnosis of, 632 

differentiation of, 632 

etiology of, 630 

latent, 659 

scarlatinal, 265 

symptoms of, 630 
cardiac, 631 
digestive, 631 
nervous, 630 
respiratory, 631 

treatment of, 633-638 
Ureter, calculus of, 660, 661 

tuberculosis of, 179 

tumor of, 662 
Uric acid in urine, 650, 738 
Urine, albumin in, 644 

alkaptone in, 651 

bile in, 589 

blood in, 647 

casts in, 620, 625, 629 

chyle in, 649 

fat in, 650 

febrile, 40 > 

hematoporphyrin in, 651 

hydrochinon in, 651 

indican in, 651 

melanin in, 579 

in nephritis, 620, 625, 628 

oxalates in, 651 

phosphates in, 650" 

pus in, 649 

tests of, elimination, 635 

urates in, 650, 738 



Urine, uric acid in, 650 
Urobilin, icterus, 588, 590 
Urobilinuria, 589 
Urostealiths, 658 

Urotropin. See Hexamethylenamina. 
Urticaria, visceral crises in, 693 
Uterus, syphilis of, 217, 222 
tuberculosis of, 180 



Vaccination, 256, 257 
Vaccine therapy, 23, 24 
in gonorrhea, 139 
in typhoid, 50 
Vaccinia, 256 
Vagina, syphilis of, 216 
Vagus. See Nerves, vagus. 
Valerian, 336, 338 
Valleix's points, 940 
Valsalva's experiment, 386 
Valvular disease, chronic. See Aortic 
insufficiency, etc. 
combined lesions, 365 
etiology, 350 
general symptoms of, 366 
insufficiency, 351 
pathology, 350 
prognosis, 370 
stenosis, 351 
treatment, 371 
heart disease. See Aortic insuffi- 
ciency, etc. 
Vaquez's disease, 691 
Varicella. See Chicken-pox. 
Variola. See Smallpox. 
Varioloid, 252 

Vas deferens, syphilis of, 216 
Vasomotor neuroses, 744 
Veins, syphilis of, 209 
Venesection. See Phlebotomy. 
Veratrum, therapeutics of, 338, 637 
Veronal, therapeutics of, 57 
Vertigo, auditory, 888 
cerebellar, 762 
e stomacho lseso, 500 
ocular, 889 
Vincent's angina, 485, 484 
Visceroptosis, 555 
Vision, centre for, 753, 874 

fields of, 875, 907 
Vocal cords, paralysis of, 891-893 

spasm of, 982 
Volvulus, 550 

diagnosis of, 552 
differentiation of, 552 
etiology of, 550 
gastric, 507 
pathology of, 550 
symptoms of, 550 
treatment of, 553 
Vomiting in brain tumor, 792, 795 
cyclic, 531 

differentiation of, 532 
in gastric cancer, 517, 521 
dilatation, 505 
ulcer, 512, 513, 517 



1022 



INDEX 



Vomiting in gastritis, 496, 499 
in meningitis, 91 
nervous, 531 

causes of, 531 
differentiation of, 532 
in pneumonia, 69 
in tuberculosis, 167 
in typhoid fever, 35 

treatment of, 54, 55 
Vomitus, coffee-grounas, 512, 517, 521, 
526 
cruentus, 527 
v. Eiselberg's sign, in hour-glass stomach, 

509 
v. Graefe's si°n, 710 , 4 , 

v. Pirqur b s test, 164 
Voussure, pericarditic, 383 
Vulva, syphilis of, 216 
Vulvovaginitis, diphtheritic, 82 



W 



Wassermann reaction, 219, 229 
Water, 635 
Weil's disease, 299 

diagnosis of, 300 

etiology of, 299 

prognosis of, 300 

symptoms of, 299 

treatment of, 300 
Werlhof's disease, 693 
Westphal's sign, 853 
Whip-worm, 315 
Whooping-cough, 106 

"after-pertussis," 109 

complications of, 108 

bronchopneumonia, 108 
convulsions, 108 
glottis, spasm of, 108 
hemorrhages, 108 

course of, 107 

diagnosis of, 109 

differentiation of, 108 

etiology of, 107 

prognosis of, 109 

sequels of, 108 * 

symptoms of, 107 

convulsive stage, 107 

treatment of, 109 
Widal test, 32 
Widal's syndrome, 590 
Winckel's disease, 694 



Wintrich change of note, 159 

Wolff-Eisner reaction, 164 

Wolfler's sign in hour-glass stomach, 509 

Wooden-tongue, 194 

Woolsorters' disease, 130 

Word-blindness, 753 

Wound diphtheria, 82 

Writers' cramo, 932 

diagnosis of, 933 

etiology of, 932 

symptoms of, 933 

treatment of, 933 
Wryneck, 895 



Xanthelasma in icterus, 590 
Xanthopsia in icterus, 590 
Xerostomia, 481 
X-rays, 458, 515, 524, 596, 660 



Yaws, 247 

Yeast, pseudotuberculosis, 165 

Yellow fever, 291 

complications of, 293 

diagnosis of, 293 

etiology of, 291 

prognosis of, 294 

sequels of, 293 

symptoms of, general, 292 
stages of, 292 
special, 292 

black vomit, 293 
circulatory, 293 
digestive, 293 
fever, 292 
hemorrhages, 293 
icterus, 293 
liver, 293 
nervous, 292 
urine, 293 

treatment of, 294 



Zinc oxide, 502 
Zomotherapy, 186 
Zoonoses, 127 
Zuckergussleber, 612, 616 






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